Infections with Chlamydia trachomatis are the major cause for infectious blindness and still represent the most common bacterial sexually transmitted disease worldwide. Considering the possible side effects of antibiotic therapy and the increasing threat of antibiotic resistance, alternative therapeutic strategies are needed.
Previous studies showed a reduction of C. trachomatis infectivity after irradiation with water filtered infrared A alone (wIRA) or in combination with visible light (wIRA/VIS).
In this study, we aimed to gain further insight into the working mechanism of wIRA/VIS by analyzing cytokine and chemokine levels of infected and non-infected HeLa cells following triple dose irradiation at 24, 36 and 40 hours post infection. Subsequently, we examined the influence of cytokines on irradiation and chlamydial infection using a cytokine/chemokine inhibitor (Azelastine) and by IL-6 and IL-8 gene silencing.
A triple dose irradiation significantly reduced chlamydial infectivity in HeLa cells without inducing the chlamydial stress response. The reducing effect was present regardless of the addition of cycloheximide (CHX), a host protein synthesis inhibitor. Chlamydial infection, wIRA/VIS treatment and the combination of both revealed a similar release pattern of a subset of pro-inflammatory cytokines (IL-6, IL-8, RANTES, Serpin E1). The addition of Azelastine induced the chlamydial stress response in non-irradiated samples. This effect was even more pronounced in wIRA/VIS-treated conditions. Silencing of IL-6 and IL-8 resulted in a lower chlamydial infectivity. However, wIRA/VIS treatment of infected and silenced cells reduced the chlamydial infectivity similar to wIRA/VIS treated control cells. Further studies are needed to elucidate the working mechanism of wIRA/VIS.
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