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Frontiers in Infectious diseases > L10 - How Bacteria Evade the Human Immune System to Cause Disease > Flashcards

L10 - How Bacteria Evade the Human Immune System to Cause Disease Flashcards

Intended Learning Outcomes (ILOs) •Understanding of ‘evolutionary arms race’ between pathogen and host •Outline of the human immune system •Specific mechanisms of bacterial immune evasion (89 cards)

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1
Q

What is the Red Queen Hypothesis in the context of host–pathogen interactions?

A

It is the idea that species must continually adapt and evolve not only for reproductive success but also for survival, because competing organisms are also evolving.

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2
Q

Who first proposed the Red Queen Hypothesis and when?

A

It was first proposed by evolutionary biologist Leigh van Valen in 1973.

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3
Q

How does the Red Queen Hypothesis apply to the interaction between hosts and pathogens?

A

It suggests that hosts and pathogens are engaged in a continuous cycle of adaptation, where hosts develop immunity and pathogens counter-evolve mechanisms to evade that immunity.

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4
Q

What does the concept imply about the ongoing development of species in a shared environment?

A

It implies that continual evolution is necessary merely to maintain relative fitness within the co-evolving system.

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5
Q

What are the two main divisions of the human immune system?

A

The immune system is divided into the innate and adaptive components.

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6
Q

What is a key feature of the innate immune system?

A

It provides an immediate, non-specific response to invading pathogens.

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7
Q

How does the adaptive immune system differ from the innate immune system?

A

It generates a specific response and retains memory of past infections, allowing for a more effective response upon re-exposure.

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8
Q

What are the three main categories of bacterial immune evasion?

A

They include manipulation of innate immune responses, disruption of adaptive immune responses, and lifecycle adaptation.

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9
Q

Give an example of a strategy used to manipulate innate immune responses.

A

Evasion of the complement system.

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10
Q

How can bacteria disrupt adaptive immune responses?

A

By targeting B cells for destruction or interfering with antibody production, and by manipulating T-cell responses using superantigens.

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11
Q

Give examples of lifecycle adaptation for evasion strategy?

A

It involves invading or internalising host cells, developing biofilms, and forming persister cells.

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12
Q

Which plasma proteins help prevent self-damage by the complement system?

A

Factor H, Factor I, C4b-binding protein, and C1 inhibitor.

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13
Q

What cell-bound regulators are used by the host to control complement activation?

A

Decay-accelerating factor (CD55), complement receptor 1 (CD35), membrane cofactor protein (CD46), and CD59.

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14
Q

How does Staphylococcus aureus inhibit complement activity?

A

It secretes evasins such as extracellular fibrinogen binding protein (Efb), extracellular complement binding protein (Ecb), and staphylococcal complement inhibitor (SCIN), which target complement components like C3d and C3b.

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15
Q

What is the mechanism by which SCIN interferes with complement activation?

A

SCIN’s N-terminal tail interacts with specific domains and components of the C3 convertase, preventing the cleavage of C3.

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16
Q

How do Efb and Ecb prevent complement-mediated damage?

A

Their TED domains attach to C3b on the bacterial surface, stabilising the proconvertase complex and preventing its cleavage by Factor D.

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17
Q

How does Streptococcus pyogenes evade the complement system?

A

It uses proteases (such as SpeB, EndoS, Mac-2, IdeS), molecules that block complement proteins, converts plasminogen to plasmin via streptokinase, and produces inhibitors of the membrane attack complex.

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18
Q

What role does Factor H play in complement regulation?

A

Factor H is a plasma glycoprotein that accelerates the decay of alternative pathway C3 convertases and acts as a cofactor for Factor I to inactivate C3b.

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19
Q

How can microbes benefit from recruiting Factor H?

A

By recruiting Factor H, microbes prevent complement activation on their surface, aiding in immune evasion.

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20
Q

What is the function of C4b-binding protein in the immune system?

