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40 Cards in this Set
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- 3rd side (hint)
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1. What are the two ways in which fever is beneficial to the immune response against antigen?
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High temperature inhibits pathogen growth in 2 ways
1. Elevates temp. above the optimum growth temp. of the pathogen 2. Activating and speeding up the number of other body defenses |
Fever:
Hypothalamus controls temperature by regulating the blood flow to the skin and the amount of sweating and respiration Higher temp is caused by pro-inflammatory cytokines Pyrogens –fever inducing substances Endogenous- fever inducing cytokines Exogenous- fever inducing substances introduces from an external source; bacterial endotoxins |
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2. How is the complement system activated? What effects can complement activation have upon foreign cells?
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The complement system can be activated in two main ways.
The first means of activation is part of the innate (natural) immune response. (i.e.; neither antibodies nor T cell receptors are involved.) For example, certain polysaccharides found on the surface of bacteria can activate the system. This can occur immediately and does not require prior exposure to the molecules. The second and most potent means occurs in a adaptive immune response when antibodies (IgG or IgM) binds to antigen at the surface of a cell. This exposes the Fc region of the antibody in a way that allows the first complement protein (C1) to bind. |
Historically, the term complement (C) was used to refer to a heat-labile serum component that was able to lyse bacteria (activity is destroyed (inactivated) by heating serum at 56 degrees C for 30 minutes). However, complement is now known to contribute to host defenses in other ways as well. Complement can opsonize bacteria for enhanced phagocytosis; it can recruit and activate various cells including polymorphonuclear cells (PMNs) and macrophages; it can participate in regulation of antibody responses and it can aid in the clearance of immune complexes and apoptotic cells. Complement can also have detrimental effects for the host; it contributes to inflammation and tissue damage and it can trigger anaphylaxis.
Complement comprises over 20 different serum proteins (see Table 1) that are produced by a variety of cells including, hepatocytes, macrophages and gut epithelial cells. Some complement proteins bind to immunoglobulins or to membrane components of cells. Others are proenzymes that, when activated, cleave one or more other complement proteins. Upon cleavage some of the complement proteins yield fragments that activate cells, increase vascular permeability or opsonize bacteria. |
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3. The activation of complement by antigen-antibody complexes is known as:
a. Classical pathway b. Alternative pathway c. Chemotaxis d. Inflammation The ultimate result in either pathway is the creation of the membrane attack complex, a large pore in the cell membrane that results in cell lysis. |
a. Classical pathway
The Classical pathway of activation of the complement system is a group of blood proteins that mediate the specific antibody response. The main activators of the Classical Pathway are antigen-antibody complexes. |
the alternative pathway is antibody independent. The alternative pathway starts with the spontaneous conversion of C3 to an active protease. C3 contains a thioester group that is spontaneously hydrolyzed at a slow rate to create C3(H2O). From there, binding of factor B (Fb) and activation by factor D (Fd) cleaves factor B to create the active protease C3 convertase (AP convertase). This enzyme cleaves C3 to form C3b, which can go on to form a C5 activating convertase. At this point the alternative pathway proceeds in the same manner as the classical pathway, recruiting additional complement factors (C6, C7, C8 and C9) to ultimately form the membrane attack complex and lyse the associated cell.
One question about the alternative pathway is how the spontaneous activation of C3 in plasma leads to the lysis of specific cells in the absence of antibody on the cell surface. Active C3b binds to the cell surface, particularly to complement activators like cell wall components and lipopolysaccharide. A constant low level of spontaneous C3b formation ensures that C3b can bind to invading cells and trigger the rest of the alternative complement pathway to lyse the cells even in the absence of an antibody response. The constant low level of C3b activation and potential activation of the alternative pathway is kept in check by a natural damper, factor H and factor I. Factors H and I in plasma inactivate C3b enzyme in solution. Factors H and I cannot inactivate C3b on the cell surface due to protection by properdin, ensuring that the alternative pathway is primarily inactive in plasma and specifically activated on the surface of invading. |
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4. What consists of tissue debris, remains of digested microorganisms, injured cells and dead phagocytes?
a. Pus b. Plasma c. Opsonin d. Tonsils e. Membrane attack complexes |
a. Pus
Pus is a whitish-yellow, yellow, or yellow-brown exudate produced by vertebrates during inflammatory pyogenic bacterial infections. Pus is viscous material composed of these dead neutrophils. Pus has a foul odor. An accumulation of pus in an enclosed tissue space is known as an abscess, whereas a visible collection of pus within or beneath the epidermis is known as a pustule or pimple. Pus is produced from the dead and living cells that travel into the intercellular spaces around the affected cells. |
Something that creates pus= suppurative, pyogenic, or purulent.
