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Microbiology & Immunity > 24- Microbial Immune Evasion Mechanisms > Flashcards

24- Microbial Immune Evasion Mechanisms Flashcards

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Biology 101 flashcards
1
Q

what is virulence?

A

the capacity of a pathogen to infect and cause disease – quantitative measure

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2
Q

what are virulence factors?

A

proteins that enable the pathogen (bacteria/virus) to infect

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3
Q

what are adhesins?

A

molecules that aid in attachment and allow bacteria to establish a niche in mucosal surfaces

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4
Q

what are the two main ways through which virulence factors evade host defences?

A

promote colonisation and adhesion to establish an infection via adhesins

promote tissue damage by toxins which
- damage cells, tamper with host cell signalling, and help growth and transmission of bacteria

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5
Q

what are the main functions of the complement system?

A

induces inflammatory response
promotes chemotaxis (via C3a and C5a as chemoattractants for immune cells)
increase/promote phagocytosis by opsonization
increase vascular permeability
mast cell degranulation
lysis of cell membranes

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6
Q

what are defensins?

A

antimicrobial peptides, form part of the innate immune response by protecting the host against microbial infections

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7
Q

what are alpha-defensins?

A

found in neutrophil granules, released upon degranulation

broad-spectrum antimicrobial activity against bacteria, fungi, and some viruses - disrupt the cell membrane, leads to cell lysis

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8
Q

what are beta-defensins?

A

produced by epithelial cells lining the skin, resp & urogenital tracts

broad-spectrum antimicrobial activity by disrupting their cell membranes = leads to cell lysis

act as chemoattractants for immune cells, aid in inflammation and fighting infection

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9
Q

list different elements bacteria have to stop complement activating (5)

A
  • LPS and capsules on bacterial cell surfaces prevent triggering complement
  • negative antibody binding mechanisms
  • disrupting CS regulation by sequestering factor H on bacterial cell surfaces
  • producing C5a proteases
  • expelling MAC complexes through blebbing
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10
Q

how do bacterial LPS and capsules prevent complement activation?

A

composition of LPS and bacterial capsules can block bacterial recognition by complements
- prevent C3b binding to PAMPs on bacterial cell surfaces
- prevent C3b receptor access

prevents activation of alternative pathway, affects opsonisation and efficient phagocytosis

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11
Q

how does negative antibody binding affect complement activation?

A

some bacteria can preferentially bind different antibodies

inappropriately bind the wrong class of antibody, prevents proper activation of the classical complement pathway

e.g. being coated in IgA which doesn’t activate the classical pathway

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12
Q

what is factor H?

A

potent complement regulatory protein

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13
Q

how does dysregulation of the complement system by sequestering factor H affect complement activation?

A

bacteria sequester factor H and negatively regulate it - prevent formation of C3 & 5 convertases = prevent complement activity

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14
Q

how do C5a proteases affect complement activation?

A

C5A proteases produced by bacteria degrade complement protein C5a

C5a acts as a chemoattractant for immune cells to the site of infection & pro-inflammatory molecule = dampens host inflammatory/ immune response

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15
Q

how does blebbing off MAC complexes affect complement activation?

A

bacteria can secrete enzymes to degrade MACs or induce blebbing to shed MAC off its surface and avoid cell lysis

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16
Q

list mechanisms bacteria have developed to prevent phagocytosis (3)

A

produce leucocidins
produce protein A
capsules

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17
Q

how do leucocidins help bacteria prevent phagocytosis?

A

potent enzyme which targets immune cells - breaks down neutrophils and macrophages, prevents phagocytosis

produced by Staphylococci

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18
Q

how does protein A help bacteria prevent phagocytosis?

A

protein A - high-affinity binding with Fc region of IgG antibodies, prevents phagocyte Fc receptors from binding

prevents phagocytosis

produced by Staphylococci

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19
Q

how does a capsule help bacteria prevent phagocytosis?