A

C4b-binding protein binds activated C4b, acts as a cofactor for Factor I to inactivate C4b, and inhibits the formation of the classical pathway C3 convertase.

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21
Q

Why is the recruitment of C4b-binding protein advantageous for pathogens?

A

It limits complement activation and thereby protects the pathogen from immune clearance.

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22
Q

How does the bacterial capsule help evade phagocytosis?

A

The capsule, composed of polysaccharides, can block the access of complement fragments to the bacterial surface and prevent recognition by phagocytic receptors.

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23
Q

What additional role does the capsule play in immune evasion?

A

It can also mask antigenic proteins, hindering antibody recognition.

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24
Q

How do IgG-binding proteins contribute to the evasion of phagocytosis?

A

They bind to IgG and IgM antibodies, preventing proper antigen–antibody interactions and reducing opsonisation.

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25
Can you provide examples of IgG-binding proteins used by bacteria?
Staphylococcus aureus expresses Protein A and Sbi, while Streptococcus pyogenes utilises members of the M-protein family.
26
What mechanism does Staphylococcus aureus use to interfere with neutrophil recruitment?
It secretes a chemotaxis inhibitory protein (CHIPS) that blocks the chemotactic signals required for neutrophil migration.
27
What are neutrophil extracellular traps (NETs) composed of?
They consist of extracellular DNA, histones, and chromatin, often coated with antimicrobial peptides.
28
How can NETs be generated by neutrophils?
can NETs be generated by neutrophils?  A: NETs can form either through the process of NETosis, which involves slow cell death, or through non-lytic NETosis, where live cells rapidly release NETs.
29
Describe one mechanism by which bacteria can reduce NET formation.
Some bacteria mimic sialic acids to dampen the generation of reactive oxygen species, thereby reducing NETosis.
30
How do bacterial capsules assist in defending against NET-mediated killing?
Capsules can help shield bacteria from the antimicrobial peptides contained within NETs.
31
What enzymatic strategy do bacteria use to dismantle NETs?
They secrete endonucleases that degrade the extracellular DNA of NETs.
32
How can certain bacteria turn NET components into a weapon against the immune system?
By secreting specialised molecules, they convert NET-derived products into toxic compounds that trigger immune cell death.
33
What bactericidal mechanisms are deployed by phagocytes?
Phagocytes use reactive oxygen species from NADPH oxidase, degradative enzymes, and cationic peptides from granules to kill bacteria.
34
How does Staphylococcus aureus counteract reactive oxygen species inside phagocytes?
It produces enzymes such as superoxide dismutases, catalase, and alkyl hydroperoxide reductase to neutralise reactive oxygen species.
35
What is the role of staphyloxanthin in bacterial survival within phagocytes?
Staphyloxanthin helps to mitigate the effects of antimicrobial peptides.
36
How do the Dlt operon and mprF genes contribute to evading cationic antimicrobial peptides?
They modify the bacterial cell surface by incorporating D-alanine into teichoic acids and L-lysine into phosphatidylglycerol, reducing the overall negative charge.
37
Why is O-acetylation of peptidoglycan important for bacterial survival?
It confers resistance to lysozyme, thereby enhancing survival within phagocytes.
38
Which other bacterial pathogens are known to survive within phagocytes?
Mycobacterium tuberculosis, Salmonella typhi, Listeria monocytogenes, and Shigella flexneri, among others.
39
What distinguishes bacterial T cell superantigens from conventional antigens?
Superantigens bind directly to MHC class II molecules and T cell receptors without prior antigen processing, leading to widespread T cell activation.
40
What is the primary consequence of superantigen activity on T cells?
It causes uncontrolled activation of large numbers of CD4+ and CD8+ T cells, contributing to conditions such as scarlet fever and toxic shock syndrome.
41
How do superantigens alter the T cell receptor–MHCII interface?