If it creates mucus=mucopurulent. (most common agents that induce pus formation are bacteria, such as Staphylococcus aureus) In addition, some chemical agents can cause pus creation. Pus consists of a thin, protein-rich fluid, "liquor puris" & dead cells (part of the body's immune response). Neutrophils are produced in the bone marrow and released into the blood. When the need to fight infection arises, they move to the site of infection by a process known as chemotaxis, usually triggered by cytokines released from macrophages that sense invading organisms. At the site of infection, the neutrophils engulf and kill bacteria. Eventually, the neutrophils die, and are then phagocytosed by macrophages, which break them down further. Pus is viscous material composed of these dead neutrophils. Neutrophils are the most abundant type of leukocyte in human blood, making up anywhere between 40% and 75% of leukocytes. When seen in a wound or dry skin, pus indicates the area is infected and should be cleaned with antiseptic. Despite normally being of a whitish-yellow hue, changes in the color of pus can be observed under certain circumstances. Pus is sometimes green because of the presence of myeloperoxidase, an intensely green antibacterial protein produced by some types of white blood cells. Blue-green pus is found in certain infections of Pseudomonas aeruginosa as a result of the pyocyanin bacterial pigment it produces; amoebic abscesses of the liver produce brownish pus. Pus can also have a foul odor. In almost all cases when there is a collection of pus anywhere in the body, the clinician will try to create an opening for it to evacuate - this principle has been distilled into the famous Latin aphorism "Ubi pus, ibi evacua!" |
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5. All of the following are true of complement EXCEPT:
a. Some of the components are involved in chemotaxis b. It is activated only by endotoxin c. It often results in the lysis of the cell membrane d. Some components can stimulate phagocytosis |
b. It is activated only by endotoxin
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Complement:
- Some of the components are involved in chemotaxis (Neutrophils in bone marrow --> most common leukocytes 40%-75% --> macrophages sense invading organisms --> and trigger cytokines --> initiates chemotaxis --> neutrophils move to site of infection to engulf and kill bacteria --> they are then phagocytosed by macrophages which break them down further -->Pus which is composed of these dead neutrophils. - It often results in the lysis of the cell membrane - Some components can stimulate phagocytosis (macrophages) |
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6. Which of the following are phagocytic cells?
a. Neutrophils and basophils b. Neutrophils and monocytes c. Basophils and monocytes d. Eosinophils and monocytes |
b. Neutrophils and monocytes
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The innate leukocytes include: Natural killer cells, mast cells, eosinophils, basophils; and the phagocytic cells including macrophages, neutrophils and dendritic cells, and function within the immune system by identifying and eliminating pathogens that might cause infection.[3]
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7. _____________________ are also known as polymorphonuclear leukocytes.
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Neutrophils
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8. Phagolysosomes fuse with a phagosome to produce a lysosome (True or False)
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False
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A lysosome fuses with the phagosome to form a phagolysosome and the virus is degraded.
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9. Phagocytes may stick to the inner lining of blood vessels before passing through the vessel wall to the damaged area; this action is called___________________.
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diapedisis
the outward passage of blood cells through intact vessel walls. |
Phagocytes adhere to the endothelium via the interaction of leukocyte and endothelial adhesion molecules and then roll down the endothelial surface. This porcess is called margination.
As the phagocyte rolls over the endothelial cells, the endothelial cells retract and additional ahdhesion molecules are expressed that allow for firm adhesion of the phagocyte to the endothelial surface. The phagocyte squeezes b/t the endothelial cells using yet another type of adhesion molecule. It then moves thru the basement membrane before moving thru the tissue to the area of injury. |
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10. The host response to tissue damage characterized by redness, pain, heat and swelling is called ___________________.
