Kuratli, Jasmin; Leonard, Cory Ann; Schoborg, Robert; Borel, Nicole (2023). Anti-chlamydial effects of azelastine hydrochloride and the impact of the histamine H1 receptor on chlamydial development. Journal of medical microbiology, 72(5) Microbiology Society 10.1099/jmm.0.001691
Full text not available from this repository. (Request a copy)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. We assessed the specificity of azelastine for the chlamydial species and host cell type, the timing of azelastine application and whether the anti-chlamydial effects could be reproduced with different H1R-modulating compounds.Results. We observed similar anti-chlamydial azelastine effects for Chlamydia muridarum as well as for an ocular CT strain in human conjunctival epithelial cells (ocular infection model). Pre-incubating host cells with azelastine before infection mildly reduced chlamydial inclusion numbers and infectivity. Incubation of cells with azelastine initiated concomitantly with the chlamydial infection, or initiated several hours post-infection, reduced inclusion size, number and infectivity, and altered chlamydial morphology. These effects were strongest when azelastine was added shortly after or with the infection. Azelastine effects were not alleviated by increased concentrations of culture medium nutrients. Additionally, we did not observe anti-chlamydial effects when incubating cultures either with a different H1R antagonist or agonist, indicating that azelastine effects are probably H1R-independent.Conclusion. Accordingly, we conclude that azelastine anti-chlamydial effects are not restricted to a specific chlamydial species, strain or culture model, and are probably not mediated by H1R antagonism. Thus, it appears likely that off-target mechanisms of azelastine may explain our observations.
Item Type: |
Journal Article (Original Article) |
|---|---|
Graduate School: |
Graduate School for Cellular and Biomedical Sciences (GCB) |
ISSN: |
1473-5644 |
Publisher: |
Microbiology Society |
Language: |
English |
Submitter: |
Pubmed Import |
Date Deposited: |
19 May 2023 13:43 |
Last Modified: |
19 May 2023 13:43 |
Publisher DOI: |
10.1099/jmm.0.001691 |
PubMed ID: |
37195751 |
Uncontrolled Keywords: |
Chlamydia azelastine histamine H1 histamine antagonists in vitro techniques receptors |
URI: |
https://boris.unibe.ch/id/eprint/182665 |
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