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Immuno Flashcards

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1
Q

What is the human microbiota?

A

a. Provide extra source of genes
b. Co-evolution → provides diverse physiological properties we have not had to evolve on our own = mutualist
c. 99.9% anaerobic (from stomach onwards; rare to grow in the stomach) → minute proportion aerobes
d. NB. Less than 30% are culturable

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2
Q

Why study the microbiome?

A

Data suggests that the microbiome is intimately associated with health and disease

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3
Q

What sort of bacteria do we find in the gut, throat, skin and vaginal canal?

A

Gut is dominated by gram negative

Skin and throat = gram positive

Vaginal = mainly gram positive

Number and species of bacteria vary greatly

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4
Q

What are the main phyla of the microbiota?

A

i. Bacteriodetes
ii. Firmicutes
iii. Actinobacteria
iv. Proteobacteria (eg. E. coli)

The relative concentration shift in different regions of the body

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5
Q

Where are most of the bacteria in the GIT found?

A

In the LI

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6
Q

What is the role of the microbiota?

A

Genes of the microbiota contribute to:
Metabolism
Immune protection

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7
Q

What phenomenon is observed in animals grown in a germ free environment?

A

Require more energy to function.

Indicates that microbiota must confer some mutualistic benefit

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8
Q

What are some factors which influence the gut microbiota?

A

Age - diversity decreases with age

Mode of delivery - i. Vaginal delivery associated with rapid acquisition of Firmicutes, Bifidobacteria
ii. Caesarian birth associated with delayed microbiota development + restricted diversity

Diet - influences diversity and numbers

Antibiotics - short term use can induce long term changes

Genetics and the environment

Chronic inflammation and the production of pro-inflammatory cytokines

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9
Q

What is the role of the microbiota in metabolic activity of the intestine?
(carbohydrates)

A

Assists in the breakdown of lactose (esp. early in life), cellulose, mucins broken down to SCFAs (10% calories)

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10
Q

What is the role of the microbiota in metabolic activity of the intestine?
(vitamins)

A

Produces vitamin K, biotin, folate (w/o microbiota problems with production of vitamins)

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11
Q

What is the role of the microbiota in metabolic activity of the intestine?
(bile acids)

A

Assists in the breakdown of bile acids and the reabosrbiton of its components

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12
Q

What is the role of the microbiota in metabolic activity of the intestine?
(Amino acids)

A

Assists in the breakdown, especially lysine and threonine; urea → NH3 allows nitrogen recycling to more aa

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13
Q

How do the microbiota alter the metabolic machinery of the host?

A 
Induce changes in host genes involved in CHO + lipid metab. (different phyla have different effects) 
Bacterial degradation of host glycans (e.g. mucin) elicits synthesis of new glycans by host 
Induces changes in host genes affecting angiogenesis→ influence supply of O2 and nutrients to tissues. 
Produce SCFAs (e.g. butyrate) that maintain enterocyte differentiation.
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14
Q

What process occurs in the colon and what are the results?

A 
Complex carbohydrates (such as dietary fibre) are metabolised by the microbiota of the colon to form oligosaccarides and monosaccarides.
These are then fermented to short chain fatty acid end products
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15
Q

What are the short chain fatty acids ends products in the colon?

A

Mainly acetate, proprionate and butyrate

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16
Q

What happens to the short chain fatty acid products of digestion?

A

They are absorbed by the colon

Butyrate provides energy for colonic epithelial cells

Acetate and proprionate reach the liver and peripheral organs where they acts as substrates for gluconeogenesis and lipogenesis

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17
Q

How to Short chain fatty acids control colonic gene expression?

A

By inhibiting the enzyme histone deacetlyase (HDAC)

Metabolic regulation through g-protein coupled receptors (GPR41/43)

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18
Q

What are the aggregates of lymphoid cells in the gut called?

A

Isolated lymphoid follicles (ILFs) - Large and Small intestine
Peyers patches - Small intestine only
These are sites for induction of T and B cell activation

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19
Q

What do goblet cells in the GIT secrete?