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inflammation
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Basophils and Mast cells contribute to inflammation
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11. A granulocyte that releases the inflammatory agent histamine
a. Neutrophil b. Basophil c. Dendritic cell d. T cell e. Natural killer cell |
b. Basophil
Basophils and Mast cells release histamine |
"Basophils release the histamine when such an allergic reaction happens. Antihistamines are medicines which prevent histamine from having the effects which make us ill, and they work well in hay fever and most kinds of hives or 'urticaria'. Basophils are very similar to another kind of cell, the mast cell, which does not live in the bloodstream but in the lungs, nose, skin, gut, heart and other organs and is important in allergy. Both kinds of cell release histamine in allergic reactions. Unfortunately they also release quite a lot of other things which are rather similar to histamine in their effects. But antihistamines don't work against these other substances. This means that antihistamines may not make much difference to some allergic illnesses. For example antihistamines help asthma so little that we usually don't use them for asthma. In anaphylactic reactions (anaphylaxis) antihistamines are utterly inadequate on their own if the reaction is at all serious."
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12. Which of the following does NOT partake in the process of phagocytosis
a. Chemotaxis b. Attachment c. Digestion d. Granulation e. Engulfment |
d. Granulation
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1. Activation of the Phagocyte = circulating phagocytes produce surface glycoprotein receptors that increase their ability to adhere to the inner surface of capillary walls, enabling them to squeeze out of the capillary and be attracted to the site of infection. In addition, they produce endocytic pattern-recognition receptors (def) that recognize and bind to pathogen-associated molecular patterns or PAMPs (def) - components of common microbial molecules such as peptidoglycan, teichoic acids, lipopolysaccharide, and mannose that are not found in human cells - to attach the microbe to the phagocyte for what is called unenhanced attachment (discussed below).
2. Chemotaxis of Phagocytes 3. Attachment of the Phagocyte to the Microbe or Cell Enhanced attachment, Extracellular trapping with NETs 4. Engulfment + Digestion = Ingestion of the Microbe or Cell by the Phagocyte |
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13. Related to the complement system is a protein named ____________________ that is found on the mucous membrane and also forms holes in bacterial cell walls.
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defensin
Defensins are short antimicrobial peptides produced by neutrophils and epithelial cells. They fxn by inserting (making holes) into bacterial membranes, forming pores that disrupt the integrity of the cell. Alpha & Beta defensins |
The epithelial cells that line our guts provide a pretty good physical barrier themselves, but they're no match for pathogens. Instead, they rely on a number of chemical barriers - proteins and other molecules that can kill or repel bacteria without harming your own cells. One of the most abundant of these so-called anti microbial peptides is human β-defensin1 (hBD-1), but there's just one problem: it kinda sucks at killing bacteria.
There are a number of different defensins, and most of them are potent microbicides, but you can dump loads of β-defensin1 on bacteria and they'll mostly shrug it off. Why would the most abundant defensin in the gut be so terrible at, you know, defending? Reduction of disulphide bonds unmasks potent antimicrobial activity of human β-defensin 1 |
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14. What two proteins inhibit microbial growth by reducing the amount of available iron found in tissue? Why would this inhibit the growth of the microorganism?
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Lactoferrin and Transferrin
Lactoferrin is an iron binding protein found in saliva, mucous and milk; it is also found in some types of phagocytic cells. Transferrin (a similar compund) is found in blood and tissue fluids. pg 349 |
Iron (important element required for growth) By sequestering iron, lactoferrin and transferrin withhold this essential element from the microbes and they can not grow. Some bacteria make compunds that capture iron from the host - thus circumventing this defense.
