Host Defense Flashcards

1
Q

Extra cellular bacteria mediate tissue distraction in what 2 ways?

A
  1. Induce inflammation

2. Release of toxins

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2
Q

the goals of host immune responses to extracellular bacteria:

A

Neutralize toxins and kill bacteria

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3
Q

Innate responses to extra cellular bacteria

A
  1. Phagocytosis via neutrophils, monocytes, and macrophages

2. Peptidoglycan and LPS can trigger alternative complement pathways to lyse or opsonize bacteria

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4
Q

Adaptive immunity towards extracellular bacteria

A

-Activated Tcell produce interferon gamma to activate macrophages and initiate B cell mediated humoral immunity.
- humoral immmnity: igG opsonizes bacteria. Toxin specific antibodies neutralize toxins
IgM and IgG activate complement pathway to Lyse Microbes

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5
Q

Immunity evasion by extracellular bacteria is achieved by what 2 mechanisms?

A
  • Polysaccharide capsules resist phagocytosis and inhibit complement activation via alternative pathway
  • genetic variation attempt to keep one step ahead of antigen specific antibodies
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6
Q

Deleterious effects of immune system responses to extracellular bacteria

A
  1. Septic shock: gram negative bacteria promote macrophage production of TNF and IL-1
  2. superantigens bind tightly to MHC class II proteins and the variable region of the TCR on tcells Causing them to be activated and release a large amount of cytokines such as TNF-alpha = shock-like presentation. Eg. Staph enterotoxins causing toxic shock syndrome
  3. Disease causing Ab’s can be made in response to strep. Eg rheumatic fever
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7
Q

Method for eradicating intercellular bacteria (innate)

A

NK cells are activated by IL-2 that is produced by macrophages. NK cells produce interferon gamma which in turn activate macrophages to high levels making them more efficient killers or intracellular microbes.

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8
Q

Adaptive immunity to intracellular bacteria…

A
  • mediated by “delayed-type hypersensitivity reaction” where T-cells become activated to release interferon gamma then macrophages eliminate the microbes
  • cytotoxic T cells are generated. Class I mhc activation occurred is bacteria if the microbe escapes a phagosome or protein antigens bend up in the cell cytosol.
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9
Q

How mycobacterium evades immune system:

A

Prevents fusion of the phagosome and lysosomes, also scavenges for reactive oxygen intermediates to prevent bacterial killing

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10
Q

How listeria evades he immune system

A

Disrupts phagosome and escapes into the cytosol

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11
Q

Deletriuus effects of the immune response towards intracellular bacteria

A

-granuloma formation, esp. in lungs

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12
Q

Innate response to viruses

A
  • stimulation of interferon alpha and beta production by infected cell hosts
    Aka type 1 interferon: acts to inhibit viral replication in surrounding host cells
  • NK cells lyse infected cells ( activity increased by interferon 1) also viruses down regulate mhc 1 molecules. The absence of mhc 1 allows more NK activity
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13
Q

Adaptive immunity to viruses

A
  • the presence of antibody is most helpful before the virus invades a cell. This prevents binding of the virus to host, opsonization, and activate complement.
  • CTC are most important during established viral infections; they can lyse cells before the virus completes replication process. They also recognize particles presented on mhc class I
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14
Q

Viral evasion of immunity

A
  • point mutations
  • reassortment of genomes
  • Eg HIV has an error probe reverse transcriptase point mutations . Influenza does antigen alterations and rearrangements
  • prevention of MHC I presentation so the cell won’t be killed by CTC’s
  • hiv kills CD4 + Tcells
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15
Q

Deleterious impacts of viral immune response

A

-CTC’s may Cause pathological lesions instead of solely targeting the virally infected cells. Hep B - liver attack
-viruses may have homologous proteins to humans –> cross reactivity with normal
Host tissues

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16
Q

Immunity to fungi innate

A

Neutrophils are the principle mediator- phagocytosis of fungus, lysosomal degradation and reactive O2
-neutropenia causes fungal susceptibility

17
Q

Fungus: adaptive immunity

A

Cell Mediated and humoral

Th1 Mediated response
Elimination by CTC or granuloma formation

Humoral - unknown

18
Q

Innate immunity to parasites

A
  • macrophages phagocytosis only works for protozoans, sometimes
  • alternative complex pathway- initiated by helminths (often there is resistance)
    Also there is resistances to granule contents of neutrophils and macrophages
19
Q

Additive immunity to protozoan

A
  • eg. Leishmania lives in macrophages and generates CD4 + activation generate th1 response. CD4+ tcells secret interferon gamma. = meaner and more efficient macrophages
20
Q

Question : intracellular protozoan cause a CD4 reaction.. why?

What are grabulomas?

A

??

21
Q

Adaptive immunity: schistosoma

A
  • th1 mediated response that causes granulomas
22
Q

Adaptive immunity: plasmodium

A

Malaria
Induces th1 response in the form of CTC’s
Ab’s are not effective against this parasite as the CTC

23
Q

Adaptive immunity: helminths

A

Helminths elicits lots of igE used by eosinophils in an ADCC attack as an example of th2 response

24
Q

How parasite avoid immunity

A
  • protective shields/hideouts in GI lumen
  • coating with host proteins (ABO or MHC)
  • outer surface does not activate complement
  • repair after MAC
  • extracellular enzymes that cleave Abs
  • continuously change surface antigen
  • she’s their antigens after being bound by an ab
  • resistance to immune effector mechanisms
25
Q

Deleterious impacts of fungal immune response

A
  • chronic infection results in large immune complexes that can get lodged in blood cells to cause vascular is, and nephritis
  • chronic activation of adaptive immunity to schistosoma mansoni causes liver fibrosis and disrupts liver venous flow= portal hrn and cirrhosis
  • filaria worms lodge in lymphatic channels, chronic th1 immnunity causes sever fibrosis and restriction of the lymph flow=lymphedema