A

Mucins
Lysozyme
Lactoferrin

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20
Q

What do paneth cells secrete?

A

Defensins

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21
Q

What are the innate defences of the gut?

A 
Peristaltic action
Acid
Mucous layer
Enterocytes
Innate leucocytes
Mechanism for controlled antigen access
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22
Q

What are the specific roles of enterocytes in the innate defence of the gut?

A

Barrier - tight epithelial junctions (regular cell turnover)
Antimicrobial factors (bile, lactoferrin, complement)
Cytokines and chemokines

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23
Q

What cells allow controlled antigen access?

A

M cells

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24
Q

What are the signs of inflammation?

A 
Swelling
Heat
Loss of function 
Pain
Redness
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25
Q

How is IL-1 formed?

A

Inactive IL-1B precursor (31kDa) is cleaved to release IL-1B (18kDa)

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26
Q

What is familial cold urticaria?

A

Inactive IL-1B precursor (31kDa) is cleaved to release IL-1B (18kDa)

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27
Q

What gene is mutated in familial cold urticaria and what family of genes is it from?

A
  • Single nucleotide mutations of a gene called cryopyrin;

* cyropyrin identified as a member of the NOD-like receptor family

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28
Q

Why was the discovery of familial cold urticaria important in the development of our understanding of IL-1?

A
  • Mutations in cryopyrin gene found to be associated with IL-1 converting enzyme (ICE).
  • Cryopyrin associated with ICE (interleukin 1 converting enzyme)
  • When these patients are cold, the mutation in Cryopyrin some how increased ICE activity and we get increased IL1. (localized inflammatory response).
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29
Q

What is the inflammasome?

A

The inflammasome is a multiprotein oligomer

The inflammasome is responsible for activation of inflammatory processes

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30
Q

How is the inflammasomes activity regulated?

A

Excessive inflammasome activity would be very dangerous thus there are two regulatory mechanisms:

  1. The production of pro-IL-1B and pro-IL-18 is regulated by the presence of certain PAMPs
  2. The inflammasome complex is only assembled if a second series of PAMPs are present
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31
Q

What is the mechanism of gout?

A
  • Input (consumption) of purines in diet
  • Output (excretion) of uric acid (urate).
  • Problem in excretion of urate → urate precipitates into crystals → deposit in joints → very painful gout.
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32
Q

What happens after gout forms urate crystals in the joints?

A 
Urate crystals causing;
(i) Physical damage 
(ii) Activating inflammasomes
(iii) Macrophages come into joint and remove crystals → macrophages phagocytose crystals but these are too large/chemically difficult to degrade; 
→ crystals activate NLRP3 inflammasome
→ IL-1B production.
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33
Q

What is alum and when is it used?

A

Alum causes inflammation and induces an immune response. It is often used in immunisations to encourage an immune response.

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34
Q

What drug is used to treat gout?

A

Anakinra

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35
Q

When is anakinra absolutely contraindicated?

A

Neutropenia

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36
Q

What is anakinra?

A

It is an IL-1 receptor anatagonist

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37
Q

What relationship does obesity have to the production of IL-1B?

A

precipitation of fat metabolites (similar to crystals in gout) → induces very low grade chronic inflammasome activation → IL-1B.

38
Q

What role is IL-1B thought to play in the disease state of people with obesity?

A

a) Acts on hepatocytes to reduce their sensitivity to glucose →increased BGL → type 2 diabetes.
b) Also, accumulation of adipocytes in liver (steatohepatitis) = fatty liver;
c) Pancreas produces less insulin, destruction of beta cells;
d) deposits of fat in vessels causing atherosclerosis → LDL accumulation in intima → fatty precipitates → activates inflammasomes in macrophages → perpetuates chronic inflammation underlying atherosclerosis.
e) People are starting using Anakinra for type 2 diabetes in the hope of reducing the inflammation that perpetuates the insulin resistance and glucose desensitisation

39
Q

What is the mechanism by which a salmonella infection drives the immune response?

