Term
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Definition
- Lack of resistance to a disease
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Definition
- Ability to ward off disease
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Definition
- defenses against any pathogen
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Term
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Definition
- immunity or resistance to a specific pathogen
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Term
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Definition
- Intact skin
- Mucous membranes and their secretions
- Normal microbiota
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Term
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Definition
- Phagocytes, such as neutrophils, eosinophils, dendritic cells, and macrophages
- Inflammation
- Fever
- Antimicrobial substances
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Term
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Definition
- Specialized lymphocytes: T cells and B cells
- Antibodies
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Term
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Definition
- 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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Term
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Definition
- 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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Term
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Definition
- 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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Term
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Definition
- 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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Term
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Definition
- Granulocytes
- Neutrophils
- Basophils
- Eisinophils
- Agranulocytes
- Monocytes
- Dendritic cells
- Lymphocytes
- T cells
- B cells
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Term
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Definition
- 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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Term
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Definition
- 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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Term
Microbial Evasion of Phagocytosis |
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Definition
- 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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Term
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Definition
- Activation of acute-phase proteins (complement, cytokine, and kinins)
- Vasodilation (histamine, kinins, prostaglandins, and leukotrienes)
- Redness
- Swelling (edema)
- Pain
- Heat
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Term
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Definition
- Vasodilation, increased permeability of blood vessels
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Term
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Definition
- Vasodilation, increased permeability of blood vessels
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Term
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Definition
- Intensify histamine and kinin effect
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Term
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Definition
- Increased permeability of blood vessels, phagocytic attachment
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Term
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Definition
- Chemicals such as histamine, kinins, prostaglandins, leukotrienes, and cytokines are released by damaged cells
- Blood clot forms
- Abscess starts to form
- Margination- phagocytes stick to endothelium
- Diapedesis- Phagocytes squeeze between endothelial cells
- Phagocytosis of invading bacteria occurs
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Term
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Definition
- 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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Term
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Definition
- Advantages
- Increases transferrins
- Increases IL-1 activity
- Produces interferon
- Disadvantages
- Tachycardia
- Acidosis
- Dehydration
- 44-46o C fatal
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Term
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Definition
- 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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Term
Outcomes of complement activation |
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Definition
- Inactivated C3 splits into activated C3a and C3b
- C3b binds to microbe, resulting in opsonization
- C3b also splits C5 into C5a and C5b
- 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.
- C3a and C5a cause mast cells to release histamine, resulting in inflammation; C5a also attracts phagocytosis
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Term
Effects of Complement Activation |
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Definition
- Opsonization: enhanced phagocytosis
- Membrane attack complex: lysis of the invader
- Attract phagocytes by chemotaxis
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Term
Classical pathway of complement activation |
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Definition
- 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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Term
Some bacteria evade complement |
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Definition
- Capsules prevent C activation
- Surface lipid-carbohydrate complexes prevent formation of membrane attack complex (MAC)
- Enzymatic digestion of C5a
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Term
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Definition
- 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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Term
Antiviral action of alpha and beta interferons |
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Definition
- Viral RNA from an infecting virus enters the cells
- The infecting virus replicated into new viruses
- The infecting virus also induces the host dcell to produce interferon mRNA (IFN-mRNA), which is translated into alpha and beta interferons.
- 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.
- New viruses released by the virus-infected host cell infect neighboring host cells
- AVP's degrade viral mRNA and inhibit protein synthesis - and thus interfere with viral replication.
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