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GIGU 2 Exam 1 > Immuno-Pathogenic Mechanisms Of IBD - Dr. Shnyra > Flashcards

Immuno-Pathogenic Mechanisms Of IBD - Dr. Shnyra Flashcards

1
Q

What happens in IBD

A
  1. Ulcerative Colitis : chronic inflammation and ulcers in innermost lining of colon + rectum
  2. Crohn’s Disease : inflammation GI lining spreading deep in to affected tissues (any part of GI, usually no rectum)
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2
Q

What 2 disease can seem like IBD only are not

A

Celiac Disease and IBS

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3
Q

IBD is what type of inflammation

A

Chronic relapsing idiopathic
= increased intestinal permeability
= irreversible impairments of function and structure of GI

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4
Q

What can increase incidence of IBD

A

Hyagien hypothesis = allergic and autoimmune diseases can

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5
Q

Reason permeability increases with IBD inflammation

A

Tight junctions are impaired and causes epithelial barrier to increase permeability

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6
Q

How does IBD happen or begin

A

The commensal bacteria of normal microbiota causes mucosal inflammation
= leading to bacteria crossing the mucosal barrier into immune cells activating innate and adaptive IS
= both cellular and humoral responses from this commensal bacteria

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7
Q

Main thing happening in Ulcerative colitis

A

Barrier is disrupted beginning the IBD

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8
Q

Main thing happening in Crohn’s disease

A

Microbe sensing by TLR in lamina Propria is disrupted beginning the IBD

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9
Q

SX CD

A

ABD pain , obstruction , fever

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10
Q

SX UC

A

Bloody D, urgency

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11
Q

CD where in GI

UC where in GI

A

CD : mouth to anus

UC : anus or rectum

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12
Q

CD pathology

A

Abscesses, fistulas, strictures, granulomas, transmural inflammation

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13
Q

UC Pathology

A

Pseudopolyps
Toxic megacolon
Mucosal / submucosal inflammation

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14
Q

DX CD

A
  1. Skip lesions
  2. Barium X -ray : String sign
  3. Cobblestone appearance = endoscopy
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15
Q

UC DX

A
  1. Ulcerations, edema, erythema or colon mucosa
    • stool cultures
  3. Continuous disease
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16
Q

TX and outcome of CD and UC

A

CD : surgery, not curable

UC : surgery, curable

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17
Q

Lab tests that are positive in CD, and UC

A

CD : ASCA + (anti-saccharomyces cerevisioe Abs)

UC : pANCA +(pernuclear Anti- neutrophil cytoplasmic Abs)

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18
Q

Environmental factors in IBD percentage in UC andCD

A

CD : 50% rate of transmission

UC : 10% rate of transmission

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19
Q

IBD develops in what types of areas

A

High bacterial concentrated area like ileum and colon

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20
Q

LN in IBD

A

Reactivity ageists fecal Ags

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21
Q

Surgery and IBD

A

Diverge the fecal system past the IBD area can prevent inflammation

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22
Q

What can one eat that helps with IBD

A

Antibiotics and probiotics

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23
Q

Most common 2 bacteria in LI + 2 other ones that are still in there

A
  1. Firmicutes
  2. Bacteroidetes
  3. Actinobacteria
  4. Proteobacteria
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24
Q

Bacterial composition in UC

A

Most common is Proteobacteria and then some Bactroidets and firmicutes

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25
Q

Bacterial composition in CD

A

Mostly Firmicutes taking up everything then a lot of Actinobacteria also

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26
Q

Colitis in mouse with germ free environments

A

Don’t get IBD

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27
Q

mice in germ free environments get IBD how

A

Introduced to commensal bacteria

Or EVER HIGHE if IBD donor transplant

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28
Q

Cytokines most important to prevent IBD

A

IL10

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29
Q

Babies from IBD mothers

A

Have ow bacterial diversity and dysbiosis = alters adaptive immune system

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30
Q

What factors effects microbiota in GI

A
  1. Diet : fibers
  2. Genetics
  3. Stress, medication
  4. Vaginal delivery is good
31
Q