A

• Salmonella typhi infects and lives happily inside macrophage (IC pathogen like M. tuberculosis).
• Local infection → gastroenteritis;
• Systemic infection (invade Ep barrier) → typhoid fever (affect other organs e.g. liver, bone marrow).
• Salmonella bacteria phagocytosed into vesicle/endosome of macrophage. Salmonella has evolved to resist phagolysosomal degradation such that the vesicle in which it resides becomes its niche.
• They effectively modify the macropgae vesicle to make it habitable for them.
• To do this, they constantly inject molecules into the cytosol via a needle apparatus. The molecules and needle apparatus is recognised by the infected macrophage.
• So the constant translocation of vesicular content into cytosol → macrophage recognition → inflammasome activation → IL-1B and IL-18 produced.
1. IL-1B causes the macrophage to burst (commits suicide, takes one for the team) → release of salmonella into ECS for other phagocytes to eat them up.
2. Meanwhile, IL-18 activates:
(i) CD8+ T cells and NK cells
(ii) → secretion of IFN-y → optimal macrophage activation to kill IC salmonella more effectively.

40
Q

Where are Intra epithelial lymphocytes found and what is there role?

A

IELs intercalating with enterocytes; multiple subtypes (both adaptive and innate lymphocytes); non-conventional.
Upon encountering antigens, they immediately release cytokines and cause killing of infected target cells

41
Q

What is an unconventional role of peristaltic action in the gut?

A

It is part of the innate defences of the gut

42
Q

What is the defence role of the mucous layer/glycocalyx

A

It acts as a molecular sieve - it keeps commensals at ‘arms length’

43
Q

What is the immune function of the enterocytes (including goblet cells and paneth cells)

A
  1. Barrier: tight epithelial (Ep) junctions, regular shedding and replacement; Ep integrity is critical to host defences.
  2. Antimicrobials: bile, lactoferrin (goblet cells), complement, AMPs (antimicrobial peptides e.g. defensins)
  3. Cytokines (e.g. TGF-B) and chemokine
44
Q

What are the methods for controlled antigen access into the cells?

A

M cells and dendritic cells

45
Q

Where are M cells located?

A

Located directly over sites of organised lymphoid aggregates (Isolated Lymphoid Follicles (ILF) in SI/LI, and Peyer’s patches in SI)

46
Q

What is the function of the M cell?

A

Allows movement (in a controlled fashion) of antigen into the aggregates of lymph tissue below.

47
Q

What are the innate lymphocytes produces in the gut?

A 
Lymphoid tissue inducer
Intraepithelial lymphocytes (IEL's)
NK-22
Macrophages 
Mucosal associated invariant T cells (MAIT cells)
Invariant NKT cells
48
Q

What is the function of the Lymphoid tissue inducer?

A

Stimulate recruitment of:

DC, T/B cells to PP and Lymphoid Follicles

49
Q

What is the function of IELs in the gut?

A

1) Involved in host protection, epithelial repair,
2) Drive tolerogenic DCs (in contrast to DCs that drive an inflammatory TH1 response),
3) Damaged enterocytes can be removed by IELs.
4) Many produce IL-22

50
Q

What is the function of NK cells (NK-22)in the gut?

A

Produce multiple cytokines including IL-22

51
Q

What is the role of IL-22 in the gut?

A

It enhances the antimicrobial defence and epithelial repair and barrier integrity

52
Q

What is common to innate lymphoid cells (ILC’s)?

A

Whilst there are multiple subsets they have a cytokine expression pattern resemebling Th subsets (produce IFN-g, IL-17, IL-22, IL-5, IL-13)

53
Q

What is the function of MAIT cells in the gut?

A

They respond rapidly to bacterial antigens, most are CD8 positive

54
Q

What is the function of macrophages in the gut?

