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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
Bacterial composition in CD
Mostly Firmicutes taking up everything then a lot of Actinobacteria also
26
Colitis in mouse with germ free environments
Don’t get IBD
27
mice in germ free environments get IBD how
Introduced to commensal bacteria | Or EVER HIGHE if IBD donor transplant
28
Cytokines most important to prevent IBD
IL10
29
Babies from IBD mothers
Have ow bacterial diversity and dysbiosis = alters adaptive immune system
30
What factors effects microbiota in GI
1. Diet : fibers 2. Genetics 3. Stress, medication 4. Vaginal delivery is good
31
High fiber diet has what bacteria
HIGH : bactericides and Firmicutes and Actinobacteria | LOW : proteobacteria
32
High fat diet has what bacteria
LOW : bacterioides, Firmicutes, Proteobacteria = dysbiosis
33
High Protein diet has what bacteria
HIGH : Proteobacteria, Bacteriodets, Firmicutes = dysbiosis
34
High Protein diet has what bacteria
HIGH : Proteobacteria, Bacteriodets, Firmicutes = dysbiosis
35
Acute infection and IBD
1. Persistent measles, Listeria | 2. Gastroenteritis : Salmonella, Campylobacter
36
IBD and acute infection that doesn’t cause it
Helming colonization | = regulate the intestinal flora and resistant to IBD
37
Common population for CD UC
CD : Caucasians UC : Asia and Africa very common Genetically
38
What in genetics leads to getting IBD
SNP (single Nuceotide Polymorphisms) , not mutations | = ALL genes encode for immune-inflammatory components
39
IBD-1 gene is what
Found on chr16 | = has the CARD15/NOD2 genes
40
CARD15 Expressed where and hen And what is it
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
Defected CARD15/NOD2 is how common and means what to getting IBD
Found in 17%-27% of pt with CD | - homozygous for SNP of CARD15 = 20x increased risk of CD
42
What happens when NF-kB is activated
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
CD caused by NOD2 mutations causes what
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
Enterocytes and microbiota specific roles
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
Commensal Bacteria uses what to protect the gut
Cellulose (fiber non-digestible polysaccharides fermentation) : leads to CO2 + short chain FAs that are ANTI-inflammatory for M, DC, CD4+, intestinal epithelial cells
46
SCFAs do what to be anti inflammatory
Bind to GPR43 and Activate and make cells into Tregs and IL10 that block effector cells
47
Which 2 bacteria’s contribute to healthy gut in lamina Propria
1. Bacteroids fragilis 2. Clostridium supp. = activate Tregs in LP, maintain Th17 at BASAL level for healthy epithelial barrier
48
What specific thing in commensal bacteria is helping GALT development
The Lipopolysaccharide into the SCFAs ——> Tregs, Tolorant DC, B-cells to recognize IgAs
49
Epithelial cells produce what
Anti-microbial peptides
50
Translocation of commensal bacteria and their Ags is stoped how
Eliminated by Tissue resident M, and DC—> LN = Tregs, Th17, IgA producing B cells
51
Peter Patches do what
Lymphocytes come here to activate Tregs for more class switching activation and IgA generation against the commensal bacteria
52
Mucosal firewall is what
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
Commensal bacteria and food tolerance works how
1. Suppresses the NF-kB pathway, DC and M dont sense he presence of microflora and dont secrete cytokines = IBD looses this tolorace
54
Chronic immune inflammatory responses activated by
Mucosa
55
Response to bacteria salmonella with no bacteroids
TLR5 activate the IkB kinase ——> activates NF-kB pathway
56
Response to Salmonella when bacteroides are present
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
Chronic inflammation involves what
Hyperactivation of : Th1, Th17 | Inhibition of : Tregs, IL10
58
Steps in how IBD develops
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
3 signals to activate a T-cell
1. HLA2 —> TCR 2. CD88/86–> CD28 (on T cell) 3. Ag MAMPs recognition = cytokines production
60
Induction of what cells are associated with CD and UC
CD : Th1 and Th17 (INF-g, TNF, IL2 + IL17)** | UC : Th2 (IL4,5,13) + NKC (IL13)**
61
What cytokines active TH1 and TH17
IL12 (Th1) , IL6(Th17), IL23 (Th17), TGF-B Th17) by M and DC
62
Which cytokines activates TH2 and NKCs
IL4
63
Follow steps of activation by Th1 as seen in CD
1. IL12 activator TH1 2. Release IFN-g : inflammation 3. Activated M 4. Release of TNF : more inflammation 4. Release of IL23 activating TH17 5. Release of IL17 : even more inflammation
64
Follow steps of activation by Th2 in UC
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
SNP in TGF-B and IL10 does what
1. Loss of function : IBD risk | 2. Gain of function : protection against IBD
66
SNPs for Cytokines promoting CD and UC does what
1. Loss of function : protection against IBD | 2. Gain of Function : risk against IBD
67
Tregs do what
= tolorance of commensal bacteria and food Ags = prevent rapid immune response to pathogenic molecules = breakdown of this leads to IBD
68
What makes a naive T-cell a Treg or Th17
1. IL2 + TGF-B ——> Treg (has a retinoic acid type that blocks Th17) 2. IL6 + TGF-B ——> Th17
69
How many cells in GALT are Tregs
10% of the cells
70
Excess TGF-B leads to
Only Tregs activated all other T cells are blocked
71
Tregs express what on its surface
1. CTLA-4 | 2. CD25 = IL2R that binds to IL2 to decrease it
72
Tx for IBD
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
Future IBD TX
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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