High fiber diet has what bacteria

A

HIGH : bactericides and Firmicutes and Actinobacteria

LOW : proteobacteria

32
Q

High fat diet has what bacteria

A

LOW : bacterioides, Firmicutes, Proteobacteria = dysbiosis

33
Q

High Protein diet has what bacteria

A

HIGH : Proteobacteria, Bacteriodets, Firmicutes = dysbiosis

34
Q

High Protein diet has what bacteria

A

HIGH : Proteobacteria, Bacteriodets, Firmicutes = dysbiosis

35
Q

Acute infection and IBD

A
  1. Persistent measles, Listeria

2. Gastroenteritis : Salmonella, Campylobacter

36
Q

IBD and acute infection that doesn’t cause it

A

Helming colonization

= regulate the intestinal flora and resistant to IBD

37
Q

Common population for
CD
UC

A

CD : Caucasians
UC : Asia and Africa very common
Genetically

38
Q

What in genetics leads to getting IBD

A

SNP (single Nuceotide Polymorphisms) , not mutations

= ALL genes encode for immune-inflammatory components

39
Q

IBD-1 gene is what

A

Found on chr16

= has the CARD15/NOD2 genes

40
Q

CARD15
Expressed where and hen
And what is it

A
  1. By M and DC
  2. Intracellular PPR recognize MDP (muramyl dipeptide, peptidoglycan* in gram - and gram +)
  3. Activated leads to NF-kB activation
41
Q

Defected CARD15/NOD2 is how common and means what to getting IBD

A

Found in 17%-27% of pt with CD

- homozygous for SNP of CARD15 = 20x increased risk of CD

42
Q

What happens when NF-kB is activated

A

It is phosphorylates by CARD15-MDP,
= release of p65-p50
= the TF go to Nucleus and transcribe cytokines ,adhesion molecules, chemokines (150 different immune genes)

43
Q

CD caused by NOD2 mutations causes what

A
  1. M defective function that chronically stimulate T-cells
  2. Epithelial response defect : loss of barrier and increased exposure to mucosal microflora
  3. Defected APC conditioning : inappropriately activated
44
Q

Enterocytes and microbiota specific roles

A
  1. High turn over rate
  2. Microbiota increased GALT (maintain basal Th17 and Th1 levels in lamina Propria) + anti-inflammatory (commensal bacteria suppress pathobionts by IL10 and Tregs
45
Q

Commensal Bacteria uses what to protect the gut

A

Cellulose (fiber non-digestible polysaccharides fermentation) : leads to CO2 + short chain FAs that are ANTI-inflammatory for M, DC, CD4+, intestinal epithelial cells

46
Q

SCFAs do what to be anti inflammatory

A

Bind to GPR43 and Activate and make cells into Tregs and IL10 that block effector cells

47
Q

Which 2 bacteria’s contribute to healthy gut in lamina Propria

A
  1. Bacteroids fragilis
  2. Clostridium supp.
    = activate Tregs in LP, maintain Th17 at BASAL level for healthy epithelial barrier
48
Q

What specific thing in commensal bacteria is helping GALT development

A

The Lipopolysaccharide into the SCFAs ——> Tregs, Tolorant DC, B-cells to recognize IgAs

49
Q

Epithelial cells produce what

A

Anti-microbial peptides

50
Q

Translocation of commensal bacteria and their Ags is stoped how

A

Eliminated by Tissue resident M, and DC—> LN = Tregs, Th17, IgA producing B cells

51
Q

Peter Patches do what

A

Lymphocytes come here to activate Tregs for more class switching activation and IgA generation against the commensal bacteria

52
Q

Mucosal firewall is what

A

Epithelial barrier + mucus layer + IgA + DC + T cells = limits passage and exposure of commensal bacteria to the GALT = prevent inflammation
= help tolerate food Ags also