A

Express lower levels of TLRs

HYPOresponsive to TLR signalling and thus contributing to promoting a tolerogenic environment in gut.

55
Q

What functions of M cells allow them to function as antigen entry points?

A

Possess a folded luminal surface, NO VILLI.
No thick glycocalyx, don’t secrete mucus = much easier microbial access (desirable since the immune system wants to sample the external environment).

56
Q

How do dendritic cells in the gut sample antigens?

A

Directly

Indirectly through M cells

57
Q

What cell types do dendritic cells in the mucosa promote?

A

In steady state, DCs induce Treg (TGF-B) and Th2 (produces IL-4 which inhibits Th1 and Th17)

Under inflammatory conditions DCs may induce TH1 and TH17

58
Q

What effects do the tolerogenic T cells have on B cell class switching?

A

Treg and Th2 bias B cell isotype switching to IgA

59
Q

Why is IgA favoured in a non inflammatory response?

A

IgA is non-inflammatory and doesn’t activate C’ - it purely neutralises

60
Q

What role do DC play with addressin?

A

DCs induce mucosal adressin α4β7 (this is a homing receptor) (on activated T/B lymphocytes) which binds to MAdCAM1 (Mucosal Adressin cellular adhesion molecule 1 receptors on vascular Endothelial cells)
These leave the payers patches and circulate till they reach lymphoid tissues

61
Q

What happens to T/B cells activated in the PP (payer’s patches) or the mesenteric lymph nodes (MLN)?

A

T/B cells activated in the PP or mesenteric lymph nodes (MLN)

  1. Leave efferent lymphatics
  2. Enter the blood circulation, and acquire homing receptors α4β7 which bind MAdCAM1 on vascular endothelium of all mucosal surfaces
  3. They also have chmeokine receptors to get into the lamina propria.
62
Q

What happens to activated T and B cells once they have migrated into the lamina propria?

A

(i) Activated B cells produce sIgA (bucket loads)
(ii) CD4+ T cells - multiple roles (mostly Tregs in steady state)
(iii) CD8+ T cells protect against IC infections
(iv) Many of these activated T/B cells persist as memory cells.

63
Q

Describe the steps of induction and its effector mechanisms (general mechanism)

A

1) Ag sampling from gut lumen: M cells capture Ags (via endocytosis probably) and deliver to underlying PP or ILF (organised lymphoid aggregates; site of Ag presentation by APCs, T/B cell interaction and activation).
2) Efferents from PP and ILF to mesenteric LNs (MLNs). A subset of DCs can extend their dendritic processes through enterocytes and directly take up Ag.
3) APC (e.g. DC) processes Ag → migrates to mesenteric LNs (MLNs) → activate T cells, B cells. B cells secrete mainly sIgA. →
4) Activated T/B cells leave MLN via efferent →enter blood → migrate into LP (α4β7MAdCAM1).
5) Both stimulation and suppression take place in the MALT. But following activation of lymphocytes, there is a predominantly suppressive/tolerogenic response.
6) Enterocytes, Paneth cells secrete AMPs (e.g. defensins); Enterocytes release cytokines (TGFB).

64
Q

What role does the intestinal microbiota play with regard to the mucous layer and gut epithelium?

A

1) Direct: Block binding sites for bacteria and produce Bacteriocins
2) Indirect: Express PAMPS/metabolites which interact with TLR’s on the enterocytes. (TLR 2 and 4 mainly).

65
Q

What are the indirect effects of the intestinal microbiota on the epithelial cells?

A
  1. ↑ in Crypt Enterocytes and Paneth Cells
  2. Induce Antimicrobial peptides from Enterocytes/Paneth Cells.
  3. Induces the regulatory cytokines from Enterocytes/Paneth Cells. (TGF B, and IL-10)
  4. SCFAs (butyrate, acetate) inhibit NF-kB → inhibit inflammatory cytokine production. PAMP interaction with LTi, IELs, NK-22 cells →release of IL-22 → promotes Ep barrier integrity.
66
Q

How does the microbiota influence the development of lymphoid structures?