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15. The complement component that aids in inflammation by forming a concentration gradient that cells of the immune system can follow to the site of infection is:
a. C3b b. C3a c. C5b d. C5a |
d. C5a
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Components of the Classical Pathway
Native component Active component(s) Function(s) C1(q,r,s) C1q Binds to antibody that has bound antigen, activates C1r. C1r Cleaves C1s to activate protease function. C1s Cleaves C2 and C4. C2 C2a Unknown. C2b Active enzyme of classical pathway; cleaves C3 and C5. C3 C3a Mediates inflammation; anaphylatoxin. C3b Binds C5 for cleavage by C2b. Binds cell surfaces for opsonization and activation of alternate pathway. C4 C4a Mediates inflammation. C4b Binds C2 for cleavage by C1s. Binds cell surfaces for opsonization. Components of the Alternate Pathway Native component Active component(s) Function(s) C3 C3a Mediates inflammation; anaphylatoxin. C3b Binds cell surfaces for opsonization and activation of alternate pathway. Factor B B Binds membrane bound C3b. Cleaved by Factor D. Ba Unknown. Bb Cleaved form stabilized by P produces C3 convertase. Factor D D Cleaves Factor B when bound to C3b. Properdin P Binds and stabilizes membrane bound C3bBb. Components of the Membrane-Attack Complex Native component Active component(s) Function(s) C5 C5a Mediates inflammation; anaphylatoxin, chemotaxin. C5b Initiates assembly of the membrane-attack complex (MAC). C6 C6 Binds C5b, forms acceptor for C7. C7 C7 Binds C5b6, inserts into membrane, forms acceptor for C8. C8 C8 Binds C5b67, initiates C9 polymerization. C9 C9n Polymerizes around C5b678 to form channel that causes cell lysis. |
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16. All cells of the blood are made in the bone marrow from a single type of stem cell. What is the name of this process and stem cell, and how does the bone marrow know which cells of the blood to make?
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Hematopoiesis is the name of the process. All originate from the same stem cell hematopoietic stem cell found in bone marrow in the medullary canal of long and flat bones.
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hematopoietic stem cell --> hemocytoblasts mature into 3 blood cells = RBC's (erythrocytes), WBCs (leukoctyes) and Thrombocytes (Platelets) WBCs (Leukocytes) --> granulocytes (neutrophils, eosinophils, basophils) and agranulocytes (B-lymphocytes and T-lymphocytes) greek for "blood" hemato and "to make" poiesis pg 350 |
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17. The skin and mucous membranes have several antimicrobial substances that deter microbial invasion. List and explain 4 of these substances.
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There are 6 first line defenses that deter microbial invasion: (skin, mucosa, PRR (Toll-like receptors and NODs or nucleotide-binding oligomerization domain), complement proteins, inflammation and fever.
In he skin and mucous membranes, 4 substances inhibit or kill microorganisms = 1. sweat (high in salt) as it evaporates, it leaves a salty residue, inhibiting many organisms that might otherwise proliferate the skin. 2. Lysozyme, enzyme found in tears, saliva and mucous that bathes mucous membranes. It degrades peptidoglycan (the cell membrane of bacteria cell wall.) It is also found in phagoctyes, blood and interstitial fluid (teh fluid that bathes tissues). 3. Peroxidase enzymes - found in saliva and milk, also found in phagocytes and body tissues. These enzymes break down hydrogen peroxide and in the process produce potent oxidizing compounds. This is called peroxidase-killing and only certain bacteria (catalase-negative bacteria) can be killed. Catalase-positive bacteria produce catalase that destroys and breaks down hydrogen peroxide and so the peroxidase enzyme has no hydrogen peroxide to combine with in order to produce potent oxidizing compounds. 4. Lactoferrin and Transferrin (defensins) Lactoferrin is an iron building protein foudn in saliva, mucous and milk, and also in phagocytes (some types). A similar compound, transferrin is found in blood & tissue fluids. Iron is a major element of growth, without they cannot grow and survive. Some bacteria though make compounds that capture iron from the host and thwarting this defense. pg 348-349 |
The epidermis is the outer layer of skin. The majority of cells (95%) are specialised epithelial cells called keratinocytes which produce a tough protein called keratin. There are five distinct sub-layers of cells that represent the different stages in the keratinisation process. New skin cells are produced at the basal membrane (deepest epidermal layer) pushing the older cells towards the surface. As the keratinocytes get older and migrate closer to the skin's surface they change from being square-shaped to flat, they become engorged with keratin and eventually die, losing all of their internal structures. These overlapping, closely packed layers of keratinized cells form a permeable barrier and are able to withstand scuffs and scrapes. It takes 40-60 days for keratinocytes to reach the surface of the skin where they are sloughed away.
