Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autism is a heterogeneous group of life-long neurologic problems that begin in childhood. Success in efforts to understand and treat autism has been mostly elusive. The role of autoimmunity in autism has gained recognition both for associated systemic autoimmune disease and the presence of brain autoantibodies in autistic children and their family members. There is an acknowledged genetic susceptibility to autism--most notably allotypes of complement C4. C4 defects are associated with several autoimmune diseases and also confer susceptibility to mycobacterial infections. Mycobacterium avium ss. paratuberculosis (MAP) causes an enteric inflammatory disease in ruminant animals (Johne's disease) and is the putative cause of the very similar Crohn's disease in humans. Humans are widely exposed to MAP in food and water. MAP has been also linked to ulcerative colitis, irritable bowel syndrome, sarcoidosis, Blau syndrome, autoimmune (Type 1) diabetes, Hashimoto's thyroiditis and multiple sclerosis. Environmental agents are thought to trigger autism in the genetically at risk. Molecular mimicry is the proposed mechanism by which MAP is thought to trigger autoantibodies. Autoantibodies to brain myelin basic protein (MBP) is a common feature of autism. This article considers the subset of autoimmunity-related autism patients and postulates that MAP, through molecular mimicry to its heat shock protein HSP65, triggers autism by stimulating antibodies that cross react with myelin basic protein (MBP).
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PMID:Mycobacterium paratuberculosis and autism: is this a trigger? 2190 38

The hypothesis proposed is that functional disorders, such as irritable bowel syndrome, chronic fatigue syndrome and anorexia nervosa are caused by auto-antibodies to neuronal proteins induced by molecular mimicry with microbial antigens. The age incidence of these conditions, the marked female excess, increase with economic and technological advance, precipitation by infection, and the paucity of histological changes are all consistent with the hypothesis. It can be tested directly using human sera to search for cross reaction with brain proteins in model systems such as Drosophila melanogaster. The conditions might be amenable to treatment using pooled immunoglobulin. Identification and elimination from the microbial flora of the bacteria that express the cross reacting antigens should be possible.
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PMID:Microbes, molecular mimicry and molecules of mood and motivation. 2682 39