A
  1. PPs and MLNs develop prenatally
  2. whereas ILFs (isolated lymphoid follicles) develop postnatally (under microbiota influence):
  3. Signalling by microbiota→initiates development of ILFs.
  4. Microbes enter via M cells → initiate further development of PPs.
  5. Germ-free mice deficient in IgA, lymphoid tissue → no microbiota signalling →deficiency in ILF development→ B cells in these lymphoid tissues don’t produce IgA = microbiota is essential in providing developmental signals for ILF formation.
67
Q

How does the microbiota influence the development of lymphocyte subsets?

A
  1. Promotes differentiation of NK22cells (which produce IL-22)
  2. Restricts differentiation of inflammatory invariant NKT cells
  3. Induces cytokines TGF-B and other factors (e.g. retinoic acid) from Ep cells and IELs → influence LP DCs to drive regulatory T cell differentiation (Tregs, TH2
68
Q

What is the difference between physiological and pathological inflammation?

A

“physiological inflammation → ”Normal microbiota→ activation of DCs (via PAMP-PRR) can directly drive tolerogenic DCs to induce Tregs, TH2. This results in effective innate/adaptive defences without damage to host

“pathological inflammation” →Pathogenic bacteria → drive immunogenic, inflammatory DCs→ induce TH1, TH17. Results in damaging

69
Q

What are the three means by which the gut epithelium and lymphoid tissue appears to discriminate between friend and foe?

A 
Location and numbers
Epithelial PRR (pattern recognition receptor) detect invasion
Differential interaction with PRRs
70
Q

What does lymphoid tissue discriminate between with regard to location and numbers when it comes to differentiating between normal flora and pathogen?

A

Epithelial PRR “sense” bacterial numbers and proximity to epithelial surface.
Commensals are found at the luminal edge of mucous layer vs. pathogens bind tightly to/invade Ep. surface (via adhesins, invasins, mucinases, toxins).

71
Q

How does Epithelial PRR detect invasion as opposed to friend?

A

(TLR5 at basolateral surface) and damage (e.g. ROS and RNIs detected by endosomal PRRs).
Only microbes that have breached the Ep barrier and invaded can bind to endosomal/basolateral TLRs.

72
Q

How do differential interactions with PRRs signal friend or foe?

A 
Normal microbiota bind weakly with TLR
Inflammasome signalling (?)
73
Q

What disease states is dysbiosis thought to be directly and indirectly associated with?

A 
Nutritional deficiencies (malabsorbtion, steatorrhea, vitamin deficiencies)
Obesity and Mets
Inflammatory bowel diseases
Allergies
Autoimmune diseases
Infectious disease 
Others
74
Q

What is kwashiorkor?

A

is a form of severe protein–energy malnutrition characterized by edema, irritability, anorexia, ulcerating dermatoses, and an enlarged liver with fatty infiltrates.

75
Q

What happens to the microbiome in kwashiorkor?

A

There is a significant difference in the microbiome between those with kwashiorkor and those who do not have it, even from the same family.
Even after being fed a regular diet those with kwashiorkor could not increase significantly the diversity in their gut. This is thought to be significant in terms of long term nutrition and health

76
Q

What is the role of the microbome in obesity?

A

In humans:

Obese people have different gut microbiota to non-obese people.
Obesity/high fat diets ass with a decrease in diversity of microbiota.
Altered (and predictable?) gut microbiome in Type 2 diabetes: study could predict >90% who had type 2 diabetes just by looking at their microbiota profile.

In animal models:

Can transfer obesity by transferring microbiota
An increase in Bifidobacteria in diet induced obese mice
Reduced adiposity
Microbiota of obese mice are enriched for genes ass with CHO metabolism, greater energy extraction.

77
Q

What are the immunological symptoms of obesity?