There are 6 first line defenses that deter microbial invasion: (skin, mucosa, PRR (Toll-like receptors and NODs or nucleotide-binding oligomerization domain), complement proteins, inflammation and fever. Skin: 1. made of stratified squamous keratinized epithelial tissue (Keratin is a poly lipid that is arid, tough & hardened and waterproof). This prevents microbes from penetrating through the skin. 2. Also, keritanocytes are constantly being produced in the basal membrane and as the new cells are produced, the older cells get pushed upward toward the surface. They change from being square shaped to flat or squamous. They become engorged with keratin and die. When they die, they are sloughed off the outermost layer and any attached microbes will get sloughed off along with them. This constant sloughing minimizes the potential for infection. 3. Mucous membranes line the digestive tract, respiratory tract and genitourinary tract. they are constantly bathed with mucus or other secretions that help wash microbes from the surface. 4. Peristalsis rhythmic contractions that push the food through the digestive tract and also push the microbes as well to an area where they are more easily expelled. Cilia propel materials away from the lungs and upward the respiratory tract so they can be exhaled or coughed up and expelled from the body. This free ride out of the respiratory tract is reffered to as mucociliary escalator. |
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18. What are the two ways that your normal flora (normal microbiota) protects you against microbial invaders.
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1. one protective effect of normal microbiota is competitive exclusion of pathogens. The normal flora prevents invading organisms from adhering to host cells by covering binding sites that might otherwise be used by less desirable organisms.
2. They produce toxic compounds. Ex. Propionibacterium species that degrades lipids found in skin glands, releasing fatty acids that inhibit the growth of many pathogens. 18. pg 349-350 |
In the GI tract, some strains of E. coli synthesize colicins, proteins toxic to other strains of bacteria. Lactobacillus species growing in the vagina produce lactic acid as a fermentation end product, resulting in an acidic pH that inhibits the growth of some potential disease causing organisms. Disruption of the normal microbiota which occurs when antibiotics are used can predispose a person to various infections. Ex. antibiotic producing diarrhea, caused by growth of toxin producing strains of Clostridium difficile in the intestine or vulvovaginitis, caused by excessive growth of Candida albicans.
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19. Exogenous and endogenous prostaglandins are fever causing substances (True or False)
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19. False
1. the fever does 2 things. It inhibits bacterial growth b/c the temperature is no longer optimal for bacterial growth. 2. it speeds up bodily processes and defense mechanisms. Fever = Heat + heat speeds up (like a catalase) molecular and metabolic /enzymatic reactions. Pathogens grow best at 37 degrees C. Anything outside of this is no longer optimal for growth. Fever also enhances inflammatory response. killing by leukocytes, multiply of lymphocytes, substances that attract more neutrophils, and production of interferons and antobodies. It also enhances the release of leukocytes from the bone marrow. Hence why it is best to see a Dr. before taking fever reducing meds. |
For many years, it was thought that bacterial products caused fever via the intermediate production of a host-derived, fever-producing molecule, called endogenous pyrogen (EP). Bacterial products and other fever-producing substances were termed exogenous pyrogens. A fever is caused by pro-inflammatory cytokines released by macrophages when their toll like receptors detect microbial products (such as peptidoglycan and double stranded RNA (dsRNA) and lipopolysaccharide cell walls of bacteria). they then send a chemical message to the hypothalamic thermoregulatory center in the brain that the body is under attack - hence to initiate fever so that the temperature will not be optimal for bacterial growth. These cytokines and other fever inducing substances are called endogeneous pyrogens (indicating that the body makes them or that they are host-derived) the microbial products are exogenous products meaning they are derived from outside the body or introduced from the external sources. |
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20. The cells of the immune system are broken into 4 groups. Name the four groups and all the cells involved in each group with their general function.
