Helicobacter pylori (H. pylori) is suspected to be one of the factors triggering systemic sclerosis (SSc). Data on the possible role of H. pylori are lacking. The aim of this study was to assess the effect of H. pylori infection in SSc patients. Forty-two SSc patients without dyspeptic symptoms were recruited--26 were H. pylori-positive and 16 were H. pylori-negative on the basis of invasive test. We evaluated the disease severity using clinical and laboratory parameters according to the Medsger Severity Scale. The level of SSc activity was evaluated according to Valentini activity score. The prevalence of H. pylori infection in population of SSc patients is 62%. Severity of skin, gastrointestinal, and joint/tendon involvement was different between H. pylori-positive and -negative SSc patients (p < 0.001 for skin involvement, p = 0.002 and p = 0.03 for gastrointestinal and joint/tendon involvement, respectively) as well as erythrocyte sedimentation rate (p = 0.002). Severity score according to Medsger was higher in the H. pylori-positive than in the H. pylori-negative SSc patients (p < 0.001). Our data suggest that H. pylori infection correlates with severity of skin, gastrointestinal, and joint/tendon involvement in SSc patients. H. pylori-positive SSc patients showed higher severity score compared to H. pylori-negative. Therefore, H. pylori infection may play a role in the pathogenesis of SSc and also can provide some prognostic information.
Essential part of a response to infection is early pathogen recognition and adequate initiation of innate immunity. One of the hallmarks of systemic lupus erythematosus (SLE) is reduced resistance to infection despite overall hyperactivity of the immune system. Immunosuppressive drugs (high‐dose corticosteroids and cytotoxic agents) are independent risk factors for infection in SLE, with bacteria as predominant cause. To investigate whether less aggressive immunomodulatory treatment may still affect recognition and response to Gram‐negative bacteria, we measured TLR4 expression in monocytes of untreated SLE patients and patients on chloroquine and low‐dose steroid therapy and examined the drugs’ influence on monocyte TLR4 expression in peripheral blood mononuclear cell (PBMC) culture. Additionally, we determined whether induction of monocyte NF‐κB signalling, TNF‐α and IL‐6 production with lipopolysaccharide (LPS), a TLR4 ligand, can be altered with dexamethasone, chloroquine or both. There was no statistically significant difference in TLR4 expression between patients with SLE and controls, even though treated SLE patients tended to have lower frequency of TLR4+ monocytes and TLR4 mean fluorescence intensity than healthy controls. However, neither dexamethasone nor chloroquine had major influence on TLR4 expression in vitro or suppressed LPS‐induced NF‐κB activation in monocytes, although dexamethasone decreased TNF‐α and IL‐6 production. Therefore, even if low‐dose steroids or chloroquine do not seem to affect TLR4 expression and signalling, steroids might decrease cytokine production in response to LPS.
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