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Host Defense Exam 2 > Infections > Flashcards

Infections Flashcards

1
Q

List the 4 categories of disease-causing pathogens.

A
  • extracellular (bacteria, parasites, fungi)
  • intracellular (bacteria, parasites)
  • viruses
  • parasitic worms
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2
Q

What are the primary barriers to infection?

A
  • physical: skin, mucosal surfaces

- chemical

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3
Q

Describe the skin as a barrier to infection.

A
  • keratinocyte layers
  • dry
  • acidic
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4
Q

Describe the mucosal surfaces a barrier to infection.

A
  • mucus
  • ciliated epithelium
  • secretory IgA
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5
Q

Describe chemical barriers to infection.

A
  • skin is dry and acidic. pathogens that can withstand acidic conditions are more likely to infect after direct tissue damage
  • lysozymes are secreted in tears and saliva. antibacterial; degrades peptidoglycan layer of both gram positive and gram negative bacteria
  • antimicrobial peptides are secreted by epithelial cells and phagocytes create pores in pathogen membranes
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6
Q

List antimicrobial peptides (AMPs) secreted by epithelium and phagocytes.

A
  • defensin and cathelicidins: anti-bacterial, viral, and fungal
  • histatins: anti-fungal
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7
Q

Define PAMPs.

A

Pathogen-Associated Molecular Pattern

  • conserved surface peptide or epitope
  • recognized by resident immune cells
  • alerts immune system of the type of pathogen and location of invasion
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8
Q

Define TLRs.

A

Toll-Like Receptors

  • primitive, highly conserved PAMP recognition receptors
  • stimulates intracellular signaling
  • increases cytokine production and immune cell recruitment
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9
Q

List TLRs responsible for recognizing bacteria.

A
  • TLR2 (both - lipoproteins)
  • TLR4 (only gram negative - LPS)
  • TLR5 (both - flagellin)
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10
Q

List TLRs responsible for recognizing viruses.

A
  • TLR3
  • TLR7
  • TLR8
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11
Q

List TLRs responsible for recognizing both bacteria and viruses.

A
  • TLR9
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12
Q

Define NOD-like receptors.

A
  • intracellular

- cytosolic PAMP receptors

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13
Q

Define NOD1.

A
  • recognizes gram NEGative
  • peptidoglycan breakdown products
  • ex: salmonella
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14
Q

Define NOD2.

A
  • recognizes BOTH gram negative and gram positive
  • recognizes myco. TB (fungal)
  • found enriched in gut cells
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15
Q

Describe the relationship between Crohn’s Disease and NOD2.

A
  • some people with Crohn’s have a NOD2 mutation
  • if you have a NOD2 mutation…can’t effectively recognize bacterial and fungal PAMPs
  • causes dysbiosis and disease symptoms
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16
Q

Define glucan receptors.

A
  • recognizes B-glucans on FUNGAL cell walls
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17
Q

Define scavenger receptors.

A
  • recognizes BACTERIAL cell wall components
18
Q

What does PAMP receptor activation lead to?

A
  • inflammatory cytokines
  • recruit immune cells
  • activates T cells (initiate adaptive immunity)
  • promote bactericidal killing by activating AMPs and ROS production
  • phagocytosis and respiratory burst
19
Q

List PAMP receptors.

A
  • TLRs (BACTERIAL, VIRAL, FUNGAL)
  • NOD (some BACTERIAL, myco. TB)
  • glucan (FUNGAL)
  • scavenger (BACTERIAL)
20
Q

Pair up complement-mediated actions with the pathogens they affect.

A
  • MACs - only gram NEGATIVE; (gram positive and fungi are resistant due to their cell wall composition)
  • Opsonization by C3/C3R - broad acting; BACTERIAL
21
Q

Complement deficiencies render patients significantly more susceptible to…?

A
  • bacterial infection

- esp. Neisseria meningidits and pneumococci

22
Q

Define respiratory burst.

A
  • after C3R PAMP receptor activation, macrophages and neutrophils are activated to kill the pathogen
  • phagosome with pathogen fuses with lysosome containing ROS to damage microorganism
23
Q

Define chronic granulomatous disease.