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1. Granulocytes
--> Neutrophils (polymorphonuclear neutrophilic leukocytes or PMNs (often called polys) = phagocytize and digest engulfed materials --> Eosinophils = participates in inflammatory rxn andimmunity to some parasites --> Basophils = release histamine and other anti-inflammatory chemicals from the granules 2. Mononuclear Phagocytes --> Monocytes = Phagocytize and digest engulfed materials --> Macrophages = Phagocytize and digest engulfed materials 3. Dendritic cells = gather antigen from the tissues and then bring it to lymphocytes that congregate in the secondary lymphoid organs. 4. Lymphocytes --> several types = participate in adaptive immune responses. pg 350-352 |
hematopoietic stem cell
1. Erythroblast --> RBCs (erythrocytes) Colony Stimulating Factors (Megakaryoblast & Myeloblast and descendents thereof) 2. Megakaryoblast --> Megakaryocyte --> Thrombocytes (Platelets) 3. Myeloblast --> Eosinophil, Basophil, Neutrophil (all Granulocytes) 4. Monoblast --> Monocyte --> Macrophage (Mononuclear phagocytes, Binuclear phagocytes and polymorphonclear phagocytes) and Dendritic cell (looks like a starfish) *all cells produced from myeloblast and monoblast are leukocytes Lymphoid Stem cell --> Natural Killer Cells (NK) and --> Lymphoblasts --> T-lymphocytes processed in thymus --> effector T-cell and B-Lymphocytes processed in bone marrow --> plasma cell ** still these are called leukocytes |
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21. Explain the process of phagocytosis.
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1. Chemotaxis = phagocytic cells attracted to site of infection by chemoattractants (products of microorganisms - such as peptidoglycan in cell wall, double stranded RNA (dsRNA) or lipopolysaccharide in cell wall), also phospholipids released by injured mammalian cells & complement component C5a (a derivative from C5).
2. Recognition & Attachment = phagocyticcells use receptors to bind (directly or indirectly) one receptor binds mannose (sugar found on surface of some bacteria and yeasts) The serum mannose-binding protein and the macrophage mannose receptor are pattern recognition molecules that link innate and adaptive immunity.The mannose receptor is a C-type lectin carbohydrate binding protein Indirect binding involves particle opsonized, enhancing phagocytes ability to attach and engulf material. Opsonins incl. Complement component C3b and certain antibody molecules. 3. Engulfment = phagocytic cell engulfs and forms a membrane bound vacuole (phagosome) --> it rearrnges phagoctyes cytoskeleton, forming arm-like extensions called pseudopods that surround the material being engulfed. Engulfment itself does not destroy the microbe. 4. Fusion of phagosome w/lysosome = within phagocyte, phagosome is transported along the cytoskeleton to a point where it fuses with lysosomes (membrane bound bodies filled with various digestive enzymes incl. lysozyme and proteases. The fusion results in a phagolysosome. 5. Destruction & digestionwithin the phagolysosome, O2 consumption increases enormously as sugars aer metabolized via aerobic respiration. Resulting in highly toxic oxygen products such as superoxide, hydrogen perxode, singlet oxygen. and hydroxyl radicals. As avail. O2 is consumed --> leads to fermentation --> lactic acid --> lower pH. various enzymes degrade peptidoglycan and other bacterial cell components. 6. Exocytosis = Following digestion of the microorganism, the membrane bound vesicle fuses with plasma membrane, expelling the digested material to the external environment. pg 358 |
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22. Monocytes will differentiate into neutrophils (True or False)
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False
Monocytes is a descendent of Monoblasts that come from Hamatopoietic stem cell They in turn produce macrophages and mononuclear phagocytes. they are wbcs (leukocytes) Neutrophils are descendents of Myeloblast which comes from hematopoietic stem cell. It is a granulocyte and also a wbc (leukocytes). |
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23. What are the three events that can trigger an inflammatory reaction?
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1. Microbial products such as LPS )lipopolysaccharide), flagellin & bacterial DNA trigger the toll-like receptors of macrophages, causing the cells to produce pro-inflammatory cytokines. One of these cytokines - tumor necrosis factor alpha, induces the liver to synthesize acute phase proteins, a group of proteins, that facilitate phagocytosis and complement activation.
2. Microbial cell surfaces can trigger the complement cascade leading to the production of C3a and C5a, both of which stimulate changes assoc. w/inflammation. The complement components also induce mast cells to release various pro-inflammatory cytokines (incl. tumor necrosis factor alpha, histamine and other substances. 3. Tissue damage results in the activation of 2 enzymatic cascades. One is the coagulation cascade, which results in blood clotting, and the other produces several molecules such as bradykinin that elicit changes involved in inflammation. pg 360 |
May induce either singly or in combination.
