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Gastro block > Micro/immuno > Flashcards

Micro/immuno Flashcards

1
Q

4 main phyla in the gut

A

bacteroidetes: bacteroides
firmicutes: clostridia, lactobaccillus, GP
actinobateria: bifidobacterium
proteobacteria: e coli

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2
Q

What species dominate in the gut?

A

anaerobes dominate 99.9% from SI to LI
aerobes stoamch: H pylori, staph, strep, lactobacillus
*NO anaerobes in stomach

Aerobes SI LI: LActobacillus, strep and staph and e coli
anaerobes SI: bacteroides, strep, bifidobacterium
anaerobes LI: bacteroides, strep, bifidobacterium, clostridium

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3
Q

what do normal microbiota provide for the host?

A

Metabolism
development of enterocytes, angiogenesis, lymphocytes,
protection against enteropathogens
immune system

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4
Q

How does our microbiota affect nutrition? (2 over-arching 1ways)

A
  1. Directly supply nutrients from metabolism of
    carbs (lactose, cellulose, mucin broken down to SCFAs),
    vitamins (vitamin B2, Vit K, biotin, folate),
    bile acids,
    and can generate amino acids (lysine, threonine)
  2. alter metabolic machinery of host by changing gene expression and producing SCFAs that affect enterocytes.
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5
Q

How do bacteria produce SCFAs and what do they do?

A

Produced from the metabolism by bacteria of complex carbohydrates (mucin, fibre) which are ultimately fermented to SCFAs

Act:
In colon to provide energy for enterocyes and control gene expression (inhibit histone deacetylase)
Regulate metabolism via signallying thorugh GPCRs
Affect gluconeogenesis and lipogenesis in liver and other organs

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6
Q

What are the “lymph nodes” or aggregates of lymphoid cells that are present in the GIT?

A

Isolated lymphoid follicles in SI and LI

Peter’s patches in SI

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7
Q

In what layer of the GIT walls are the immune cells located?

A

lamina propria

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8
Q

What do goblet cells do?

A

produce and secrete mucins that protect enterocytes

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9
Q

What is the role of the enterocytes?

A

Secrete antimicrobial peptides
Physical barrier
Absorb water and nutrients

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10
Q

What/where are Paneth cells?

A

In crypts

Secrete antimicrobial peptides and defensins

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11
Q

What/where are intraepithelial lymphocytes?

A 
Between enterocytes
CD8 and CD4 T cells
Protect from commensals  
Induce tolerance 
Clear damaged/dying commensals
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12
Q

Innate defences of the gut

A

Peristalsis
Acid
Mucous
Enterocytes (barrier, secrete antimicrobial factors, cytokines, chemokines)
Innate leukocytes
M cells and DCs Control access of Ag to underlying lymphoid tissue

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13
Q

What cells are important in inducing tolerance?

A

Enterocytes and intraepithelial lymphocytes

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14
Q

What is the role of DCs in the mucosa when no Ag is present?

A

Sample Ag from intestinal mucosa
-> No Ag present: promote non-inflammatory envrionement: secrete TGFbeta -> induces Treg and Th2 ( induces IgA isotype switching)

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15
Q

Alpha4beta7

A

Homing receptor/adressin upregulated on T and B cells once they have seen Ag in their mucosal lymphoid tissue. They leave to enter circulation, then return to mucosal tissues because mucosal endothelial cells express MAdCAM1 which is ligand for alpha4beta7 and lamina propria expresses chemokine (CCR5 and CCL25)

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16
Q

What are different innate lymphoid cells in the GIT mucosa?

A 
Lymphoid tissue inducer cells
Intraepithelial lymphocytes
NK22
Mucosal associated invariable T cells (MAIT cells)
Invariant NKT cells
Macrophages
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17
Q

What is the role of M cells?

A

Between epithelial cells, overlying Peyer’s patches
Lack villi, glycocalyx and mucus secretion so Ag have easier access.
Sample the GI lumen and deliver antigens to underlying lymphoid aggregates where APC and lymphocytes reside.

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18
Q

What is the role of DC in the mucosa when Ag is present?

A

Sample the GIT lumen
-> Ag present activates PRR: promote inflammatory environment -> induce Th1, Th17
Promote expression of homing receptors/addressins (alpha4beta7) on T and B cells once they have been activated

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19
Q

Role of CD4 and CD8 T cells in the gut

A

CD4: innate immune system -> mostly Tregs in steady state
CD8: adaptive immune system, protect against intracellular infections

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20
Q

How do intestinal microbiota directly interact w gut immune system?

A
  1. bind and block binding sites on enterocytes for other microbiota
  2. produce bacteriocidins
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21
Q

How do intestinal microbiota INdirectly interact w gut immune system?

