Microbiota And Immune System (innate) Flashcards
Where in the gut are the most microbiota
Colon followed by ileum
What can dysbiosis be caused by
Diet, stress, genetics, antibiotics, hygriene
What is the genetic link to Crohn’s disease which is inappropriate response to microbiota
Mutation in the nod 2 receptors (intracellular)
What do nod 2 have as their pamps
Muramyl dipeptide (in peptidoglycan cell wall)
Which types of cells in gut (epithelial) produce defensins and what are defensins a and b
Paneth cells
Defensins are antimicrobial peptides which are cationic (+ve) and produce pores in bacteria
Normally , what would happen at gut epithelial to kill bacteria
Muramyl dipeptide will be recognised by nod 2 and this causes release of defensins to kill bacteria
What are defensins attracted to
-ve cell membranes
Which types of things can allow for over proliferation of microbiota in gut
Diet/ nutrients
What would happens when a lot of microbiota are in gut
Muramyl dipeptide will break through the cells via endocytosis
Pamp detected via nod 2 and many defensins released which attract macrophages etc
Why would mutation to nod 2 end up in crohns inflammation
Defensins can’t be released bc no signalling from nod 2
This means macrophages will form a cytokine storm to try to eradicate it
This causes inflammation
How would steroid treatment help crohns
Anti inflammatory via stopping prostaglandin and leukotrienes
Also blocks th1 macrophages
What is rheumatoid arthritis
Complex autoimmune genetic disease
Deposits at joints cause inflammation and edema swelling
Which bacteria were found to increase RA likeliness
Segmented filamentous bacteria (dysbiosis if increased)
How do segmented filamentous cause RA and it’s symptoms
Bind to receptors and form signalling cascade
This stimulates th 17 proliferation and therefore more IL 17 release
IL 17 cytokines cause inflammation via attraction of cells and Edema
IL 17 also activate auto reactive B cells which then produce auto antibodies (auto immunity)
What produces deposits in RA
The auto antibodies produced via auto reactive B cells
How does lactobacillus prevent uti usually
Lower ph via glucose metabolism production of lactic acid
Which bacteria causes uti
UPEC E. coli
How can e coli upec move from urethra opening up the UT eg to bladder or kidney
Via flagella
Which 3 things protect the UT
Urine (flush bacteria)
Epithelial barrier
Defensins
Which receptor when not mutated can identify UPEC
Toll like 5
What does toll like 5 identify on UPEC
Their flagellins
What do the bladder epithelium then release when roll like 5 bind to flagellin from UPEC
Defensins
Which type of mutation is common to toll like 5 causing uti
SNP from C to T
How does cystitis (bladder uti) occur due to C to T mutation in toll 5
Lack of signalling to release defensins
Inflammatory markers released instead eg macrophages and neutrophils
Causes inflammation and bleeding in bladder = cystitis
Do toll 5 still recognise flagellum when they have the C to T mutation
Yes