A
  1. Associated with low grade chronic inflammation
  2. Induction of inflammatory cytokines (TNF, IL-1B, IL-6)
  3. Increase in mast cells, T cells, macrophages
  4. ↓ in Tregs.
78
Q

What is the relationship between Inflammatory bowel disease (U.C. and Crohn’s disease) and the microbiota?

A
  1. Microbiota diversity reduced in IBD patients
  2. Patients have increased intestinal permeability
  3. Gene polymorphisms (e.g. NLR polymorphisms) → loss/gain of function.

Postulate
That defective PAMP-PRR signalling →persistence of microorganisms and their products → recurrent or chronic (pathological) inflammation.
Appendectomy as well associated with chronic inflammation?

79
Q

What is the link between allergies and the microbiota?

A

Link between early microbial colonisation and development of appropriate gut microbiome and immune response development.

  1. 20% increase in asthma in C-section births
  2. Children of mothers exposed to range of animals (and their microbiota) during pregnancy → less asthma and allergies.
  3. Antibiotic use, excessive hygiene interrupts this perhaps? (Hygiene hypothesis).

Postulate that pre- and postnatal microbial interactions very early in childhood by certain commensal signal for differentiation to a regulatory phenotype

80
Q

What are the roles of intestinal microbiota in infectious disease?

A

Intestinal microbiota escape the GIT to cause infections (opportunistic) at extraintestinal sites
- Requires abnormal Host: (i) Anatomically (ii) Functionally (iii) Immunocompromised

Intestinal microbiota are a source of DNA → Spread of virulence and antibiotic resistance genes (e.g. VRE, CRE, C. difficile); Intestinal bacteria always having a rave party, promiscuously exchanging their genes via conjugation

81
Q

What happens when the commensals are altered?

A
  1. Lead to increased susceptibility to infection by GI pathogens (e.g. Salmonella spp.)
  2. Overgrowth of certain commensals
    Candida → diarrhoea;
    Clostridium difficle → pseudomembranous colitis.
82
Q

What causes Pseudomembranous colitis?

A

overgrowth of C. Difficile

83
Q

What type of bacteria is C. Difficile?

A

GPR,
Anaerobic
Spore forming

84
Q

When does pseudomembranous colitis arise?

A

C. Difficile is carried by around 3% of people
pseudomembranous colitis arises when gut microbiota is altered (e.g. antibiotic treatment, cytotoxic drugs) allowing for overgrowth.

85
Q

What is the MOA of C. Difficile?

A

Adheres to mucosal Ep → produces cytotoxic toxins → cell death, inflammation, bowel necrosis

86
Q

What are the clinical implications of C. Difficile infections?

A

Major cause of hospital-acquired (nosocomial) infection – these strains are hypervirulent and antibiotic resistant.

87
Q

What is the treatment for C. Difficile infections?

A

Metronidazole (works on strict anaerobes) +/- Vancomycin (works well on GP cells)
(? fidaxomicin if can afford it)

88
Q

Chronic C Difficile Infection

A

BUT some patients develop recurrent C. difficle infections (4-fold greater incidence in those with appendectomy) → recurrent infections due to reduced diversity of microbiota (in people who do not recover their normal microbiota).
Increased incidence in people without appendix
Theory that the appendix serves as a “library” of our microbiota such that when microbiota is disturbed, appendix perhaps replenishes supply and restores the microbiota balance.

89
Q

Treatment of chronic c. Difficile infection?

A

Bacteriotherapy (faecel transplants by ingesting a faecal capsule) is the most successful form of treatment  normal microbiota re-established,
C. difficile disease resolves (91-98% success rate).
Recently, a mixture of 33 different intestinal bacteria isolated in pure cultures has been successful

90
Q

What are prebiotics

A

Dietary supplements that promote beneficial bacteria

91
Q

What are probiotics?

A

Ingesting live organisms in adequate amounts (e.g. lactobacillus, bifidobacteria)
This can work but need a lot of work - there are very few RCT but some suggestion that it may be of use in aiding a variety of conditions

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