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24. Define cytokine and explain its function in the definition
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Cytokines serve as molecular messengers between cells. Cytokines are proteins that are produced by cells. Cytokines interact with cells of the immune system in order to regulate the body's response to disease and infection. Cytokines also mediate normal cellular processes in the body.
Types of Cytokines Cytokines are diverse, meaning, they are not all alike. The body produces different types of cytokines: colony stimulating factors (stimulate production of blood cells) growth and differentiation factors (function primarily in development) immunoregulatory and proinflammatory cytokines (interferon, interleukins, and TNF-alpha that function in the immune system) How Cytokines Work The immune system is complex -- different types of immune cells and proteins do different jobs. Cytokines are among those proteins. Explaining how cytokines work is difficult. It's a lesson in cell physiology. But to understand inflammation, you must understand the role that cytokines play. Cytokines are released by cells into the circulation or directly into tissue. The cytokines locate target immune cells and interact with receptors on the target immune cells by binding to them. The interaction triggers or stimulates specific responses by the target cells. Overproduction of Cytokines Overproduction or inappropriate production of certain cytokines by the body can result in disease. For example, it has been found that interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are produced in excess in rheumatoid arthritis where they are involved in inflammation and tissue destruction. |
Types of Cytokines
Cytokines are diverse, meaning, they are not all alike. The body produces different types of cytokines: colony stimulating factors (stimulate production of blood cells) growth and differentiation factors (function primarily in development) immunoregulatory and proinflammatory cytokines (interferon, interleukins, and TNF-alpha that function in the immune system) How Cytokines Work The immune system is complex -- different types of immune cells and proteins do different jobs. Cytokines are among those proteins. Explaining how cytokines work is difficult. It's a lesson in cell physiology. But to understand inflammation, you must understand the role that cytokines play. Cytokines are released by cells into the circulation or directly into tissue. The cytokines locate target immune cells and interact with receptors on the target immune cells by binding to them. The interaction triggers or stimulates specific responses by the target cells. Overproduction of Cytokines Overproduction or inappropriate production of certain cytokines by the body can result in disease. For example, it has been found that interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are produced in excess in rheumatoid arthritis where they are involved in inflammation and tissue destruction. Biologic Drugs Are Cytokine Inhibitors Biologic drugs have been developed to inhibit IL-1 or TNF-alpha. Kineret (anakinra) was developed as a treatment for rheumatoid arthritis that works by inhibiting IL-1 binding to its receptor. TNF-alpha inhibitors (also called TNF blockers) bind TNF and prevent TNF from attaching to cell surface receptors. Enbrel (etanercept), Remicade (infliximab), and Humira (adalimumab) are TNF blockers. Other anti-cytokine therapies are in development. |
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25. Differentiate between a macrophage an a neutrophil
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neutrophils release IL1 which attracts Macrophages, but they both seem to do the same job (engulfing foreign objects, bacteria, etc)
First of all, they do have very similar functions, but the thing with neutrophils is that they are the first type of inflammatory cell on site where there is some kind of inflammatory response. Neutrophils are also known as polymorphonuclear cells (PMN) because of their histological appearance of having more than one "lobe" in their nucleus. Neutrophils are more involved in the first part of the inflammation reaction by recruiting other cells through chemotaxis. In a pathological specimen, the presence of neutrophils often signifies acute inflammation. Macrophages are an example of a monocyte (their nucleus only has one "lobe") and they come to the scene a little later than neutrophils. Macrophages are specialized cells (either present already in the tissues...i.e. tissue macrophages....or come from the blood as an offspring of a monocyte) which can engulf cells and kill them with radicals formed from breaking hydrogen peroxide using the energy from NADPH. Neutrophils can also engulf foreign organisms, but not as proficiently as macrophages, and they can't present things to T-cells like macrophages can. Neutrophils can release granules which contain cytokines (like IL-1 and TNF) to attract other immune cells, and also granules that contain enzymes that can break down the walls of foreign invaders. pg 353 |
Well, when a foreign invader enters your system tissue macrophages and neutrophils can recognize invaders due to certain tags (antigens) they have on their surface. The neutrophils and tissue macrophages are hardwired to recognize and kill bacteria that possess these antigens.