A

PAMPs interact with PRRs and signal to:
Stimulate mucin production
Proliferation of enterocytes and crypt paneth cells -> antimicrobial peptides released
Induce regulatory cytokines (TGFbeta) that maintain non-inflammatory state
Differentiation of NK22 cells -> Production of IL22 -> promotes epithelial barrier integrity
Produce SCFAs which inhibit inflammatory cytokines

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22
Q

At what stage of development do mesenteric lymph nodes, peyer’s patches and ILFs develop?

A

PP and MLN: prenatally, but PP continue to mature once exposed to Ag
ILFs postnatally, after exposure to Ag

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23
Q

How does the gut immune system differentiate normal microbiota from pathogens?

A

Pathogens bind tightly to/invade epithelial surface (use adhesions, invasins, mucinases, toxins) whereas commensals are found at luminal edge
Thus Epithelial PRR detect invasin AND damage (RO and nitrogen intermediates)
Differential interaction with PRRs and inflammasomes

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24
Q

What is the interaction of micro biome and gut immune system at steady state?

A

Constant interaction between intestinal microbiota and epithelial cells and immune cells of gut which drives non-inflammatory (physiological inflammation) state.

DC produce TGF beta -> Treg and Th2
Th2 -> IgA production against commensals
NK22 -> IL22 acts on epithelial cells to produce more defencins and TGFbeta

