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Define nonspecific resistance
innate immunity: defences against ANY pathogen
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Outline and describe the role of the components of the nonspecific defenses
- First line of defense: intact skin, mucous membranes and their secretions, normal microbiota
- Second line of defense: phagocytes, such as neutrophils, eosinophils, dendritic cells, and macrophages, inflammation, fever, antimicrobial substances
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Physical factors of the first line of defence (innate)
- skin: physical barrier (epidermis, dermis)
- consists of tightly packed cells with keratin
- dryness inhibits microbial growth (lack of H2O)
- shedding removes microbes
- Mucous membranes:
- mucous traps many microorganisms (+ nose hairs)
- ciliary escalator moves trapped microorganisms away from lungs
- epiglottis physically covers lungs
- cleansing actions - tears, saliva, bodily fluids (urine, vaginal secretions, mucous, semen)
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Chemical factors of the first line of defense (innate)
- Skin: fungistatic fatty-acid in sebum-protective film
- Lysozyme: in perspiration, tears, saliva, urine, and tissue fluids
- Low pH: skin (3-5), gastric juice (1.2-3.0), vaginal secretions (3-5)
- Transferrins: in blood, bind iron
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Describe the role of normal microbiota in nonspecific resistance
- Microbial antagonism/competition against pathogenic microbes
- 1. physical barrier
- 2. compete for space/food
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Classify phagocytic cells, describe the functions of neutrophils and macrophages
- Neutrophils, monocytes, macrophages, dendritic cells
- Neutrophils: protects against microbes during initial phase of infection
- Macrophages: develop from monocytes, dominate as infection progresses
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Explain the process of phagocytosis
- Host TLRs attach to PAMPs
- Chemotaxis and adherance of microbes to phagocyte
- Ingestion from pseudopods
- Formation of phagosome
- Formation of phagolysosome (phagosome + lysosome)
- Digestion of microbe
- Residual body contains indigestible material
- Discharge of waste
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Describe the stages of inflammation
- Response to tissue damage - intended to limit damage and restore function
- Signs and symptoms include redness, pain, heat, and swelling
- Tissue damage: release of chemical mediators trigger vasodilation, blood clot forms, absess starts to form,
- Vasodilation: increased vascular permeability
- Phagocyte migration and phagocytosis: [first neutrophils then macrophages] margination (phagocytes stick to endothelium), diapedesis, phagocytosis of invading bacteria
- Tissue repair: scab, blood clot, regenerated epidermis, regenerated dermis
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Describe the cause and effects of fever
- Pyrogens (fever inducing endotoxins) cause phagocytes to release IL-1, which causes the hypothalamus to release prostaglandins which reset the hypothalamus to a higher temperature
- When fever increases rate of metabolism increases, however sweating causes fever to go down.
- Advantages: speeds up tissue repair, increase in speed/activation of other body defenses
- Disadvantages: tachycardia, acidosis, dehydration, too high can be fatal
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Discuss the role of complement activation and 3 consequences.
- Serum proteins are activated in a cascade
- 1. Opsonization: C3b enhances phagocytosis
- 2. Inflammation: C3a + C5a
- 3. Cytolysis: C5b + C6 + C7 + C8 + C9 membrane attack complex
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Antimicrobial substances
- Interferons: inhibit viral replication
- Transferins: host protein, bind serum iron
- Antimicrobial peptides: lyse bacterial cells
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Interferons
- Properties: short lived, antiviral, specific to host cell NOT to virus
- Function: inhibit viral replication in surrounding cells
- Mechanism: binds to surface of surrounding cells causing them to secrete antiviral proteins
- Alpha IFN: leukocytes
- Beta IFN: fibroblast (connective tissues)
- Gamma IFN: lymphocytes (enhances ability to phagocitize bacteria)
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