Since the discovery of Helicobacter pylori infection, several authors have investigated the immunological properties expressed by the bacterium in relation to the host. Those studies were expressly aimed at demonstrating how H. pylori may cause gastric mucosal damage and, at the same time, elude the immunological response evoked by the host. Data collected from those studies clearly showed that the immunological response caused by this bacterium is not only locally oriented but also systemically and that this immunological response may virtually cause local damage as well as influence the clinical course of other diseases, outside the stomach, thus opening the field of extragastric manifestations of H. pylori infection that we review in this manuscript.
Cardiovascular DiseasesSome reviews have suggested a possible role of H. pylori infection in ischemic heart disease (IHD) [1][2][3][4][5][6][7]. Furthermore, there are also original studies conducted in this field, showing very interesting results. A study by Ayada et al. clearly showed that H. pylori promotes atherogenesis in heterozygous apoe (+ ⁄ )) ldlr (+ ⁄ )) mice. In particular, H. pylori infected and noninfected mice were fed a high fat diet from the age of 6 weeks; development of atherosclerotic lesions was observed in infected animals and correlated with an elevation of Th1-immune response against H. pylori heat shock protein 60. To confirm the plausibility of this hypothesis, H. pylori eradication significantly reduced the progression of atherosclerosis in infected mice [8]. A study by our group also showed a highly positive correlation between H. pylori and IHD. In particular, we performed a clinico-pathological study on patients with stable angina, unstable angina and normal controls and a meta-analysis in the attempt to shed new light on this complex issue. Anti-urease B and anti-CagA antibodies were assessed in all patients; moreover, coronary atherosclerotic plaque specimens were obtained by patients with stable and unstable angina and used for immunohistochemistry using anti-CagA antibodies. Interestingly, the anti-CagA but not anti-urease B antibody titer was significantly higher in patients with unstable angina compared to stable. Moreover, anti-CagA antibodies recognized antigens localized inside coronary atherosclerotic plaques. In the meta-analysis, seropositivity to CagA was significantly associated with the occurrence of acute coronary events with an adjusted odds ratio (OR) of 1.34 (95% confidence interval (CI), 1.15-1.58, p = .003). Thus, taken together, these findings suggest that in a subset of patients with unstable angina, an intense immune response against CagA-positive strains might act as a trigger for the precipitation of coronary instability via a molecular mimicry mechanism [9]. Another study by Jia et al.[10] reported a strong correlation between H. pylori infection and decreased levels of HDL cholesterol, which has been Keywords Idiopathic thrombopenic purpura, iron deficiency anemia, obesity, CagA, molecular mimicry.Reprint ...