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Introduction . Chlamydia trachomatis (Ct) is an obligate intracellular bacterium, causing a range of diseases in humans. Interactions between chlamydiae and antibiotics have been extensively studied in the past. Hypothesis/Gap statement: Chlamydial interactions with non-antibiotic drugs have received less attention and warrant further investigations. We hypothesized that selected cytokine inhibitors would alter Ct growth characteristics in HeLa cells. Aim.
Introduction. Azelastine hydrochloride a second-generation histamine H1 receptor (H1R) antagonist exhibits anti-chlamydial effects against Chlamydia trachomatis (CT) in HeLa cells (genital infection model). Hypothesis/Gap Statement. Non-antibiotic pharmaceutical interactions with CT are an understudied field and the anti-chlamydial effects of azelastine are a potential interaction requiring further elucidation. Aim. To explore the underlying anti-chlamydial mechanisms of azelastine. Methodology.
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