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Genes associated with microbiota

From what I can make out scientists have been looking for years for what controls PGE2 and this gene PTGER4 may control it.

There is also a link with il-10 and for that part I become a bit lost.
Its important, but they are just signaling molecules for the inflammatory/immune response. Thing is, lots of things influence this pge2, the research is needed, but I don't think there is anything groundbreaking here. And many other genetic studies will come up with similar conclusions, the same risk genes found in crohn's patients can be found in people that never develop the disease at all, this is why the microbiome should get more focus and actually is getting more focus now. There really is a reason so many private corporations are investing in microbiome startups, it's a really big deal. my guess is these gene associations are no more important to a susceptibility to inflammation as the genes that determine your muscle size make one person more susceptible for fatigue in a bout of resistance exercise.
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Effect of aspirin on prostaglandin E2 and leukotriene B4 production in human colonic mucosa from cancer patients

Mucosal samples were obtained during sigmoidoscopy from the colons of 17 subjects with a history of colonic cancer prior to and following 60 days of self-administration of 325 mg aspirin/day and again 60 days after administration of 650 mg aspirin/day. PGE2 and LTB4 concentrations were determined by enzyme immunoassay for tissue samples that were flash frozen after removal from the biopsy forceps and also in medium that was collected from tissue samples that were incubated for 4 h following removal from the subject. PGE2 concentrations were decreased significantly in samples collected after 60 days of consumption of 325 mg aspirin. An additional 60 days of consuming 650 mg aspirin/day did not result in a further significant decrease relative to that attained after consumption of 325 mg/day.
Interesting thanks for pointing that out Bill, I did not know asprin blocked this pathway and that took me by shock.

I have took asprin and i know i cant take that it makes me flair.

Also on this article appears the team who did this study were even aware asprin already does this.

Appears they are taking the investigation further in 2022 even after knowing this.

What a puzzle this disease is that is all i can say, we dont even have any decent medication for it yet that works very effecive for every patient and has minimal side effects.
thing is, most aspirin available is full of additives that likely feed bad microbes in the gut, i looked into it and you can get pure aspirin powder, havent tried it yet though.
Hmm so PGE2 is to high, in a normal person take asprin it lowers it, if a crohns pattient takes asprin it makes the inflamation worse.

Yes your right there are more than likely addatives in it.

I wonder is PGE2 still high in a crohns patient after taking asprin?, or unless it has two switches, the gene and the intestine and in needs to be struck in the gene rather than the cells in the intestine.
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San Diego
Aspirin is an NSAID and like the other NSAIDs it is well known to have a corrosive effect on the gut. In fact, aspirin consumption is one of the major confounders that GIs check for when trying to diagnose IBD, since both aspirin and IBD commonly cause gut bleeding. This is the reason why GIs advise IBD patients to avoid taking aspirin and other NSAIDs. You don't need that extra stress on an already fragile and damaged gut.

Thus, no matter what effect aspirin may or may not have on prostaglandin E2 and leukotriene B4 production, Crohn's patients should be very cautious about consuming any aspirin, pure or otherwise.
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Yes that is very good advice, it is really best to avoid at all costs pain killers narcotics and make sure proper medication is taken for the disease.
Acetylsalicylic Acid Reduces the Severity of Dextran Sodium Sulfate-Induced Colitis and Increases the Formation of Anti-Inflammatory Lipid Mediators

This article has been cited by other articles in PMC.

Go to:
The role of non-steroidal anti-inflammatory drugs in inflammatory bowel disease is controversial, as they have been implicated in disease aggravation. Different from other cyclooxygenase inhibitors, acetylsalicylic acid (ASA) enhances the formation of anti-inflammatory and proresolution lipoxins derived from arachidonic acid as well as resolvins from omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA). In this study, we examined the effect of ASA on murine dextran sodium sulfate colitis. A mouse magnetic resonance imaging (MRI) protocol and post mortem assessment were used to assess disease severity, and lipid metabolites were measured using liquid chromatography-coupled tandem mass spectrometry. Decreased colitis activity was demonstrated by phenotype and MRI assessment in mice treated with ASA, and confirmed in postmortem analysis. Analysis of lipid mediators showed sustained formation of lipoxin A4 and an increase of DHA-derived 17-hydroxydocosahexaenoic acid (17-HDHA) after treatment with ASA. Furthermore, in vitro experiments in RAW264.7 murine macrophages demonstrated significantly increased phagocytosis activity after incubation with 17-HDHA, supporting its proresolution effect. These results show a protective effect of ASA in a murine colitis model and could give a rationale for a careful reassessment of ASA therapy in patients with inflammatory bowel disease and particularly ulcerative colitis, possibly combined with DHA supplementation.

Aspirin linked to reduction in risk of several cancers of the digestive tract
Date : April 15, 2020

So strange the conflicting results on this topic.

There must be some logic, wonder what happens when it's given iv

8 weekly dose of asprin or clopidogrel via iv infusion at hospital lol. Probably doesn't stay in the blood longer than 6 hours I would guess.