We appreciate the letter from Dr. Abenavoli and Dr. Arena. Helicobacter species are mainly classified as gastric Helicobacter spp. (such as Helicobacter pylori) and enterohepatic Helicobacter spp. (such as H. bilis and H. hepaticus) found in the liver, biliary tract, and intestinal tract. Helicobacter species other than H. pylori have been identified in recent years, and so the relationship between infection with these species and various diseases has been of high interest. In our recent article [1], we concluded, from the results of the measurement of serum anti-H. hepaticus antibody levels, that H. hepaticus infection might play a role in the development of liver diseases.. In particular, H. hepaticus might increase the risk of viral hepatitis developing into liver cirrhosis and hepatocellular carcinoma. About the association of primary biliary cirrhosis (PBC) and Helicobacter species, Dohmen et al. [2.] reported that H. pylori infection could induce autoimmune responses in the development of both PBC and atrophic corpus gastritis. Their hypothesis is that molecular mimicry, possibly resulting from H. pylori infection, might be responsible for initiating an autoimmune response in a predisposed host owing to cross-reactivity among gastric mucosal, bile ductular, and bacterial antigens. H. pylori infection is reported [3] to be frequently detected in subjects with early gastric autoimmunity, indicated by the presence of parietal cell antibodies, suggesting that H. pylori could have a crucial role in the induction and/or the maintenance of autoimmunity at the gastric level. There are many reports [4] suggesting that infectious agents might be associated with the autoimmune pathogenesis of PBC. It has also been reported that the DNA of Helicobacter species was detected relatively frequently in the liver tissues of patients with PBC and those with primary sclerosing cholangitis, both of which diseases have an autoimmune etiology [5]. Moreover, Helicobacter species have also been proposed to be implicated in the pathogenesis of PBC, because their DNA was found in liver tissue, and antibodies to the microbe were found in the serum and the bile of patients with PBC [6]. Abenavoli et al. [7] reported a patient with celiac disease (CD), PBC, and H. pylori infection. Strict adherence to a gluten-free diet, associated with ursodeoxycholic acid (UDCA) administration and eradication treatment for H. pylori infection, led to a marked improvement of the patient’s clinical status. Abenavoli et al. speculate that increased intestinal permeability has a pathogenetic role in the course of CD and that H. pylori infection could induce PBC. In reply to the point raised by Dr. Abenavoli and Dr. Arena in their letter, we did not investigate for or detect blood CD markers in our PBC patients, and we note that CD is a very rare disease in Japan. Results with several animal models [8, 9] have suggested that commensal bacteria may have important role(s) as initiating factors in the pathogenesis of autoimmune disorders such as PBC. Under the pathogenetic conditions of increased intestinal permeability that occur in CD and ulcerative colitis, infection with Helicobacter species could induce hepato-biliary autoimmune abnormalities. This author’s reply refers to the letter to the editor at doi:10.1007/s00535-012-0583-2.
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May 1, 2013
Sadegh Massarrat + 7
Open Access
