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99 Cards in this Set
- Front
- Back
species resistance
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When the cells and certain basic physiological processes of a speicies are incompatible with those of most plant and animal pathogens, humans have what is termed species resistance to these pathogens
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innate immunity
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the first two lines of defense are called innate immunity because they are present at birth prior to contact with infectious agents or their products. Innate immunity is rapid and works against a wide variety of pathogens, including parasitic worms, protozoa, fungi, bacteria, and viruses.
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adaptive immunity
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the third line of defense, adaptive immunity, responds against unique species or strains of pathogens and alters the body’s defenses such that they act more effectively upon subsequent infection with the specific strain
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epidermis and dermis
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The skin–the organ of the body with the greatest surface area–is composed of two major layers: an outer epidermis, and a deeper dermis, which contains hair follicles, glands, and nerve endings. Both the physical structure and the chemical components of skin enable it to act as an effective defense
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dendritic cells
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The epidermis also contains phagocytic cells called dendritic 1 cells. The slender, fingerlike processes of dendritic cells extend among the surrounding cells, forming an almost continuous network to intercept invaders. Dendritic cells both phagocytize pathogens nonspecifically and play a role in adaptive immunity
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defensins
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Antimicrobial peptides (also called defensins) are chains of about 40 amino acids that act against microorganisms.
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dermicidins
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Sweat glands secrete a class of antimicrobial peptides called dermicidins. Dermicidins are broad-spectrum antimicrobials that are active against many Gram-negative and Gram-positive bacteria and fungi. As expected of a peptide active on the surface of the skin, dermicidins are insensitive to low pH and salt.
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Lysozyme
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Lysozyme is an enzyme that destroys the cell walls of bacteria by cleaving the bonds between the sugar subunits of the walls. Bacteria without cell walls are more susceptible to osmotic shock and digestion by other enzymes within phagocytes
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sebum
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sebaceous (oil) glands secrete sebum , an oily substance that not only helps keep the skin pliable and less sensitive to breaking or tearing but also contains fatty acids that lower the pH of the skin’s surface to about pH 5, which is inhibitory to many bacteria.
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Staphylococcus epidermidis
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Although salt, defensins, lysozyme, and acidity make the surface of the skin an inhospitable environment for most microorganisms, some bacteria, such as Staphylococcus epidermidis , find the skin a suitable environment for growth and reproduction.
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epithelium
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Mucous membranes are moist and have two distinct layers: an outer covering of superficial (closest to the surface, in this case the lumen) cells called the epithelium...
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stem cells
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epithelial cells are continually shed and then replaced via the cytokinesis of stem cells, which are generative cells capable of dividing to form daughter cells of a variety of types; one effect of such shedding is that it carries attached microorganisms away.
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Dendritic cells
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Dendritic cells reside below the mucus epithelium to phagocytize invaders. These cells are also able to extend pseudopodia between epithelial cells to “sample” the contents of the lumen, which helps prepare adaptive immune responses against particular pathogens that might breach the mucosal barrier
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goblet cells
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the epithelia of some mucous membranes have still other means of removing pathogens. In the mucous membrane of the trachea, for example, the stem cells produce both goblet cells, which secrete an extremely sticky mucus that traps bacteria and other pathogens, and ciliated columnar cells, whose cilia propel the mucus (and the particles and pathogens trapped within it) up from the lungs
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cilia
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The effect of the action of the cilia is often likened to that of an escalator. Mucus carried into the throat is coughed up and either swallowed or expelled.
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lysozyme,
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Nasal mucus contains lysozyme, which chemically destroys bacterial cell walls. Mucus contains antimicro-bial peptides (defensins).
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lacrimal apparatus
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The lacrimal apparatus is a group of structures that produce and drain away tears
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Lacrimal glands
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Lacrimal glands, located above and to the sides of the eyes, secrete tears into lacrimal gland ducts and onto the surface of the eyes.
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microbial antagonism.
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This normal microbiota plays a role in protecting the body by competing with potential pathogens in a variety of ways, a situation called microbial antagonism.
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axenic environment
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animals raised in an axenic environment–that is, one free of all other organisms or viruses–are slower to defend themselves when exposed to a pathogen
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Toll-like receptors (TLRs) and their microbial binding partners
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Cells produce antimicrobial peptides when microbial chemicals bind to Toll-like receptors (TLRs) 3 on host cells’ cytoplasmic or internal membranes. Scientists have discovered at least 10 different TLRs, each of which recognizes a particular microbial chemical.