A

consists of polysaccharides - acts as a protective barrier and helps bacteria evade immune recognition

may contain PAMPs the immune system won’t recognise

present in meningitidis and Hib bacteria

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20
Q

list mechanisms bacteria have developed to prevent phagocytosis (5)

A

promote their uptake through safe routes
prepares cell for invasion beforehand
inhibits phagosome-lysosome fusion
evade phagosome-lysosome by escaping to cytoplasm
resist oxidative killing

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21
Q

intracellular pathogens promote their uptake through safe routes - how?

A

promote their own uptake through specific Fc receptors - e.g. CR3 or mannose-lectin receptors

direct phagocytosis through safe routes and avoid macrophages’ killing machinery - e.g. avoid lysosome fusion, ROS and degradative enzymes

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22
Q

intracellular pathogens prepare host cell for invasion beforehand - how? example?

A

e.g. Shigella toxin - uses type 3 secretion systems to inject effector proteins into host cells, prevents its killing mechanisms before phagocytosis

helps bacteria evade host immune responses and survive in phagocyte

23
Q

intracellular pathogens inhibit phagosome-lysosome fusion - how? example of pathogen?

A

e.g. M-TB inhibits PL fusion

bacteria contained with phagosome

prevents acidification of phagosome and release of antimicrobial enzymes, allows bacteria to replicate and survive inside phagosome

24
Q

intracellular pathogens evade phagosome-lysosome - how? example?

A

e.g. Listeria

escapes from phagosome into lysosome before PL fusion and acidification

avoids lysosomal degradation in the cytoplasm, continues to replicate

25
Q

intracellular pathogens resist oxidative killing - how?

A

bacteria produce enzymes like catalases and peroxidases to neutralise ROS generated by immune cell (e.g. neutrophil)

26
Q

enzymes intrac. pathogens produce to resist oxidative killing?

A

catalases
peroxidases

27
Q

how are bacteria normally destroyed by macrophages via C3b / alternative complement pathway?

A

macrophages have complement receptors - recognise C3B coated bacteria and activate the alternative complement pathway

bacteria is phagocytosed into phagosome - destroyed through phagosome-lysosome fusion
- degradative enzymes release
- acidification
- ROS and NOS production cause respiratory burst

peptides from pathogen are processed and presented on MHC 2 to naïve CD4+ T cells

28
Q

list different mechanisms that enable life of intracellular pathogens inside macrophages

A

directs phagocytosis via CR3

actin rearrangement

type 3 secretion systems to prepare cell

resists digestion via oxidative killing

pathogen escapes into cytoplasm e.g. Listeria

inhibits phagolysosome fusion – e.g. mycobacteria TB

controls antigen presentation

29
Q

intracellular pathogens directing phagocytosis via CR3 - how?

A

C3B coated pathogens can manipulate host cell CR3 receptors - facilitates pathogen entry into macrophage via a safe route

evades immune detection

30
Q

intracellular pathogens directing actin cytoskeleton rearrangement to survive in host cell - why?

A

induce actin cytoskeleton rearrangement to direct phagocytosis in a safe manner

31
Q

type 3 secretion systems used to enable pathogen life inside host cells - how?

A

specialised molecular needles inject effector proteins directly into the host cell, prepare cell for bacterial invasion and survival

32
Q

intracellular pathogens resist digestion via ROS - how?

A

pathogen is phagocytosed, immune cell starts producing ROS for oxidative killing of pathogen

pathogen produces enzymes like catalases and superoxidases to neutralise immune cell ROS and prevent oxidative damage

33
Q

intracellular pathogens control antigen presentation - how?

A

pathogens interfere with host cell antigen presenting machinery by producing peptides themselves to be presented on MHC

false peptides stimulate a decoy immune response, allows bacteria to thrive inside cell and evade CD8+ T cells, prevent macrophage activation

34
Q

example of a bacteria that escapes into cytoplasm?

A

Listeria

35
Q

example of a bacteria that inhibits phagosome-lysosome fusion?

A

mycobacterium tuberculosis

36
Q

example of a bacteria that uses type 3 secretion systems to prepare host cell for bacterial invasion beforehand?

A

Shigella

37
Q

example of bacteria that produces leucocidins and protein A to prevent phagocytosis?

