Afaik the most probable trigger of IBDs (Crohn's, colitis ulcerosa) are changes in the gut microbiota due to western lifestyle (high intake of some nutrients e.g. milk fat). These changes cause an inflammation in the susceptible (genetic factors) people. So the cause of IBDs is very likely not an allergic reaction.
According to wikipedia IBS is not an IBD (inflammatory bowel disease). It is a functional disorder of the bowel, so not so serious as the IBDs. Its possible causes are low grade inflammation of the bowels and neuroendocrine disregulation. It has genetic factors as well. The pathomechanism is not fully understood yet.
There are many bowel diseases which can be caused by specific foods, e.g. celiac disease, lactose intolerance, and so on, the list is long, many of them can be caused by food protein intolerance. It is my understanding of protein sensitivity that skin conditions are caused by B-cell (IgE) mediated immune response, while bowel conditions are caused by T-cell mediated immune response. Ofc. there is connection between them, so it is possible that a certain type of protein induces skin symptoms and intestinal symptoms as well. Based on the current studies I think food sensitivity is not related to IBDs, and probably not related to IBS as well.
CD is associated with dramatic changes in the gut microbiota and this
was particularly evident for individuals with ileal CD.
Molecular profiling of faecal bacteria revealed abnormalities of
intestinal microbiota in UC and IBS patients, while different patterns
of Bacteroides species loss in particular, were associated with UC and
Breakdown of the normal microbial community increases the risk of
pathogen infection, the overgrowth of harmful pathobionts and
inflammatory disease. Understanding the interaction of the microbiota
with pathogens and the host might provide new insights into the
pathogenesis of disease, as well as novel avenues for preventing and
treating intestinal and systemic disorders.
Crohn's disease and ulcerative colitis are idiopathic, chronic,
relapsing, inflammatory conditions that are immunologically mediated.
Although their exact etiologies remain uncertain, results from
research in animal models, human genetics, basic science and clinical
trials have provided important new insights into the pathogenesis of
chronic, immune-mediated, intestinal inflammation. These studies
indicate that Crohn's disease and ulcerative colitis are heterogeneous
diseases characterized by various genetic abnormalities that lead to
overly aggressive T-cell responses to a subset of commensal enteric
bacteria. The onset and reactivation of disease are triggered by
environmental factors that transiently break the mucosal barrier,
stimulate immune responses or alter the balance between beneficial and
pathogenic enteric bacteria. Different genetic abnormalities can lead
to similar disease phenotypes; these genetic changes can be broadly
characterized as causing defects in mucosal barrier function,
immunoregulation or bacterial clearance. These new insights will help
develop better diagnostic approaches that identify clinically
important subsets of patients for whom the natural history of disease
and response to treatment are predictable.
The composite human microbiome of Western populations has probably
changed over the past century, brought on by new environmental
triggers that often have a negative impact on human health1. Here we
show that consumption of a diet high in saturated (milk-derived) fat,
but not polyunsaturated (safflower oil) fat, changes the conditions
for microbial assemblage and promotes the expansion of a
low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia2.
This was associated with a pro-inflammatory T helper type 1 (TH1)
immune response and increased incidence of colitis in genetically
susceptible Il10−/−, but not wild-type mice. These effects are
mediated by milk-derived-fat-promoted taurine conjugation of hepatic
bile acids, which increases the availability of organic sulphur used
by sulphite-reducing microorganisms like B. wadsworthia. When mice
were fed a low-fat diet supplemented with taurocholic acid, but not
with glycocholic acid, for example, a bloom of B. wadsworthia and
development of colitis were observed in Il10−/− mice. Together these
data show that dietary fats, by promoting changes in host bile acid
composition, can markedly alter conditions for gut microbial
assemblage, resulting in dysbiosis that can perturb immune
homeostasis. The data provide a plausible mechanistic basis by which
Western-type diets high in certain saturated fats might increase the
prevalence of complex immune-mediated diseases like inflammatory bowel
disease in genetically susceptible hosts.
The pathogenesis of IBS seems to be multifactorial, with the following
factors playing a central role in the pathogenesis of IBS:
heritability and genetics, dietary/intestinal microbiota, low-grade
inflammation, and disturbances in the neuroendocrine system (NES) of