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25
What happens when pathogens interact with epithelial cells and immune cells of gut?
Invade layers of commensals and mucosa to infect M cells or epithelial cells activate PRR or inflammasomes -> production of IL1beta and IL18 -> Th1, Th17 type response -> IgG production by B cells
26
Acute hepatitis vs chronic hepatitis Symptoms
Acute: non specific, flu-like symptoms, dark urine, pale faeces, jaundice Chronic: jaundice, malaise, fatigue, weightloss, easy bruising and bleeding, peripheral oedema, ascites (chronic inflammation of liver -> cirrhosis and fibrosis)
27
Which hepatitis stains are passed via the faecal-oral route? via blood/bodily fluids? (sex/IV drugs)
A and E B,C,D
28
What virus causes HepA?
Hepatovirus (Picornaviridae family)
29
What virus causes HepE?
Hepevirus (Hepeviridae family)
30
What serum markers indicate an acute infection?
Rising IgG titre High IgM Presence of viral protein and liver enzymes
31
What serum markers indicate a chronic or convalescent infection?
Low IgM, high IgG
32
How do hep infection prognoses/symptoms vary w age of infection?
Infection in child: mild symptoms but more likely to become chronic (weaker immune response - virus not cleared) vise versa in adult.
33
What is the pathogenesis of Hep A?
Virus ingested -> low level replication in intestine -> portal circulation to liver -> replication in hepatocyte cytoplasm -> secreted in bile -> excreted in faeces
34
Treatment for Hep A
Supportive rehydration and nutrition, immune globulin can be given pre and post-exposure, if given within 14 days of infection.
35
For Hep A: What is the incubation period? How long do symptoms last? What are possible sequelae?
30 days 2-3 weeks None! Once virus is cleared, it is gone.
36
Hep E: What is the incubation period? How long do symptoms last? What are possible sequelae?
40 days 4 weeks None! Once virus is cleared, it is gone.
37
How does Hep E differ from Hep A in terms of cholestasis?
Cholestasis is more common w Hep E (bile flow ceases)
38
Which Hep virus has an increased mortality rate for pregnant women?
Hep E: increased to 20-25% vs 1-3% for overall population
39
For Hep A and E, when is the virus transmitted in the stool?
10-14 days before symptom onset, and up to a week after symptoms subside for Hep E For Hep A, virus stops being shed just after symptoms onset
40
Which hep viruses can be transmitted perinatally?
Hep B
41
Which hep viruses are self-limiting?
Hep A and E
42
Which hep viruses can become chronic?
Hep B, D, C
43
2 Virus structures of Hep B
ds DNA virus with double wall: outer envelope containing HBsAg particles and inner capsule made of "core protein" (HBcAg) containing genome. HBs Antigens can also assemble into incomplete and noninfectious virus particles that act as decoy for Ab directed against HB
44
Replication cycle of Hep B
1. Infectious particles enter hepatocyte in liver and release core containing incomplete circular dsDNA genome 2. Genome released into nucleus where it is repaired so it is a complete ds circle of DNA 3. DNA transcribed and translated into viral RNA and proteins 4. Viral proteins and RNA assembled in cytoplasm to form pre-genomic core particle 5. polymerase reverse transcribes RNA into DNA 5. Core particle w DNA can now assemble w lipid and other proteins to form fully infectious viral particle, OR can go into nucleus to continue making more copies of itself
45
What is the life cycle of Hep B?
Transmitted sexually or injected into blood -> circulates in blood to liver where it replicates -> secreted back into environment through bodily fluids *ONLY replicates in liver
46
Incubation period for Hep B
60-90 days, but can be shorter or longer
47
Serum markers of recovery following acute Hep B
HBsAg decr Anti-HBs incr Anti-HBe incr and HBeAg decr
48
Serum markers of chronic Hep B infection
HBsAg remains elevated, lack of antibodies against it Total Anti-HBc remain elevated
49
Serum markers of acute infection with Hep B
Anti-HBc IgM elevated
50
What is the role of the HBcAg?
Turns off expression of viral proteins, making them invisible to the immune system and initiates RNA transcription of viral DNA genome
51
What is the role of the HBeAg?
Dampens immune response so virus can persist | Regulate viral replication Promote excess of empty virus particle decoys
52
What does elevated Anti-HBc IgG represent in regards to HepB?
Past OR chronic infection
53
The presence of what serum marker, in Hep B, indicates that the virus is actively replicating and that the patient is therefore contagious?
HBeAg AND HBV DNA (more accurate than HBeAg) Anti-HBeAg indicates the virus isn't replicating, but if HBsAg is still elevated it means that although the patient isn't infectious, there is still ongoing immune response and damage being done to the liver.
54
What is the natural history of Hep B?
Acute infection can resolve OR progress to chronic HB. Chronic HB can stabilise or progress to cirrhosis. Cirrhosed liver can compensate OR become decompensated -> death from liver failure. Cirrhosed liver can also become cancerous -> liver cancer
55
Treatment for HepB
IFNalpha antiviral (30-40% response rate) Nucleoside/nucleotide analogues that are picked up by reverse transcriptase and terminate production of DNA copy (most patients relapse bc of incomplete viral clearance) HBV vaccine: post-exposure administration is also effective!
56
What is the Hep B vaccine composed of?
Subviral particles composed of HBsAg
57
What is an example of a nucleotide analogue that treats HBV?
Adefovir
58
Is there a vaccine for HDV?
Yes, the same one that treats HBV made of HBsAg, because HDV is packaged/transferred within the HBsAg
59
What virus is the HDV?
Deltavirus
60
How is HDV transmitted?
Packaged within the HBsAg and passed on WITH the HBV
61
What are the 2 methods (and their main outcomes) that HDV can co-infect withHBV?
1. Co-infection => severe acute illness w low risk of chronic infection 2. Superinfected (already infected w HBV, then you are infected w HBV+HDV on top of that) => chronic infection, probably severe
62
What virus is HCV?
Flavivirus
63
Replication cycle of HCV
Virus in blood enters hepatocytes in liver via receptor-mediated endocytosis Endosome acidifies and uncoats capsid -> releases viral +ssRNA -> In RER, RNA translated into structural and non-structural viral proteins -> these proteins then replicate viral RNA (+ to -, then produce many + copies) New viral particles are assembled which are coated in a lipid droplet and released into lumen OR passed to neighbouring cell directly.
64
Genome of HCV
Single linear strand of +ssRNA encoding 3 structural proteins and a series of non-structural proteins
65
Sequelae of HCV
Chronic infection (70-90% of those infected) Liver fibrosis, cirrhosis, liver failure Primary hepatocellular carcinoma
66
Treatment of HCV
IFNalpha (but toxic) +/- Ribavirin (neucleoside analogue but can only be used w patients with certain genotypes) Various lifecycle inhibitors Direct-acting antivirals (Ledipasvir, Sofosbuvir) - v effective in curing! New!
67
Example of direct acting antivirals to treat HCV
Ledipasvir | Sofosbuvir
68
When do you do a laboratory diagnosis for diarrhoea?
Only if it persists (diarrhoea > 2weeks) or is bloody
69
When a laboratory diagnosis is made for diarrhoea, what techniques are used? Think about for bacterial, viral, protozoal causes?
Microscopy Culture bacteria: use enrichment then selective/indicator media if you are looking for a specific bacteria (i.e. Salmonella-very common cause in Australia) PAthotyping -detects nucleic acids (PCR, electrophoresis) Biochemical tests Ag detection (ELIZA) Electron microscopy (viruses when no Ag detecting kits are avail)
70
What does the oral rehydration therapy for diarrhoea contain and how does it work?
Contains NaCl, KCl, Sodium bicarbonate, glucose Normally, Na couples to Cl and is taken up from lumen into enterocyte into blood, and water and ions follow passively down the []gradient. But this is shut down in diarrhoea. Accounts for 90% of absorption The other 10% of absorption occurs via Na coupling to solute (glucose) and water follows passively down this [] gradient. Still works in diarrhoea - what the oral rehydration therapy capitalises to cure the fluid and electrolyte imbalance.

Gastro block (6 decks)

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