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Printable Handouts
Navigable Slide Index
- Introduction
- Complexity of the intestinal microbiota
- Managing intestinal bacteria
- Toll-like receptors (TLRs) sense bacterial products
- Flagellin activates pro-inflammatory genes
- A model based on an in vitro work
- Loss of flagellin/TLR5 interaction
- Blockade of pro-inflammatory signaling pathway
- T5KO mice develop spontaneous colitis
- Innate immune gene expression TLR5KO colons
- Non-colitic T5KO mice develop colitis
- Summary (1)
- Non-colitic T5KO mice are overweight
- T5KO vs. Leptin-KO mice
- Embryo transfer changes only the environment
- Rederivation via embryonic transplant (1)
- Rederivation via embryonic transplant (2)
- Elevated fecal lipocalin-2 in T5KO mice
- T5KO mice develop obesity
- T5KO mice exhibit visceral fat inflammation
- T5KO mice have high lipids and blood pressure
- T5KO exhibit hyperglycemia/insulin resistance
- High fat diet & metabolic syndrome in T5KO mice
- T5KO mice exhibit hyperphagia
- Calorie restriction improves metabolic syndrome
- T5KO mice have increased adhered bacteria
- TLR5 loss & composition of gut microbiota
- Metabolic/inflammatory parameters in T5KO mice
- T5KO mice have less stable microbiota
- Taxonomical alterations in T5KO gut microbiota
- Increased volatility in T5KO microbiota
- Antibiotics treat metabolic syndrome
- Lack of phenotype in germ-free T5KO mice
- T5KO microbiota transfers metabolic syndrome
- Overview: gut microbiota in metabolic syndrome
- IEC TLR5 loss changes microbiota composition
- Bacterial localization by confocal microscopy
- IEC TLR5 loss decreases microbiota-IEC distance
- Bacterial encroachment in humans
- TLR5 null homozygotes
- What changed microbiota?
- Emulsifiers
- Evidence: emulsifiers might promote IBD
- CMC & PS80 in WT mice
- CMC & PS80 in IL10-KO mice
- Emulsifiers: bacterial adherence & composition (1)
- Emulsifiers: bacterial adherence & composition (2)
- CMC & PS80 promote colitis in IL10-KO mice
- CMC & PS80: low-grade inflammation in WT mice
- CMC & PS80: metabolic syndrome in WT mice
- Emulsifiers & presence of microbiota
- Altered microbiota transfers metabolic syndrome
- What dose of emulsifier is required?
- PSU creamery
- Concluding remarks
- Microbiota and potential effects
- Acknowledgements
Topics Covered
- Managing intestinal bacteria
- Toll-like receptors
- Flagellin
- Enhancing inflammation through blockade of a pro-inflammatory signaling pathway
- T5KO mice
- Embryo transfer
- Loss of TLR5 and alteration of the composition of the gut microbiota
- Possible role of gut microbiota in metabolic syndrome and relevance in humans
- The human gut microbiota in the last 50-100 years
- Dietary disturbance of the gut microbiota & metabolic syndrome
Links
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Talk Citation
Gewirtz, A. (2018, February 28). Gut microbiota, chronic inflammation and metabolic syndrome [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 14, 2024, from https://doi.org/10.69645/VJGB4493.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Andrew Gewirtz has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Gut microbiota, chronic inflammation and metabolic syndrome
A selection of talks on Microbiology
Transcript
Please wait while the transcript is being prepared...
0:00
Hi I'm Andrew Gewirtz from
Georgia State University's Center for Inflammation Immunity and Infection.
My presentation is entitled Gut Microbiota Chronic Inflammation and Metabolic Syndrome.
0:18
This illustration is an artist's rendition of the intestinal microbiota,
designed to show the great diversity that exists in this complex ecosystem.
0:31
This is a photograph of the intestinal mucosa
showing the population of 100 trillion bacteria,
50 percent of the lumenal contents by weight,
that live in close proximity to the intestinal epithelium.
This population of bacteria is quite diverse,
comprised of over 5000 distinct species and 2 million distinct genes.
These bacteria are a functional continuum with
some being mutualistic and that they benefit the host,
a few being pathogenic and that they can cause disease.
But the vast majority being somewhere in between either commensal or opportunists.
These bacteria are inhabiting a large area,
specifically the surface area of the intestine is approximately that of a tennis court.
Unlike the skin, which is essentially a closed barrier,
the intestines should be thought of as an active port.
The microbiota is acquired or inherited early in life and once
its composition is stable it tends to remain that way over the lifetime of the host.
The microbiota is essential for immune development and metabolic health,
but has also been linked to a variety of
chronic inflammatory diseases in the gut and beyond.
Thus, it's reasonable to think of
the enteric microbiota as your BFF or Best Frenemy Forever.
In that context, a goal of the Mucosal Immune system
is to expediently detect and clear pathogens,
while keeping opportunists in check.
This must be done while avoiding harm to beneficial microbes and host tissues.
This is analogous to managing a large bustling metropolis.
The overall message of this talk is that,
poorly managed gut microbiota can result in multiple flavors of gut inflammation,
including inflammatory bowel disease and metabolic syndrome.
This slide is a simplified schematic of the function of Toll-like receptors,