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NOD 4 proteins
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NOD 4 proteins are intracellular receptors for microbial components, particularly components of bacterial cell walls. regulate genes to mediate inflammation, apoptosis (cell suicide), and possibly other innate immune responses
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second line of defense
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the second line operates against a wide variety of pathogens-the second line includes no barriers; instead, it is composed of cells (esp. phagocytes), antimicrobial chemicals (peptides, complement, interferons), and processes (inflammation, fever).
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Plasma
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Plasma is mostly water containing electrolytes (ions), dissolved gases, nutrients, and–most relevant to the body’s defenses–a variety of proteins
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serum
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When clotting factors have been removed from the plasma, as for instance when blood clots, the remaining liquid is called serum
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Staphylococcus aureus
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Staphylococcus aureus , respond to a shortage of iron by secreting their own iron-binding proteins called siderophores. Because siderophores have a greater affinity for iron than does transferrin, bacteria that produce them can in effect steal iron from the body. In response, the body produces lactoferrin, which retakes the iron from the bacteria by its even greater affinity. Thus, the body and the pathogens engage in a kind of chemical “tug-of-war” for the possession of iron.
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Neisseria meningitidis
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Neisseria meningitidis , a pathogen that causes often fatal meningitis, produces receptors for transferrin and plucks iron from the bloodstream as it flows by.
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S. aureus
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S. aureus and related pathogens can secrete the protein hemolysin, which punches holes in the cytoplasmic membranes of red blood cells, releasing hemoglobin.
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formed elements
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Cells and cell fragments suspended in the plasma are called formed elements
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hematopoiesis
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In a process called hematopoiesis, blood stem cells located principally in the bone marrow within the hollow cavities of the large bones produce three types of formed elements: erythrocytes , platelets , and leukocytes
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Erythrocytes
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Erythrocytes, the most numerous of the formed elements, carry oxygen and carbon dioxide in the blood.
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Platelets
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Platelets, which are pieces of large cells called megakaryocytes that have split into small portions of cytoplasm surrounded by cytoplasmic membranes, are involved in blood clotting.
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Leukocytes
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Leukocytes, the formed elements that are directly involved in defending the body against invaders, are commonly called white blood cells because they form a whitish layer when the components of blood are separated within a test tube
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Granulocytes
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Granulocytes have large granules in their cytoplasm that stain different colors depending on the type of granulocyte and the dyes used: basophils stain blue with the basic dye methylene blue; eosinophils stain red to orange with the acidic dye eosin; and neutrophils , also known as polymorphonuclear leukocytes (PMNs), stain lilac with a mixture of acidic and basic dyes.
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iapedesis
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Both neutrophils and eosinophils phagocytize pathogens, and both can exit the blood to attack invading microbes in the tissues by squeezing between the cells lining capillaries (the smallest blood vessels). This process is called diapedesis or emigration
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eosinophils
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eosinophils are also involved in defending the body against parasitic worms and are present in large number during many allergic reactions, though their exact function in allergies is disputed.
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Basophils
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Basophils can also leave the blood, though they are not phagocytic; instead, they release inflammatory chemicals, an aspect of the second line of defense
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lymphocytes
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lymphocytes , which are the smallest leukocytes and have nuclei that nearly fill the cells
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monocytes
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monocytes , which are large agranulocytes with slightly lobed nuclei. Monocytes leave the blood and mature into macrophages
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macrophages
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Monocytes leave the blood and mature into macrophages , which are phagocytic cells of the second line of defense. Their initial function is to devour foreign objects, including bacteria, fungi, spores, and dust, as well as dead body cells.
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Wandering macrophages
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Wandering macrophages leave the blood via diapedesis and perform their scavenger function while traveling throughout the body, including extracellular spaces. Other macrophages are fixed and do not wander. These include, alveolar macrophages 10 of the lungs, microglia of the central nervous system, and Kupffer 11 cells of the liver.
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Fixed macrophages
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Fixed macrophages generally phagocytize within specific organs, such as the heart chambers, blood vessels, and lymphatic 12 vessels.
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dendritic cells
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A special group of phagocytes are dendritic cells. These multibranched cells are plentiful throughout the body, particularly in the skin and mucous membrances, where they await microbial invaders
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differential white blood cell count
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The proportions of leukocytes, as determined in a differential white blood cell count, can serve as a sign of disease
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eosinophils-as part of a differential white blood cell count
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an increase in the percentage of eosinophils can indicate allergies or infection with parasitic worms
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leukocytes and neutrophils-as part of a differential white blood cell count
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bacterial diseases typically result in an increase in the number of leukocytes an increase in the percentage of neutrophils
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lymphocytes-as part of a differential white blood cell count
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viral infections are associated with an increase in the relative number of lymphocytes.