In reply to: ...I know that of course with lymphocytes the T lymphocytes will promote the B lymphocytes to create antibodies which block the bacteria/viruses ability to infect...and they recognize the invaders through the MHC Well, re: the MHC molecules. The macrophages (and dendritic cells) in our system are actually constantly eating cells in our system (including normal ones), breaking them down, and with the help of the MHC molecules, presenting pieces of these broken cells and proteins to the T-cells. If the protein (properly called an antigen) is familiar to the T-cell, nothing will happen...if it is NOT familiar (i.e. a piece of a bacteria), then an adaptive immune response will be activated. But you have to remember here to differentiate between adaptive immunity and innate immunity. Innate cellular immunity deals does NOT deal with T and B-cells. Macrophages and neutrophils take care of the job....adaptive immunity (i.e. employing T and B-cells) is only used when an invader has gotten past our innate immunity. In reply to: And why are there more than one kind of leukocyte to do the same job? I think it would be more appropriate to say that there are different leukocytes which have different jobs, but they overlap somewhat. Leukocytes differ in the timing in which they function, how they function (through granules or phagocytosis, or both), what their specialty is (phagocytosis, opsonization, mounting an immune response)......it's just that, there's only so much to do, and they tend to have some actions in common. |
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Immunology-
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study of the many mechanisms that the body uses to defend itself against invading microbes
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Autoimmunity-
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effects of the immune response that target self molecules and cause self damage
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Hypersensitivity reactions-
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reactions where the immune system is responding to an antigen that is foreign, but not dangerous
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Innate immunity-
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non-specific protection that we are born with that is always active
Found in all organisms in some form Involves skin and mucous membranes Involves sensor systems Involves phagocytic cells |
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phagocytic cells engulf and digest foreign material
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sensor systems (detect molecules associated with danger; compounds unique to bacteria and compounds released only when tissues are damaged)
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Vertebrates have evolved a more specialized response to foreign invasion called ______________.
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adaptive immunity
Only in vertebrates Develops throughout life “learns and remembers” the most effective response to that specific material Responds to antigens First exposure the response develops slowly during which time the microbe may cause damage, exposures following will have a swifter and greater immune response |
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antigens
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foreign material to which the immune system responds
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Toll-like receptors and NOD proteins
Found on variety of cells NOD proteins are found inside the cell and Toll-like receptors outside the cell. What do they do? |
Recognize families of compounds unique to bacteria such as LPS and peptidoglycan
Enables cells to sense invasion Sends signal to body to respond |
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first line defense
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Barriers that separate and shield the interior of the body from surrounding environments; initial obstacles that invading microbes must overcome to invade tissue
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Anatomical barriers
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Skin and mucous membranes that provide a physical barrier and are bathed in secretions containing substances that have antimicrobial properties
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Streptokinase (SK),
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a protein secreted by several species of streptococci can bind and activate human plasminogen.
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A protease (also termed peptidase or proteinase)
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is any enzyme that conducts proteolysis, that is, begins protein catabolism by hydrolysis of the peptide bonds that link amino acids together in the polypeptide chain forming the protein.
any of a subclass of proteolytic enzymes that catalyze the hydrolysis of peptide linkages; it comprises the exopeptidases and endopeptidases. |
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Amylase
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is an enzyme that catalyses the breakdown of starch into sugar
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Keratinase
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are proteolytic enzymes in nature. Keratinases are produced only in the presence of keratin containing substrate. It mainly attacks on the disulfide (-S-S-) bond of the keratin substrate
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Lysozyme,
aka. muramidase or N-acetylmuramide glycanhydrolase, are glycoside hydrolases, enzymes |
The enzyme functions by attacking peptidoglycans (found in the cell walls of bacteria, especially Gram-positive bacteria) and hydrolyzing the glycosidic bond that connects N-acetylmuramic acid with the fourth carbon atom of N-acetylglucosamine. It does this by binding to the peptidoglycan molecule in the binding site within the prominent cleft between its two domains. This causes the substrate molecule to adopt a strained conformation similar to that of the transition state
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