Background Previously, we demonstrated that urinary white cell count increases in proportion to pathogen load in cases of urethritis caused by Mycoplasma genitalium but not Chlamydia trachomatis. We further investigated urethritis pathogenesis caused by these organisms by comparing concentrations of 23 cytokines present within first void urine (FVU) specimens of male urethritis cases.

Methods FVUs from 52 symptomatic male patients (all underwent Gram stain urethral smear) were collected and patients stratified into those with non-specific urethritis (n = 12), M. genitalium urethritis (n = 13), C. trachomatis urethritis (n = 14) and non-urethritis controls (n = 13). Cytokines measurements from FVUs specimens were obtained using a Human 30-Plex Luminex assay. Concentrations were obtained for 23 of the 30 cytokines analysed and compared between the four groups using multivariate ANOVA.

Results Overall, there was a significant difference in urinary cytokine profile between groups (p = 0.042). For individual cytokines, clinical group was associated with differences in concentrations of IL-1β (p = 0.007), GCSF (p = 0.042), CCL11 (p = 0.012), MIP-1α (p = 0.029), TNF-α (p = 0.026), IL-7 (p = 0.029), EGF (p = 0.030), VEGF (p = 0.049) and IFNa (p = 0.008). When compared with uninfected non-urethritis controls, cytokine concentrations in: M. genitalium samples, were increased for IL-1β (p = 0.017), GCSF (p = 0.010) but decreased for EGF (p = 0.017); C. trachomatissamples, were decreased for EGF (p = 0.049); and in non-specific urethritis samples, were increased for CCL5 (p = 0.049), IL-1β (p = 0.05), IL-1RA (p = 0.033) and decreased for EGF (p = 0.032). No significant differences were demonstrated in cytokine concentrations between C. trachomatis and M. genitalium groups.

Conclusion The increased levels of pro-inflammatory cytokines present in the urethritis groups when compared to non-urethritis controls reflect the acute inflammatory state. The data suggests that M. genitaliumgenital infection may be associated with a discrete mucosal immunological profile potentially explaining the link between cellular inflammatory response and bacterial load, previously observed