Helicobacter pylori participates in the pathogenesis of IgA nephropathy.

Increasing evidences have shown that Helicobacter pylori (Hp) is a pathogen closely related to extra-gastric disorders. Our previous in vitro studies had demonstrated that Hp infection, at least via cytotoxin-associated gene A protein (CagA), might play an important role in the pathogenesis of IgA nephropathy (IgAN) by stimulating proliferation and ectopic synthesis of aberrantly glycosylated IgA1 of B cells. However, the relevant clinical evidence of IgAN resulted from Hp infection remain to be elucidated. This study aimed to investigate the risk incidence of IgAN caused by Hp infection. 22 primary IgAN, 20 non-IgA nephropathy (n-IgAN), and 30 healthy controls were included in this study. We found that the rate of IgG anti-Hp seropositivity was significantly improved in IgAN, but the current Hp infection was similar in all groups. The production and underglycosylation of IgA1 tended to increase in IgAN patients with IgG anti-Hp seropositivity. A tendency toward increased the risk of clinical prognosis was seen in IgAN with Hp infection. Hp antigen and CagA were only deposited in renal tubules, and enhanced antigen deposition in response to Hp was observed in IgAN. Our study suggested that Hp infection might have a pathogenic role in IgAN through giving rise to strongly mucosal immune response, and based on damage of renal tubular.

Colonization by Various Morphological Forms of Helicobacter pylori in the Gingival Sulcus and Antrum of the Stomach.

BACKGROUND: Helicobacter pylori eradication therapy can be considered effective if the result of its implementation is removed including all roots and rootlets from which surviving H. pylori can repopulate in the gastric mucosa. One of the reasons for the ineffectiveness of eradication therapy can be the continuous presence of viable coccoid forms of H. pylori in the oral cavity. Therefore, anti-Helicobacter eradication therapy should be supplemented by the sanitation of the oral cavity. OBJECTIVES: The objective of this study is to determine the frequency of occurrence of H. pylori in the gastric mucosa and in the oral cavity in patients with chronic periodontitis or with chronic gastritis using immunocytochemical method and to evaluate the pathophysiological relationship between periodontitis and HP-associated acid-dependent stomach diseases mediated by H. pylori. METHODS: A group of patients with chronic gastritis (70 participants, 46 women, 24 men, age: 24 - 55 years) and another group with chronic periodontitis before the start of surgical treatment (61 participants, 30 women, 31 men, age: 20 - 60 years) were examined for НР bacterial cells using immunocytochemical methods of staining gastric biopsy and exfoliate samples from the gingival sulcus surface. The participants did not take any antimicrobial medication before and during the examination. Routine staining was also performed to view microbiota in smears for both groups. The participants signed a voluntary consent agreement to undergo routine medical examinations and join the study at the Nikiforov Russian Centre of Emergency and Radiation Medicine, EMERCOM of Russia, where the ethical committee was made. RESULTS: Immunocytochemical method could identify all stages of bacillary-coccoid transformation of H. pylori which accounted for 63.4-67.5% of cases. HP-antigenpositive bacteria were found in the oral cavity in both groups of examined patients. It was apparent that spiral forms of H. pylori were dominant over coccoid forms in the gastric mucosa in the antrum of the stomach, whereas coccoid forms of H. pylori were frequently found more in the oral cavity. Helicobacteriosis in the oral cavity was identified in chronic periodontitis. CONCLUSION: We found certain pathogenetic connections between inflammatory lesions of the oral cavity and diseases of the internal organs of the gastrointestinal tract. Accordingly, we suggest the necessity to use proper medication for oral cavity sanitation along with anti-Helicobacter eradication therapy to influence the HP reservoir in the oral cavity and gingival sulcus. Additionally, bacterial cells of HP reside in the oral cavity in coccoid forms; therefore, the coccoid form of HP should become the second principal target in treating HP.