Page 10 - Introduction to FMT
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FMT Introduction





         Alterations in the intestinal flora have also been observed in patients with chronic fatigue syndrome (CFS)
         [83]. The proportion of gram-negative Escherichia coli was reduced in CFS patients versus that in healthy
         controls (49% vs 92.3%). More recent research examined a larger cohort of 60 CFS patients with
         gastrointestinal symptoms who had underwent FMT[84]. The results showed that 42/60 (70%) patients
         responded to treatment and 7/12 (58%) retained complete resolution of symptoms during a 15- 20 year
         follow-up period. These results, suggest that FMT may play a role in the treatment of CFS.


         Autoimmune diseases


         The incidence of autoimmune diseases has dramatically increased, but the causes of these conditions
         remain poorly understood. Idiopathic thrombocytopenic purpura (ITP) is caused by the production of
         autoantibodies against platelet surface antigens. In a patient with ITP who was treated with FMT for UC,
         prolonged reversal of ITP was reported and the normalization of platelet levels was achieved[85].


         The onset of rheumatoid arthritis (RA) is multifactorial and requires both genetic and environmental
         influential factors, with the commensal intestinal microbiota playing a major role[13,86,87]. Alterations in
         the intestinal microbiome can have an extended effect on RA through mucosal immune activation.
         Previous reports have implicated Prevotella copri in the pathogenesis of RA[88]. A recent study used the
         interleukin-1 receptor antagonist deficient (IL-1Ra ) mouse model, which can spontaneously develop T
         cell-driven IL-17-dependent autoimmune arthritis[86]. It was shown that IL- 1Ra mice had increased Th17
         and a reduced proportion of Th1 in small intestinal lamina propria compared with wild-type mice. GF IL-
         1Ra mice had lower levels of both Th1 and Th17. Interestingly, IL-1Ra mice previously treated by
         antibiotics was recolonized by segmented filamentous bacteria, a prominent Th17 inducer, leading to full-
         fledged arthritis. Moreover, elimination of intestinal Gram-negative commensals suppressed the
         progression of arthritis[86]. Understanding the role of the intestinal microbiota in the onset of RA may
         provide significant attention to FMT with regards to management of the disease; the potential is therefore
         worthy of consideration.


         In both Sjögren’s syndrome (SS) and systemic lupus erythematosus (SLE), Sjögren’s syndrome antigen
         A/Ro60 is one of the main autoantigens. Ro60 reactive autoantibodies are associated with manifestation
         severity in SS[89] and with photosensitivity in SLE[90]. Escherichia coli expresses von Willebrand factor
         type A domain protein, which can activate Ro60-reactive T cells[91]. Therefore, immune responses to the
         gut microbiota may play a pivotal role in the initiation of autoimmunity in SLE and SS. This sheds a light
         on a novel therapeutic strategy for the diseases.


























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