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Home Page Flashcards Micro: Chapter 16 - Flashcards

Micro: Chapter 16 – Flashcards

Jason Westley
7 July 2022

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Susceptibility
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  • Lack of resistance to a disease
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Immunity
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  • Ability to ward off disease
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Innate Immunity
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  • defenses against any pathogen
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Adaptive Immunity
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  • immunity or resistance to a specific pathogen
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First line of defense
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  • Intact skin
  • Mucous membranes and their secretions
  • Normal microbiota
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Second line of defense
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  • Phagocytes, such as neutrophils, eosinophils, dendritic cells, and macrophages
  • Inflammation
  • Fever
  • Antimicrobial substances
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Third line of defense
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  • Specialized lymphocytes: T cells and B cells
  • Antibodies
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The Concept of Immunity
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  • Host Toll-like resceptors (TLRs) attach to pathogen-associated molecular patterns (PAMPs)- rectptors on human cells that recognize various common bacterial substances such as peptidoglycan
  • TLRs induce cytokines that regulate the intensity and duration of immune responses
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Physical Factors
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  • Skin
  • Epidermis consists of tightly packed cells with 
    • Keratin, a protective protein
  • Mucous membranes
  • Mucus: traps microbes
  • Ciliary escalator: transports microbes trapped in mucus away from the lungs
  • Lacrimal apparatus: washes eye
  • Saliva: washes microbes off
  • Urine: flows out
  • Vaginal secretions: flow out
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Chemical factors
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  • Fungistatic fatty acid in sebum
  • Low pH (3-5) of skin
  • Lysozyme in perspiration, tears, saliva, and urine
  • Low pH (1.2-3.0) of gastric juice
  • Low pH (3-5) of vaginal secretions
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Normal microbiota
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  • Microbial antagonism/competitive exclusion: normal microbiota compete with pathogens or alter the environment
  • Commensal micrbiota: one organism (microbe) benefits, and the other (host) is unharmed
    • May be opportunistic pathogens
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Types of Leukocytes
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  • Granulocytes
    • Neutrophils
    • Basophils
    • Eisinophils
  • Agranulocytes
    • Monocytes
    • Dendritic cells
    • Lymphocytes
    • T cells
    • B cells
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Phagocytosis
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  • Phago: from Greek, meaning eat
  • Cyte: from Greek, meaning cell
  • Ingestion of microbes or particles by a cell performed by phagocytes
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Oxidative Burst
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  • Bacterium adheres to membrane of neutrophil
  • NADPH is produced
  • NADPH oxidase uses electron from NADPH to produce superoxide
  • Superoxide dismutase converts superoxide to hydrogen peroxide 
  • Hydrogen peroxide burst kills bacterium
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Microbial Evasion of Phagocytosis
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  • Inhibit adherence: M proten, capsules- Streptococcus pyogenes, S. pneumoniae
  • Kill phagocytes: leukocidins- Staphlyococcus aureus
  • Lyse phagocytes: membran attack complex- Listeria monocytogenes
  • Escape phagosome- Shigella, Rickettsia
  • Prevent phagosome-lysosome fusion- HIV, Mycobacterium tuberculosis
  • Survive in phagolysosome- Coxiella burnettii
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Inflammation
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  • Activation of acute-phase proteins (complement, cytokine, and kinins)
  • Vasodilation (histamine, kinins, prostaglandins, and leukotrienes) 
  • Redness
  • Swelling (edema)
  • Pain
  • Heat
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Histamine
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  • Vasodilation, increased permeability of blood vessels
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Kinins
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  • Vasodilation, increased permeability of blood vessels
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Prostaglandins
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  • Intensify histamine and kinin effect
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Leukotrienes
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  • Increased permeability of blood vessels, phagocytic attachment
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Process of inflammation
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  1. Chemicals such as histamine, kinins, prostaglandins, leukotrienes, and cytokines are released by damaged cells
  2. Blood clot forms
  3. Abscess starts to form
  4. Margination- phagocytes stick to endothelium
  5. Diapedesis- Phagocytes squeeze between endothelial cells
  6. Phagocytosis of invading bacteria occurs
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Fever
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  • Abnormally high body temperature
  • Hypothalamus is normall set at 37o C
  • Gram-negative endotoxins cause phagocytes to release interleukin-1 (IL-1)
  • Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature
  • Body increases rate of metabolism, and shivering occurs, which raise temperature 
  • Vasodilatin and sweating: body temperature falls (crisis)
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Advantages/Disadvantages
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  • Advantages
    • Increases transferrins
    • Increases IL-1 activity
    • Produces interferon
  • Disadvantages
    • Tachycardia
    • Acidosis
    • Dehydration
    • 44-46o C fatal
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The complement system
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  • Serum proteins activated in a cascade
  • Activated by 
    • Antigen-antibody reaction
    • Proteins C3 and a pathogen
  • C3b causes opsonization
  • C3a+ C5a cause inflammation
  • C5b+ C6 + C7 + C8 + C9 cause cell lysis
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Outcomes of complement activation
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  1. Inactivated C3 splits into activated C3a and C3b
  2. C3b binds to microbe, resulting in opsonization
  3. C3b also splits C5 into C5a and C5b
  4. C5b, C6, C7, and C8 bind together sequentially and insert into the microbial plasma membrane, where they function as a recptor to attract a C9 fragments are added to form a channel. Together, C5b through C8 and the multiple C9 fragments form the membrane attack complex, resulting in cytolysis. 
  5. C3a and C5a cause mast cells to release histamine, resulting in inflammation; C5a also attracts phagocytosis
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Effects of Complement Activation
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  • Opsonization: enhanced phagocytosis
  • Membrane attack complex: lysis of the invader
  • Attract phagocytes by chemotaxis
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Classical pathway of complement activation
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  • C1 is activated by binding to antigen-antibody complexes
  • Activated C1 splits C2 into C2a and C2b, and C4 into C4a and C4b
  • C2a and C4b combine and activate C3, splitting it into C3a and C3b
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Some bacteria evade complement
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  • Capsules prevent C activation
  • Surface lipid-carbohydrate complexes prevent formation of membrane attack complex (MAC)
  • Enzymatic digestion of C5a
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Interferons
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  • IFN-alpha and IFN-beta: cause cells to produce antivirla proteins that inhibit viral replication
  • IFN-gamma: causes neutrophils and macrophages to phagocytize bacteria
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Antiviral action of alpha and beta interferons
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  1. Viral RNA from an infecting virus enters the cells
  2. The infecting virus replicated into new viruses
  3. The infecting virus also induces the host dcell to produce interferon mRNA (IFN-mRNA), which is translated into alpha and beta interferons.
  4. Interferons released by the virus-infected host cell bind to plasma membrane or nuclear membrane receptors on unlimited neighboring host cells, inducing them to synthesize antiviral proteins (AVPs). These include oligoadenylate synthetase and protein kinase.
  5. New viruses released by the virus-infected host cell infect neighboring host cells
  6. AVP's degrade viral mRNA and inhibit protein synthesis - and thus interfere with viral replication. 
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Transferrins
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  • Bind serum ion
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Antimocrobial peptides
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  • Lyse bacterial cells
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