Chlamydia psittaci infection induces IFN-I and IL-1β through the cGAS-STING-IRF3/NLRP3 pathway via mitochondrial oxidative stress in human macrophages

Chlamydia psittaci increased mitochondrial reactive oxygen species (mtROS) production in human macrophages.

• Mitochondrial oxidative stress and damage were induced by C. psittaci post-infection.
• The increase in mtROS led to the release of oxidized mitochondrial DNA (mtDNA) into the cytoplasm.
• Activation of the cGAS-STING-IRF3/NLRP3 pathway was associated with elevated production of interferon type I (IFN-I) and interleukin-1 beta (IL-1β).
• Pre-treatment with mtROS inhibitor mito-TEMPO reduced oxidized mtDNA and subsequently lowered IFN-I and IL-1β production.
• mtROS production may inhibit C. psittaci proliferation by enhancing the action of IFN-I and IL-1β.

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