A

Staphylococci

38
Q

list mechanisms from bacteria that enable antibody inhibition

A

produce proteins to mimic Fc region of antibodies

sequester antibodies incorrectly - bind them non-functionally

block effector functions of macrophage Fc receptors

39
Q

some bacteria produce proteins to mimic Fc region of antibodies - why? how?

A

bacteria produce mimic proteins that bind competitively to macrophage Fc receptors, prevent antibody binding

inhibits opsonisation and phagocytosis = bacteria can evade immune clearance

40
Q

how do some bacteria bind antibodies non-functionally?

A

bacteria bind antibodies through their Fc regions, block access of antibodies to their surface antigens

prevent opsonisation and phagocytosis via macrophages

41
Q

list different adaptive immunity mechanisms that allow bacteria to live inside cells

A

concealing antigen
immunosuppression
antigenic variation
persistence, latency or reactivation of pathogen

42
Q

bacteria concealing antigens to evade adaptive immunity - how?

A

hide in immunologically privileged sites/ cells

block antigen-MHC presentation to conceal antigen, avoids triggering adaptive immune responses
- e.g. herpes altering TAP protein activity

incorporate host molecules into their own surfaces
- e.g. CMV and beta2microglobulin

43
Q

how does herpes prevent MHC-antigen presentation?

A

affects TAP protein, interferes with mechanisms involved in antigen presentation

44
Q

how does CMV incorporate host molecules into its own surfaces to evade adaptive immune responses?

A

incorporates beta2microglobulin (component of MHC 1) into its own surface

45
Q

bacteria inducing immunosuppression to evade adaptive immunity - how?

A

downregulate MHCs and receptors essential for T cell activation

stop apoptosis of infected cell

alters expression of cytokines beneficial for pathogen’s survival

some pathogens produce IgA proteases, destroys IgA present on mucosal surfaces so it can establish an infection

46
Q

what is antigenic diversity?

A

the range of different antigens produced by a pathogen - leads to different strains/ serotypes expressing distinct surface antigens

47
Q

what is antigenic variation?

A

process by which a single pathogen alters its surface proteins/ antigens to evade the host’s immune response with phenotypic changes

pathogen presents different antigens over time to evade immune detection

48
Q

examples of changes from antigenic variation?

A

changes in capsules
lose flagella
surface sugars
colony morphology or virulence

49
Q

pathogenic mechanism of Streptococcus pneumoniae

A

invades and colonises nasopharynx through adhesins, secretes IgA proteases to prevent IgA-mediated killing

produces mucosal specific inflammation/ otitis

Strep migrates to resp tract, bypasses surfactant protein defences and reaches endothelium - produces pneumolysin
- causes damage to endothelial cells, allows bacteria to enter tissue

infection reaches lung - evades phagocytosis from alveolar macrophages by capsule traits

detection of specific PAMPs and secreted pneumolysin toxins induces inflammation, causes bystander tissue damage = contributes to lung damage

potentially leads to - pneumonia, otitis, toxic shock, septicaemia, meningitis

50
Q

affect of many different serotypes?

A

antigenic variation through capsules preserves transmission at a population level

51
Q

how does VZV use latency as an immune evasion mechanism & transmission?

A

first infects person as chickenpox - establishes latency in dorsal ganglions of the CNS

reactivates later as shingles

within its period of latency the population will have changed - can infect the next generation of new, susceptible members

52
Q

differentiate antigenic variation and phase variation

A

PHASE variation - reversible on/off switching of gene expression, causes changes in specific surface proteins

ANTIGENIC variation - ability of pathogens to alter the antigens presented on their surface

53
Q

antigenic variation in Neisseria?

A

pilins - structural proteins involved in pili attachment to host surfaces for initial infection

undergoes antigenic variation to evade immune detection and maintain infection

54
Q

phase variation in Neisseria?

A

capsule and Opa proteins of Neisseria undergo phase variation

expression altered in response to environmental cues or host immune responses

pathogen changes surface properties, helps immune evasion

Microbiology & Immunity (37 decks)

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