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phagocytes
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cells of the body that are capable of phagocytosis–collectively known as phagocytes –play a role against pathogens that get past the body’s first line of defense.
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five steps:of the process of phagocytosis
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process of phagocytosis five steps: (1) chemotaxis, (2) adherence, (3) ingestion, (4) killing, and (5) elimination
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chemotaxis
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chemotaxis is movement of a cell either toward a chemical stimulus (positive chemotaxis) or away from a chemical stimulus (negative chemotaxis).
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pseudopodia
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positive chemotaxis involves the use of pseudopodia to crawl toward microorganisms at the site of an infection
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Chemicals that attract phagocytic leukocytes
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Chemicals that attract phagocytic leukocytes include microbial components and secretions, components of damaged tissues and white blood cells, and chemotactic factors.
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chemotactic factors.
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Chemotactic factors include defensins, peptides derived from complement (discussed later in this chapter), and chemicals called chemokines , which are released by leukocytes already at a site of infection.
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adherence
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After arriving at the site of an infection, phagocytes attach to microorganisms through the binding of complementary chemicals such as glycoproteins found on the membranes of cells . This process is called adherence.
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virulence factors
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Some bacteria have virulence factors, such as M protein of Streptococcus pyogenes , or slippery capsules that hinder adherence of phagocytes and thereby increase the virulence of the bacteria. Such bacteria are more readily phagocytized if they are pushed up against a surface such as connective tissue, the wall of a blood vessel, or a blood clot.
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opsonization
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All pathogens are more readily phagocytized if they are first covered with antimicrobial proteins such as complement proteins or the specific antimicrobial proteins called antibodies This coating process is called opsonization, and the proteins are called opsonins.
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opsonins
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Generally, opsonins increase the number and kinds of binding sites on a microbe’s surface.
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phagosome
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After phagocytes adhere to pathogens, they extend pseudopodia to surround the microbe The encompassed microbe is internalized as the pseudopodia fuse to form a food vesicle called a phagosome.
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phagolysosomes
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Lysosomes within the phagocyte fuse with newly formed phagosomes to form phagolysosomes , or digestive vesicles
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residual body
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In the end after killing, a phagolysosome is known as a residual body.
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exocytosis
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Digestion is not always complete, and phagocytes eliminate remnants of microorganisms via exocytosis, a process that is essentially the reverse of ingestion
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Eosinophilia
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Eosinophilia , an abnormally high number of eosinophils in the blood, is often indicative of helminth infestation.
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Natural killer lymphocytes (or NK cells)
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Natural killer lymphocytes (or NK cells) are another type of defensive leukocyte of innate immunity that works by secreting toxins onto the surfaces of virally infected cells and neoplasms (tumors).
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NETs - neutrophil extracellular traps
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another way that neutrophils disable microorganisms in their vicinity. They generate webs of extracellular fibers nicknamed NETs for neutrophil extracellular traps.
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complement
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The complement system–or complement for short–is a set of serum proteins designated numerically according to the order of their discovery. These proteins initially act as opsonins and chemotactic factors, and indirectly trigger inflammation and fever. The end result of full complement activation is lysis of foreign cells
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cascades
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Complement proteins react with one another in an amplifying sequence of chemical reactions, in which the product of each reaction becomes an enzyme that catalyzes the next reaction many times over. Such reactions are called cascades
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Classical Pathway Complement
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The Classical Pathway Complement In this pathway the various proteins act to “complement,” or act in conjunction with, the action of antibodies, which are part of adaptive immunity.
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fragments.
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Complement enzymes in early events cleave other complement molecules to form fragments. Most fragments have specific and important roles in achieving the functions of the complement system. Some combine together to form new enzymes; some act to increase vascular permeability, which increases diapedesis; others enhance inflammation; still others are involved as chemotactic factors or in opsonization.
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membrane attack complex (MAC)
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One end product of the cascade is a membrane attack complex (MAC), which forms a circular hole in a pathogen’s membrane. The production of numerous MACs leads to lysis in a wide variety of bacterial and eukaryotic pathogens. Gram-positive bacterium, which has a thick layer of peptidoglycan overlying its cytoplasmic membrane, is typically resistant to the MAC-induced lytic properties of complement, though it is susceptible to the other effects of the complement cascade.
