RRC ID 54871
Author Matsuo J, Sakai K, Okubo T, Yamaguchi H.
Title Chlamydia pneumoniae enhances Interleukin 8 (IL-8) production with reduced azithromycin sensitivity under hypoxia.
Journal APMIS
Abstract Obligate intracellular bacterium Chlamydia pneumoniae causes respiratory tract infections such as community-acquired pneumonia. During infection, C. pneumoniae induces inflammatory responses in host cells and the oxygen concentration at the infection sites subsequently decreases. Because hypoxic conditions influence further inflammatory responses and reduced antibacterial effects, this may exacerbate the C. pneumoniae infection. Here, we show inflammatory responses and drug sensitivity in C. pneumoniae-infected cells under hypoxic conditions. First, we confirmed the enhanced growth of C. pneumoniae under hypoxia, which indicates that the hypoxic condition we used could adequately reproduce past reports. We then demonstrated a significant increase in production of the pro-inflammatory cytokine Interleukin 8 (IL-8) in C. pneumoniae-infected cells under hypoxic conditions. Furthermore, hypoxia decreased the antibacterial effects of azithromycin against C. pneumoniae compared with normoxic conditions. Together, our data suggest that inflammatory responses and drug sensitivity may have been underestimated in C. pneumoniae infection in previous studies. Thus, to accurately understand the Chlamydia infection, it may be necessary to perform in vitro experiments under hypoxic conditions.
Volume 127(3)
Pages 131-138
Published 2019-3-1
DOI 10.1111/apm.12924
PMID 30746791
MeSH Anti-Bacterial Agents / pharmacology Azithromycin / pharmacology* Cell Hypoxia / immunology* Cell Line Chlamydophila Infections* / immunology Chlamydophila Infections* / microbiology Chlamydophila pneumoniae / drug effects* Chlamydophila pneumoniae / growth & development Chlamydophila pneumoniae / physiology* Drug Resistance, Bacterial / physiology Host-Pathogen Interactions* Humans Interleukin-8 / metabolism* Microbial Sensitivity Tests
IF 2.225
Times Cited 1
Resource
Human and Animal Cells HEp-2(RCB1889)