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Abstract
Neisseria gonorrhoeae, the pathogen causing gonorrhea, establishes asymptomatic infections by modulating host immune responses. This study demonstrates that N. gonorrhoeae represses pro-inflammatory cytokine production through upregulation of the host transcriptional regulator ATF3, a process enhanced by Type IV pilus retraction. The commensal Neisseria elongata also induces ATF3 but at lower levels, correlating with reduced cytokine suppression. These findings suggest ATF3 plays a key role in immune modulation by pathogenic and commensal Neisseria, facilitating persistence and asymptomatic infection.