They force the interface apart, preventing normal antigen recognition while still triggering T cell activation.
42
Which signalling pathway is predominantly involved in superantigen-induced T cell activation?
The lymphocyte-specific protein tyrosine kinase (LCK) pathway, which leads to sequential phosphorylation events and activation of phospholipase Cγ1.
43
How can superantigens influence the balance of T cell responses?
They may skew responses towards various T helper subsets or regulatory T cells, with low concentrations sometimes promoting an immunosuppressive, IL-10-rich environment.
44
What type of pathogen is Listeria monocytogenes, and what disease does it cause?
It is a Gram-positive bacterium responsible for listeriosis, a foodborne illness.
45
Which groups are most at risk from Listeria monocytogenes infection?
The young, the elderly, pregnant individuals, and immunocompromised people.
46
How does Listeria monocytogenes evade extracellular immune detection?
By invading host cells, it creates a protected intracellular niche.
47
Which bacterial surface proteins enable Listeria to enter host cells?
Internalins, such as InlA and InlB, bind to host receptors like E-cadherin and c-Met.
48
What critical process must Listeria complete after internalisation to ensure survival?
It must escape from the phagosome before it fuses with the lysosome, a step mediated by listeriolysin O (LLO) and phospholipase C.
49
Once in the cytosol, how does Listeria propagate?
It replicates within the cytosol and utilises the host’s actin polymerisation machinery for intracellular motility.
50
Which protein drives actin-based motility in Listeria monocytogenes?
ActA, which induces the formation of actin comet tails that facilitate movement and cell-to-cell spread.
51
How do LLO and phospholipase C contribute to bacterial dissemination?
They mediate the rupture of neighbouring cell membranes, allowing Listeria to move into adjacent cells.
52
What cell wall modifications does Listeria employ to avoid intracellular immune detection?
It utilises peptidoglycan N-deacetylation and O-acetylation to evade pattern recognition receptors and increase resistance to lysozyme.
53
In what way does Listeria dampen the host’s pro-inflammatory response?
The secretion of InlC inhibits NF-κB-dependent signalling by interfering with IKKa, preventing IκB phosphorylation and reducing pro-inflammatory cytokine production.
54
How does InlB protect infected cells from T cell-mediated killing?
InlB upregulates FLIP, which inhibits procaspase-8 cleavage and blocks Fas-mediated cell death, thereby prolonging the survival of infected cells.
55
What is the overall relationship between immune evasion strategies and bacterial pathogenicity?
The ability to evade the immune system is closely aligned with a bacterium’s capacity to cause disease.
56
How extensive are the immune evasion mechanisms used by bacteria?
Nearly every component of the host immune defence can be targeted, demonstrating the complexity of host–pathogen interactions.
57
Despite these evasion strategies, what is generally true about a healthy immune system?
A robust immune system typically manages to control most infections, even in the face of sophisticated bacterial evasion tactics.
58
What is the Red Queen hypothesis in the context of immune evasion?
It describes an evolutionary arms race where pathogens evolve to overcome host defenses, while the host simultaneously adapts to resist infection, leading to continuous cycles of adaptation.
59
What are the two main branches of the human immune system?
Innate Immunity: Provides rapid, non-specific defense using physical barriers (e.g., skin), chemical defenses (e.g., stomach acid), and cellular responses (e.g., phagocytes, complement proteins). Adaptive Immunity: Involves T cells and B cells, enabling antigen recognition, antibody production, and immunological memory.
60
How do bacteria evade the complement system?
Some, like Staphylococcus aureus and Streptococcus pyogenes, produce complement inhibitors (EFB and SPI) that block critical steps in the complement activation cascade, preventing opsonization and lysis.
61
What role does capsule formation play in immune evasion?
Bacterial capsules act as physical barriers that obstruct complement deposition and hinder phagocytosis, making it harder for the immune system to detect and eliminate bacteria.
62