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The Alternative Pathway
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The Alternative Pathway - activation occurs independently of antibodies. and begins with the cleavage of C3 into C3a and C3b. This naturally occurs at a slow rate in the plasma but proceeds no further because C3b is cleaved into smaller fragments almost immediately. However, when C3b binds to microbial surfaces, it stabilizes long enough for a protein called factor B to adhere. Another plasma protein, factor D, then cleaves factor B, creating an enzyme composed of C3b and Bb. This enzyme, which is stabilized by a third protein–factor P (properdin)–cleaves more molecules of C3 into C3a and C3b, continuing the complement cascade and the formation of MACs.
The alternative pathway is useful in the early stages of an infection, before the adaptive immune response has created the antibodies needed to activate the classical pathway. |
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The Lectin Pathway
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The Lectin Pathway - a third pathway for complement activation that acts through the use of lectins. Lectins are chemicals that bind to specific sugar subunits of polysaccharide molecules; in this case, to mannose sugar in mannan polysaccharide on the surfaces of fungi, bacteria, or viruses. Mannose is rare in mammals. Lectins bound to mannose act to trigger a complement cascade by cleaving C2 and C4. The cascade then proceeds like the classical pathway
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Lectins
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Lectins are chemicals that bind to specific sugar subunits of polysaccharide molecules; in the lectin pathway binds to mannose sugar in mannan polysaccharide
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Interferons
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Interferons are protein molecules released by host cells to nonspecifically inhibit the spread of viral infections. Their lack of specificity means that interferons produced against one viral invader protect somewhat against infection by other types of viruses as well. However, interferons also cause malaise, muscle aches, chills, headache, and fever, which are typically associated with viral infections.
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alpha and beta interferons
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type I interferons–also known as alpha and beta interferons–are present early in viral infections, whereas type II (gamma) interferon appears somewhat later - their actions are identical
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Type I (Alpha and Beta) Interferons
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Type I (Alpha and Beta) Interferons Within hours after infection, virally infected monocytes, macrophages, and some lymphocytes secrete small amounts of alpha interferon (IFN-α); similarly, fibroblasts, which are undifferentiated cells in such connective tissues as cartilage, tendon, and bone, secrete small amounts of beta interferon (IFN-β) when infected by viruses. The structures of alpha and beta interferons are similar, and their actions are identical.
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antiviral proteins (AVPs)
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binding triggers the production of antiviral proteins (AVPs), which remain inactive within these cells until AVPs bind to viral nucleic acids, particularly double-stranded RNA, a molecule that is common among viruses but generally absent in eukaryotic cells
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oligoadenylate synthetase and protein kinase
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At least two types of AVPs are produced: oligoadenylate synthetase, the action of which results in the degradation of mRNA, and protein kinase, which inhibits protein synthesis by ribosomes. They destroy the protein production system of the cell, preventing viruses from being replicated.
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Type II (Gamma) Interferon
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Type II (Gamma) Interferon Gamma interferon (IFN-γ) is produced by activated T lymphocytes and NK lymphocytes. Because T lymphocytes are usually activated as part of an adaptive immune response days after an infection has occurred, gamma interferon appears later than either alpha or beta interferon. Its action in stimulating the activity of macrophages gives IFN-γ its other name: macrophage activation factor. Gamma interferon plays a small role in protecting the body against viral infections; mostly IFN-γ regulates the immune system, as in its activation of phagocytic activity.
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Inflammation
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Inflammation is a general, nonspecific response to tissue damage resulting from a variety of causes, including heat, chemicals, ultraviolet light (sunburn), abrasions, cuts, and pathogens
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Acute inflammation
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Acute inflammation develops quickly, is short lived, is typically beneficial, and results in the elimination or resolution of whatever condition precipitated it.
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chronic inflammation
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Long-lasting (chronic) inflammation cause damage (even death) to tissues, resulting in disease. Both acute and chronic inflammation exhibit similar signs and symptoms, including redness in light-colored skin, (rubor), localized heat (calor), edema (swelling), and pain (dolor).
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importance of acute inflammation
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acute inflammation is an important part of the second line of defense because it results in (1) dilation and increased permeability of blood vessels, (2) migration of phagocytes, and (3) tissue repair. Although the chemical details of inflammation are beyond the scope of our study, we now consider these three aspects of acute inflammation.