53
Q

Commensal bacteria and food tolerance works how

A
  1. Suppresses the NF-kB pathway, DC and M dont sense he presence of microflora and dont secrete cytokines
    = IBD looses this tolorace
54
Q

Chronic immune inflammatory responses activated by

A

Mucosa

55
Q

Response to bacteria salmonella with no bacteroids

A

TLR5 activate the IkB kinase ——> activates NF-kB pathway

56
Q

Response to Salmonella when bacteroides are present

A

TLR5 activate that then activate the PPARgamma = it binds to RelA and then exporters the NF-kB out from the nucleus = no activation of cytokines

57
Q

Chronic inflammation involves what

A

Hyperactivation of : Th1, Th17

Inhibition of : Tregs, IL10

58
Q

Steps in how IBD develops

A
  1. Genetics and environmental factors casue impaired barrier function
  2. Bactria and commensal bacteria enter translocation, cytokines and immune activation
  3. ACUTE inflammation : try to clear this by Tcells in LP, however in susceptible pts ——> CHRONIC inflammation
  4. Fibrosis, stenosis, abscess, fistula, cancer can happen
59
Q

3 signals to activate a T-cell

A
  1. HLA2 —> TCR
  2. CD88/86–> CD28 (on T cell)
  3. Ag MAMPs recognition = cytokines production
60
Q

Induction of what cells are associated with CD and UC

A

CD : Th1 and Th17 (INF-g, TNF, IL2 + IL17)**

UC : Th2 (IL4,5,13) + NKC (IL13)**

61
Q

What cytokines active TH1 and TH17

A

IL12 (Th1) , IL6(Th17), IL23 (Th17), TGF-B Th17) by M and DC

62
Q

Which cytokines activates TH2 and NKCs

A

IL4

63
Q

Follow steps of activation by Th1 as seen in CD

A
  1. IL12 activator TH1
  2. Release IFN-g : inflammation
  3. Activated M
  4. Release of TNF : more inflammation
  5. Release of IL23 activating TH17
  6. Release of IL17 : even more inflammation
64
Q

Follow steps of activation by Th2 in UC

A
  1. DC activated and activate naive T-cell
  2. Release IL4
  3. Activated TH2
  4. Release of IL4, IL5, IL13 : inflammation and increased permeability, no Tregs to block this
  5. NKC also activated for same inflammatory response
65
Q

SNP in TGF-B and IL10 does what

A
  1. Loss of function : IBD risk

2. Gain of function : protection against IBD

66
Q

SNPs for Cytokines promoting CD and UC does what

A
  1. Loss of function : protection against IBD

2. Gain of Function : risk against IBD

67
Q

Tregs do what

A

= tolorance of commensal bacteria and food Ags
= prevent rapid immune response to pathogenic molecules
= breakdown of this leads to IBD

68
Q

What makes a naive T-cell a Treg or Th17

A
  1. IL2 + TGF-B ——> Treg (has a retinoic acid type that blocks Th17)
  2. IL6 + TGF-B ——> Th17
69
Q

How many cells in GALT are Tregs

A

10% of the cells

70
Q

Excess TGF-B leads to

A

Only Tregs activated all other T cells are blocked

71
Q

Tregs express what on its surface

A
  1. CTLA-4

2. CD25 = IL2R that binds to IL2 to decrease it

72
Q

Tx for IBD

A

TNF blockers for (membrane bound and soluble) —> apoptosis
= moderate to severe IBD
= by IV or subQ
= risk of worsening heart failure, infections, or malignancy
= induce outside to inside , can lead to cytotoxicity

73
Q

Future IBD TX

A

Fecal Microbiota Transplantation (FMT)
= generating healthy microflora and transplanting them
= short term remission (can only transplant a little)
= super bacteria can be resistant and take over microflora

GIGU 2 Exam 1 (12 decks)

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