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Background   Mycoplasma genitalium  is an emerging sexually transmitted pathogen that has been associated with significant reproductive tract inflammatory syndromes in women. In addition, the strong association between severity of  M. genitalium  infection and Human Immunodeficiency Virus type 1 (HIV-1) shedding from the cervix suggests that innate responses to  M. genitalium  may influence pathogenesis of other sexually transmitted infections. Epithelial cells (ECs) of the reproductive mucosa are the first cells contacted by sexually transmitted pathogens. Therefore, we first characterized the dynamics of intracellular and extracellular localization and resultant innate immune responses from human vaginal, ecto- and endocervical ECs to  M. genitalium  type strain G37 and a low-pass contemporary isolate, M2300.    Results  Both  M. genitalium  strains rapidly attached to vaginal and cervical ECs by 2 h post-infection (PI). By 3 h PI,  M. genitalium  organisms also were found in intracellular membrane-bound vacuoles of which approximately 60% were adjacent to the nucleus. Egress of  M. genitalium  from infected ECs into the culture supernatant was observed but, after invasion, viable intracellular titers were significantly higher than extracellular titers at 24 and 48 h PI. All of the tested cell types responded by secreting significant levels of pro-inflammatory cytokines and chemokines in a pattern consistent with recruitment and stimulation of monocytes and macrophages. Based on the elaborated cytokines, we next investigated the cellular interaction of  M. genitalium  with human monocyte-derived macrophages and characterized the resultant cytokine responses. Macrophages rapidly phagocytosed  M. genitalium  resulting in a loss of bacterial viability and a potent pro-inflammatory response that included significant secretion of IL-6 and other cytokines associated with enhanced HIV-1 replication. The macrophage-stimulating capacity of  M. genitalium  was independent of bacterial viability but was sensitive to heat denaturation and proteinase-K digestion suggesting that  M. genitalium  protein components are the predominant mediators of inflammation.    Conclusion  Collectively, the data indicated that human genital ECs were susceptible and immunologically responsive to  M. genitalium  infection that likely induced cellular immune responses. Although macrophage phagocytosis was an effective method for  M. genitalium  killing, intracellular localization within vaginal and cervical ECs may provide  M. genitalium  a survival niche and protection from cellular immune responses thereby facilitating the establishment and maintenance of reproductive tract infection.

bmc microbiology

Intracellular Mycoplasma genitalium infection of human vaginal and cervical epithelial cells elicits distinct patterns of inflammatory cytokine secretion and provides a possible survival niche against macrophage-mediated killing