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bradykinin
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Part of the body’s initial response to an injury or invasion of pathogens is localized dilation (increase in diameter) of blood vessels in the affected region. The process of blood clotting triggers the conversion of a soluble plasma protein into a nine-amino-acid peptide chain called bradykinin , which is a potent mediator of inflammation
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prostaglandins and leukotrienes
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patrolling macrophages, using Toll-like receptors to identify invaders, release other inflammatory chemicals, including prostaglandins and leukotrienes .
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mast cells
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Basophils, platelets, and specialized cells located in connective tissue–called mast cells–also release inflammatory mediators, such as histamine , when they are exposed to complement fragments C3a and C5a (Figure 15.14). Recall that these complement peptides were cleaved from larger polypeptides during the complement cascade
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abscess
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an isolated site of infection is called an abscess. Pimples, boils, and pustules are examples of abscesses.
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antihistamines
antiprostaglandins |
The signs and symptoms of inflammation can be treated with antihistamines, which block histamine receptors on blood vessel walls, or with antiprostaglandins. One of the ways aspirin and ibuprofen reduce pain is by acting as antiprostaglandins.
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margination
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Increased blood flow due to vasodilation delivers monocytes and neutrophils to a site of infection. As they arrive, these leukocytes roll along the inside walls of blood vessels until they adhere to the receptors lining the vessels, in a process called margination.
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phagocytes: neutrophils, monocytes. wandering macrophages
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The first phagocytes to arrive are often neutrophils, which are then followed by monocytes. Once monocytes leave the blood, they change and become wandering macrophages, which are especially active phagocytic cells that devour pathogens, damaged tissue cells, and dead neutrophils. Wandering macrophages are a major component of pus.
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tissue repair,
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The final stage of inflammation is tissue repair, which in part involves the delivery of extra nutrients and oxygen to the site. Areas of the body where cells regularly undergo cytokinesis, such as the skin and mucous membranes, are repaired rapidly. Some other sites are not fully reparable and form scar tissue.
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fibroblasts
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If the damaged tissue contains undifferentiated stem cells, tissues can be fully restored. For example, a minor skin cut is repaired to such an extent it is no longer visible. However, if cells called fibroblasts are involved to a significant extent, scar tissue is formed, inhibiting normal function. Some tissues, such as cardiac muscle and parts of the brain, do not replicate and thus tissue damage cannot be repaired. As a result, these tissues remain damaged following heart attacks and strokes
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the characteristic events in the process of inflammation.
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the events in inflammation. The process, which is characterized by redness, swelling, heat, and pain, ends with tissue repair.
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Fever
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Fever is a body temperature above 37°C. Fever augments the beneficial effects of inflammation, but like inflammation it also has unpleasant side effects, including malaise, body aches, and tiredness.
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pyrogens
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Fever results when the presence of chemicals called pyrogens trigger the hypothalamic “thermostat” to reset at a higher temperature. Pyrogens include bacterial toxins, cytoplasmic contents of bacteria that are released upon lysis, antibody-antigen complexes formed in adaptive immune responses, and pyrogens released by phagocytes that have phagocytized bacteria
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prostaglandin
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Chemicals produced by phagocytes cause the hypothalamus to secrete prostaglandin, which resets the hypothalamic thermostat by some unknown mechanism
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hypothalamus
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The hypothalamus then communicates the new temperature setting to other parts of the brain, which initiate nerve impulses that produce rapid and repetitive muscle contractions (shivering), an increase in metabolic rate, and constriction of blood vessels of the skin
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(vasodilation)
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Because blood vessels in the skin constrict as fever progresses, one effect of inflammation (vasodilation) is undone. The constricted vessels carry less blood to the skin, causing it to feel cold to the touch, even though the body’s core temperature is higher. This symptom is the chill associated with fever.
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the crisis of a fever
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Fever continues as long as pyrogens are present. As an infection comes under control and fewer active phagocytes are involved, the level of pyrogens decreases, the thermostat is reset to 37°C, and the body begins to cool by perspiring, lowering the metabolic rate, and dilating blood vessels in the skin. These processes, collectively called the crisis of a fever, are a sign that the infection has been overcome and that body temperature is returning to normal.
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increased temperature of fever
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The increased temperature of fever enhances the effects of interferons, inhibits the growth of some microorganisms, and is thought to enhance the performance of phagocytes, the activity of cells of specific immunity, and the process of tissue repair. However, if fever is too high, critical proteins are denatured; additionally, nerve impulses are inhibited, resulting in hallucinations, coma, and even death.
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