A
  • defective NADPH oxidase
  • cannot carry out respiratory burst
  • cannot kill pathogens
  • susceptible to recurrent fungal and catalase postive bacteria
24
Q

What are the 2 innate anti-viral effectors?

A
  • interferon type 1

- NK cells

25
Q

Describe the role of Type 1 interferons in anti-viral immunity.

A
  • release of Type 1 IFN is stimulated by anti-viral TLRs (3, 7, 8)
  • IFNa and IFNb are secreted from the infected cell and stimulate transcription of IFN-Stimulated Genes (ISGs) in neighboring cells
  • prevent viral synthesis and spread
26
Q

What is the difference between Type 1 and Type 2 IFN?

A
  • Type 1 (a, b) = antiviral

- Type 2 (g) = antiviral and antibacterial

27
Q

Describe the role of NK cells in anti-viral immunity.

A
  • recruited to site of infection
  • stimulated by IFN
  • occurs before stimulation of T cells and adaptive immunity
28
Q

Describe the role of antibody-mediated opsonization in infection clearing.

A
  • works for EXTRAcellular BACTERIA and FUNGI
  • antibody binds to surface markers => allows for phagocytosis by macrophages
  • S. aureus can evade this with Protein A
29
Q

Describe the role of antibody-mediated neutralization in infection clearing.

A
  • specific to BACTERIA (NOT virus)
  • antibody binds to bacterial toxins and clears them
  • ex: cholera in the gut
30
Q

Describe the role of antibody-mediated complement activation in infection clearing.

A
  • recall: only gram negative bacteria are susceptible to MACs
31
Q

Describe the role of T cells in infection clearing.

A
  • only for INTRAcellular bacteria

- Th1 mediated

32
Q

Describe the mechanism by which virally infected cells are cleared.

A
  • CD8 T cell mediated

- NK cells (IFN)

33
Q

How are parasitic infections controlled?

A
  • complement
  • IgE (antibody-dependent cellular cytotoxicity)
    ==> bound to eosinophils; eosinophil-mediated killing
34
Q

Describe the immune response against: influenza virus.

A
  • recognition by TLR3, 7, 8, 9
  • activates Type 1 IFN and NK cells
  • extracellular pathogen
  • T-cell: CD8 mediated killing
  • resistant to antibody-mediated neutralization
35
Q

Describe the immune response against: candida albicans (extracellular fungi).

A
  • recognition by glucan receptor
  • affected by AMPs (defensin, cathelicidins, histatins)
  • resistant to MACs
  • affected by antibody-mediated opsonization
36
Q

Describe the immune response against: staphylococcus aureus (gram positive, extracellular, bacterial)

A
  • recognition by TLR2, 5, 9, scavenger
  • affected by AMPs: defensins, cathelicidins
  • resistant to MACs
  • affected by chemical barrier lysozymes
  • affected by antibody-mediated opsonization and neutralization
37
Q

Describe the immune response against; neisseria meningiditis (gram negative, extracellular, bacterial).

A
  • recognition by TLR2, 4, 5, 9, scavenger
  • affected by AMPs: defensins, cathelicidins
  • affected by MACs, opsonization, complement
  • affected by chemical barrier lysozymes
38
Q

Describe the immune response against: Vibrio cholera (gram negative, extracellular, bacteria, toxin).

A
  • recognition by TLR2, 4, 5, 9, scavenger
  • affected by AMPs: defensins, cathelicidins
  • affected by chemical barrier lysozymes
  • affected by antibody-mediated neutralization
  • affected by MACs, opsonization, complement
39
Q

Describe the immune response against: mycobacterium tuberculosis (intracellular, bacteria).

A
  • recognition by NOD2
  • affected by AMPs: defensins, cathelicidins
  • affected by chemical barrier lysozymes
  • Th1 mediated response
  • resistant to antibody-mediated processes
40
Q

Describe the immune response against: schistosoma mansoni (parasite).

A
  • complement

- IgE and eosinophil mediated killing

Host Defense Exam 2 (11 decks)

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