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28 Cards in this Set
- Front
- Back
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Differences between innate and adaptive immunity |
Innate: *present at birth *Rapid response, not specific, no memory *1st and 2nd lines of defense Adaptive: *specific response to specific microbe *memory component *Lymphocytes, T & B cells *Passively & actively acquired *3rd line of defense |
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PAMPS & TLRs (innate immunity only) |
PAMPS = Pathogen-associated molecular patterns--molecules on the outside of bacteria, fungi, or viruses that trigger the immune response TLRs= toll-like receptors--protein receptors in the plasma membranes of defensive cells; attach to PAMPs and induce defensive cells to release cytokines |
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Common PAMPs |
*Lipopolysaccharides in outer layer of gram- negative bacteria *Peptidoglycan layer of gram-positive cells *Flagellin (protein found in a flagella) *Foreign DNA *Cell membrane proteins (esp. glycoproteins) |
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Cytokines |
Soluble, small proteins serving as signals to the immune system. The more cytokines released, the more intense the immune response. Recruit and activate more immune cells |
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First line of defense: Physical Factors: Skin |
*tightly layered epithelial cells prevent entry
*sheds regularly to remove pathogens *Keratin: protein that dries top layer of skin out |
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First line of defense: Physical Factors: Mucus Membranes |
*Epithelial layer and underlying connective tissue *goblet cells secrete mucus, maintain moisture *Can shed mucus (ciliary elevator) *some pathogens can survive these conditions |
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First line of defense: Physical Factors: Other |
*Peristalsis, defecation, vomiting propel microbes out of body *Urine, vaginal secretions, earwax, tears wash pathogens out of body |
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First line of Defense: Chemical Factors |
1. Sebum: forms protective film made of unsaturated fatty acids, which inhibit the growth of pathogenic bacteria & fungi 2. Perspiration: flushes microorganisms from surface of skin. 3. Lysozyme: Enzyme in sweat, saliva, tears, nasal secretions, urine; breaks down gram-positive walls and some gram-negative walls by disrupting chemical bonds in peptidoglycan 4. Low pH: slows growth of bacteria (gastric = 1-2; earwax, vaginal secretions, skin = 3-5; Urine= 6, saliva = 6.55) |
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First line of Defense: Normal Microbiota |
*antagonism (outcompetes pathogenic microbes for space & resources) *Can alter pH, O2 levels, and nutrient availability *Probiotics |
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Second line of defense |
*triggered by penetration of first line *production of phagocytes *inflammation *fever *antimicrobial substances (complement) |
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Leukocytes: Granulocytes |
*Neutrophils (early responder, phagocytic, motile, can leave bloodstream) *Basophils (release histamine in inflammation and allergy responses) *Eosinophils (can leave bloodstream; produce toxic proteins for helminths) |
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Leukocytes: Agranulocytes |
2nd responders in 2nd line of defense *Monocytes (not actively phagocytic until they leave blood and mature into macrophages; common in lymph nodes) *Dendritic cells (long extensions; phagocytic) *Lymphocytes (NK cells with perforin, T cells, B cells |
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5 steps of phagocytosis |
1. Chemotaxis & adherence (via TLR) 2. Ingestion 3. Formation of phagosome 4. Fusion of phagosome with lysosome to digest debris 5. Form residual body to discharge indigestible waste materials |
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Ways Bacteria Evade Phagocytosis (3) |
1. Prevent adherence *M proteins (strep pyogenes) *Capsules (strep pneumoniae) 2. Survive in phagocyte *Absorb digestive enzymes *Lyse phagocyte *Live in phagocyte either dormant or dividing 3. Biofilms *community of a variety of types of bacteria *phagocytes cannot detach bacteria from the biofilm easily |
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Second line of defense: Inflammation |
Acute: short-lived; gone after source is removed (ex: boil caused by S. aureus) Chronic: long-term; source is permanent (ex: lung inflammation caused by M. tuberculosis) |
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Functions of inflammation (3) |
1. Remove pathogen and products 2. If can't destroy, then contain problem (i.e. in abscess) 3. Repair tissues |
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Cytokine: Tumor necrosis factor alpha |
*released into blood, activates proteins *proteins induce local and systemic responses *inflammatory response cells (B &T) have TNF receptors--make more cells and amplify response *Ongoing response and continued production of TNF after an infection can lead to chronic disorders (autoimmune diseases) |
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Inflammation: Stage 1 |
Vasodilation & increased blood vessel permeability *so macrophages can squeeze thru capillary walls to get to affected tissue *Defensive substances move to area of injury; causes edema; histamine released; triggers more immune response *Localized clot contains microbes to prevent infection of the circulatory system *Abscess forms (focus of infection) |
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Inflammation: Stage 2 |
Phagocyte migration & phagocytosis *Cytokines alter cellular adhesion molecules (CAMs) allowing phagocytes to stick *Diapedesis occurs (phagocytes squeeze between endothelial cells in capillaries to damaged area) *Phagocytosis action destroys microbes |
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Inflammation: Stage 3 |
Tissue Repair *dead cells replaced by living cells *replace parenchymal (functional) cells *replace stroma (structural) cells *more activity in stroma results in scar tissue |
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Second line of defense: Fever |
*Systemic response caused by infection by bacteria or viruses, OR by toxins *Hypothalamus sensitive to cytokines in blood; when they are present, the body temp is reset *Fever intensifies antiviral interferons, speeds up body reactions |
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Second line of defense: Complement |
*innate *not specific for a type of pathogen *works in cascade; each event triggers next event *serum proteins activate one another to destroy invading mircoorganisms *includes interferons, iron-binding proteins, and antimicrobial peptides (AMPs) |
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Complementary pathway |
C3-->C3a & C3b-->C5-->C5b-->C6-C9 (MAC) *C3b coats pathogen, makes it more visible to phagocytes *C3b activates C5, which triggers C5b, and C6-C9 form MAC *C5 is a chemotaxic draw for phagocytes to the infection site |
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Interferons |
*proteins produced by virus-stimulated animal cells *interferes with viral replication *Host-cell specific, not virus specific |
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Interferon alpha, Interferon beta, interferon gamma |
1. Alpha & beta: host cells produce and secrete them to infected and uninfected neighbors to disrupt virus replication 2. Gamma: produced by lymphocytes; induces macrophages and neutrophils to kill bacteria; increases MHC 1 & II |
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Other defenses: Iron-binding proteins |
*host & pathogen compete for iron *Hemoglobin, ferritin, & transferrin bind iron in the body *Bacterial siderophores "steal" iron |
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Other defenses: Antimicrobial Peptides (AMPs) |
*short peptide chains, critical to innate immunity *produced when TLRs are triggered *Multiple nonspecific actions to cover a wide range of bacteria (inhibiting cell wall synthesis, pore formation, DNA/RNA deconstruction) |
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How does inflammation help combat infection? |
1. Localizing to 1 area 2. Histamines make capillaries permeable |