How do superantigens impact the immune system?
They cause massive T cell activation by bypassing normal antigen recognition, leading to immune dysregulation and excessive inflammation, which can impair an effective immune response.
63
How can bacteria manipulate T cells to avoid immune detection?
Some bacteria, such as Listeria monocytogenes, produce proteins like InlB, which allow them to evade T cell detection and even induce T cell apoptosis, aiding bacterial survival.
64
How does intracellular survival aid in immune evasion?
Certain bacteria, like Listeria monocytogenes, invade host cells and resist degradation. They hijack actin polymerization to move within and between cells, avoiding immune detection.
65
What are some immune evasion strategies used by Staphylococcus aureus?
It produces secreted complement inhibitors and surface structures that prevent opsonization and phagocytosis.
66
How does Streptococcus pyogenes evade the immune system?
It uses proteases to degrade complement proteins and forms a capsule to block phagocytosis.
67
What makes Listeria monocytogenes a particularly effective intracellular pathogen?
It moves between cells using actin tails, avoiding phagocytosis and immune signaling inhibition to persist in host tissues.
68
Why is studying bacterial immune evasion important?
Understanding bacterial strategies provides insights into chronic infections, acute diseases, and vaccine development, helping researchers find ways to counteract bacterial infections.
69
How does the immune system typically overcome bacterial evasion?
Despite bacterial adaptations, a healthy immune system can generally control infections through its complex and adaptive responses.
70
What are antimicrobial peptide evasion strategies used by bacteria?
Protease secretion (e.g. S. aureus), outer membrane modifications, efflux pumps, capsule shielding.
71
How does antigenic variation differ from phase variation?
Antigenic: changes protein sequence; Phase: ON/OFF expression switching.
72
What are roles of bacterial capsules in immune evasion?
Prevent phagocytosis, reduce complement deposition, mimic host molecules, aid in adhesion.
73
How do leukocidins aid immune evasion?
Kill neutrophils, reduce phagocytic clearance, promote pus formation, e.g. PVL in S. aureus.
74
What are examples of intracellular survival mechanisms?
Inhibit phagosome-lysosome fusion, resist oxidative burst, escape to cytoplasm.
75
What features make biofilms immune-resistant?
Physical barrier, altered gene expression, quorum sensing, resistance to NETs.
76
How do bacteria inhibit complement activation?
Bind factor H or C4BP, secrete proteases, sialylate LOS, inhibit MAC formation.
77
How is IgA neutralization achieved by pathogens?
IgA1 protease cleaves IgA, prevents mucosal neutralization, aids colonisation.
78
What is the role of phase variation in pathogenesis?
Stochastic ON/OFF switching of surface proteins to evade immune detection.
79
How does fHbp aid Neisseria in complement evasion?
Binds host factor H, prevents C3b deposition, inhibits complement-mediated lysis.
80
What is the function of the S. pneumoniae capsule?
Inhibits phagocytosis, prevents opsonisation, reduces complement, vaccine target.
81
How does Neisseria gonorrhoeae vary its pili?
Recombination between pilE and pilS loci leads to antigenic variation.
82
What is the effect of LOS sialylation?
Mimics host glycans, inhibits complement activation, reduces antibody binding.
83
What do IgA proteases do?
Cleave IgA1 at hinge, disrupt mucosal immunity, produced by Neisseria and Haemophilus.
84
How do bacterial capsules affect opsonophagocytosis?
Prevent complement and antibody deposition, shield surface antigens.
85
What does the Type III secretion system do?
Injects effectors into host cells, modulates immune signalling, e.g. Salmonella.
86
How does Salmonella survive in macrophages?
Prevents lysosome fusion, detoxifies ROS, resides in SCVs.
87
What is the role of PVL in S. aureus infections?
Kills neutrophils, promotes pus and necrosis, enhances immune evasion.
88
Why are biofilms hard to treat?
Resist immune cells and antibiotics, promote chronic infection, alter gene expression.
89
How does molecular mimicry benefit pathogens?
Avoids immune recognition, may induce tolerance or autoimmunity.

Frontiers in Infectious diseases (21 decks)

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