Have you got a stomachache after eating? Nature: It could be a local allergy to the intestines

Irritable bowel syndrome (IBS) is mainly manifested in abdominal pain and changes in intestinal activity, the signature symptoms of which are abnormal pain signals or visceral allergies (VHS).
reported that as many as 20 percent of the world's people have gastrointestinal symptoms after a meal, and if this response can be intervened, the quality of life of this population can be greatly improved.
mucous membrane immune system exists in the intestines, which provides a balanced response to pathogens and harmless symblobacters as well as food antigens, thereby limiting unnecessary inflammation and the tissue damage it causes.
viral and bacterial infections can interfere with dietary antigen tolerance, infectious gastroenteritis is an important risk factor for IBS.
recently suggested that damage to oral food antigen tolerance caused by bacterial infections is the basis of food-induced VHS.
recently, Nature magazine published online a study by Guy E. Boeckxstaens of the University of Leuven, Belgium, entitled "local immune response to food antigens drives meal-induced abdominal pain", suggesting that the local immune response of the intestines to food antigens causes abdominal pain after meals.
in mice, oral tolerance to food antigens may decrease after infection with gut bacteria, which can lead to food-induced pain, similar to irritable bowel syndrome.
researchers infected mice with BacillusC. Rodentium and then stimulated the mice's intestines with egg white protein (OVA) and found that mice showed only a local immune response, but no performance of a systemic immune response.
further studies have shown that gastrointestinal bacterial infections can break oral tolerance to food antigens, leading to increased intestinal permeability and abnormal pain signals when exposed to antigens again.
mechanisms of IBS after infection may be associated with "low-level" inflammation and increased activation of fat cells.
researchers found that locally produced OVA-specific antibodies in B cells and plasma cells sensitive fat cells and then mediated activation of fat cells when exposed to OVA again, contributing to the occurrence of VHS.
the increase in visceral pain signals mediated by hypertrophic cells is mediated by histamine type 1 (H1R) and is related to the sensitivity of vanilla acid transient subsumption 1 (TRPV1), which is the channel through which histamines participate in regulating the body's many important physiological pathological functions, while TRPV1 is a channel protein widely distributed in the peripheral and central nervous systems.
researchers injected soy, wheat, gluten and milk solutions into the colon mucous membranes of 12 IBS patients and eight healthy volunteers.
although the participants were not allergic to these dietary antigens, all participants in the IBS group developed mucous membrane reactions to at least one food antigen, while only two healthy volunteers showed a single positive reaction.
further analysis showed that food antigens caused hypertrophobic cell activation in IBS patients and may have been mediated through IgE.
, however, the fundamental difference with food allergies is that these participants only detected OVA-specific IgE antibodies in colon tissue, meaning that subjects showed only partial, not systemic, immune responses.
, this study shows that IBS is a diet-induced disease that is activated by fat cells.
concept is important for the treatment of IBS and related diseases.
Blocking hypertroller may be effective, and IgE-mediated hypertroller cell activation may also be a prognostic biomarker and therapeutic target for IBS patients, creating new possibilities for the treatment of irritable bowel syndrome and related abdominal pain disorders.
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