Food allergen-related skin reactions and intestinal inflammation?
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.



2008 - Molecular analysis of the gut microbiota of identical twins with Crohn's disease



  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
  IBS.



2010 - Ulcerative colitis and irritable bowel patients exhibit distinct abnormalities of the gut microbiota



  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.



2013 - Role of the gut microbiota in immunity and inflammatory disease
2014 - Role of the gut microbiota in inflammatory bowel disease
pathogenesis: What have we learnt in the past 10 years?



  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.



2006 - Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis.
2011 - Proinflammatory Cytokines in the Pathogenesis of Inflammatory Bowel Diseases 
2014 - Role of Regulatory B Cells in Chronic Intestinal Inflammation: Association with Pathogenesis of Crohn's Disease
2013 - Effects of Enteral Nutrition on Crohn’s Disease: Clues to the Impact of Diet on Disease Pathogenesis



  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.



2012 - Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice



  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
  the gut



2012 - Irritable bowel syndrome: Diagnosis and pathogenesis
2014 - Melatonin Regulation as a Possible Mechanism for Probiotic (VSL#3) in Irritable Bowel Syndrome: A Randomized Double-Blinded Placebo Study
2012 - Irritable Bowel Syndrome: Methods, Mechanisms, and Pathophysiology. The confluence of increased permeability, inflammation, and pain in irritable bowel syndrome