Apr6 M3-GI immunity Flashcards
part of GIT that is very different from the rest of the GIT
oropharynx
- is a large absorptive surface where things are dealt with and absorbed differently
- ex. sublingual meds
functions of saliva
- lubricate
- protect against pathogens
- neutralize acids
oral manifestations of immune salivation deficiencies
- gingivitis
- fungal infections
- teeth fall out
- periodontal area infections
- esophageal abrasions
- dental caries
- ulcers
non infectious ulcers of the mouth: cause
often because not enough saliva production
ddx of mouth ulcer
- malignancy
- trauma
- immune deficiency
- infection
- etc
oral mucosa immune system components
is part of the MALT 3 sites are -oral mucosa -salivary glands -gingival crevice
defensive mechanisms in the oral mucosa
- barrier by squamous epith (tight junctions) + LP
- intraepith dendritic cells (Langerhans cells) = surveillance
- IgA secretion in saliva against invaders
- defensins and pro-inflam cytokines released by EPITH and immune cells
most important oral health problem and why
caries
-gingival crevices and other places = places where microbes can stay
immune mechanisms at the gingival crevice
- neutrophils clearing microbes and ctly moving from gingival capillaries into the sulcus (crevice)
- are activated by local cytokine prod and co-Rs
important thing not to miss on ddx of teeth loss
neutropenia
why periodontal attachment is related to neutrophils (not bc neutrophils clear organisms that you necessarily lose your teeth in neutropenia…)
- osteoblasts and osteoclasts are of same lineage as neutrophils
- pathway affecting neutrophils = affects them too
mechanical barrier + 1st lines of defense in GIT below oropharynx
- mucosal barrier
- tight junctions
- cilia to keep microbes moving DOWN GIT
- IgA and commensal organisms
how pathogens are recognized in the GIT
- TLRs
- NOD-Rs see commensals
NOD-R mutation consequence
- higher risk of Crohn’s (IBD)
- don’t see commensal and say it’s ok (regulating (down) the immune system)
immune cells inside the mucosal barrier of the GIT
- dendritic cells pick Ags and may go show them at lymph nodes
- T cells INSIDE the intraepith compartment (immunoregulatory + for repair)
- CD8+ T cells can kill infection cells
- IgA neutralizes toxins and prevents virus and bacteria adherence to epith
Peyer’s patches def
-sites of active mucosal immune resp in GIT (are in SI, appendix, lymphoid follicles of colon)
special cells in Peyer’s patches and what they do
M cells (superabsorbers)
- interact with gut lumen and eat some of everything
- present Ags to lymphocytes AND dendritic cells
best way to make sure all the gut is protected against a known Ag
have gut derived lymphocytes that go to blood and lymph circulation of GI mucosa but that also come back to home mucosal sites
how do you get lymphocytes to home to mucosal sites in the GIT
homing Rs expressed on T cells recognize chemokines expressed by gut epith cells
when is gut inflammation bad and what determines that
ALWAYS BAD
- bad bowel vmvmt
- upset gut
- obstruction
- poor abso
- leaky gut
- perforation
- etc.
IPEX (disease where can’t make foxp3+ T reg cells) consequence on GIT
- most immune resp in GIT is tolerant
- you can’t make tolerance
- 1st thing you get i colitis (and is also what kills IPEX pts)
- MAIN PROB IS COLITIS IN IPEX
- also skin problems, primary autoimmune diabetes
class 3 MHC molecules fct in GIT
- MIC-A and MIC-B
- role in maintenance of balance in GIT immune system
- infected cells turn on MIC expression
- ALLOWS intraepith lymphs and NK cells to see and kill infected cells
c.diff cause and pathology you get
- often bc of Abx use
- pseudomembranous colitis
c.diff type of disease
- toxemia (c.diff toxin produced)
- toxin causes leakiness in GIT.
- microbes pass, secretory diarrhea, cells are killed
salmonella how affects GIT
- gets in M cells and grows in them and then goes out of them
- infects the next normal cells
- YOU GET DIARRHEA
shigellae how infects GIT
gives diarrhea
helicobacter pylori how affects GIT
- no problems initially but problems after replicates with time and thrives in high acid environment
- causes ULCERS and ongoing inflammation
- because slow inflammation, not enough stimulus to call enough immune cells
long term effects of H pylori infection
- cells keep turning over = higher risk of genetic mutations in lymphocytes
- increased risk of GASTRIC LYMPHOMA
definition of colitis
more inflammation in the GIT than T reg cells
treatments of IBD and colitis caused by poor regulation
immunosuppressants
diverticular disease and associated problems
- outpouching
- diverticulitis = inflammation of outpouching + infection + perforatin
- microbes found are COMMON MICROBES IN THE GIT (but it’s just the place and situation made the immune system unable to tolerate)
