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Background:   Ureaplasma  species have been associated with chorioamnionitis and preterm birth and have been implicated in the pathogenesis of neonatal short and long-term morbidity. However, being mostly commensal bacteria, controversy remains on the pro-inflammatory capacity of  Ureaplasma . Discussions are ongoing on the incidence and impact of prenatal, perinatal, and postnatal infection. The present study addressed the impact of  Ureaplasma  isolates on monocyte-driven inflammation.   Methods:  Cord blood monocytes of term neonates and adult monocytes, either native or LPS-primed, were cultured with  Ureaplasma urealyticum  ( U. urealyticum ) serovar 8 (Uu8) and  Ureaplasma parvum  serovar 3 (Up3). Using qRT-PCR, cytokine flow cytometry, and multi-analyte immunoassay, we assessed mRNA and protein expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-8, IL-12p40, IL-10, and IL-1 receptor antagonist (IL-1ra) as well as Toll-like receptor (TLR) 2 and TLR4.   Results:  Uu8 and Up3 induced mRNA expression and protein release of TNF-α, IL-1β and IL-8 in term neonatal and adult monocytes ( p  < 0.01 and  p  < 0.05). Intracellular protein expression of TNF-α, IL-1β and IL-8 in  Ureaplasma -stimulated cells paralleled those results.  Ureaplasma -induced cytokine levels did not significantly differ from LPS-mediated levels except for lower intracellular IL-1β in adult monocytes (Uu8:  p  < 0.05). Remarkably, ureaplasmas did not induce IL-12p40 response and promoted lower amounts of anti-inflammatory IL-10 and IL-1ra than LPS, provoking a cytokine imbalance more in favor of pro-inflammation (IL-1β/IL-10, IL-8/IL-10 and IL-8/IL-1ra:  p  < 0.01, vs. LPS). In contrast to LPS, both isolates induced TLR2 mRNA in neonatal and adult cells ( p  < 0.001 and  p  < 0.05) and suppressed TLR4 mRNA in adult monocytes ( p  < 0.05). Upon co-stimulation, Uu8 and Up3 inhibited LPS-induced intracellular IL-1β ( p  < 0.001 and  p  < 0.05) and IL-8 in adult monocytes ( p  < 0.01), while LPS-induced neonatal cytokines were maintained or aggravated ( p  < 0.05).   Conclusion:  Our data demonstrate a considerable pro-inflammatory capacity of  Ureaplasma  isolates in human monocytes. Stimulating pro-inflammatory cytokine responses while hardly inducing immunomodulatory and anti-inflammatory cytokines, ureaplasmas might push monocyte immune responses toward pro-inflammation. Inhibition of LPS-induced cytokines in adult monocytes in contrast to sustained inflammation in term neonatal monocytes indicates a differential modulation of host immune responses to a second stimulus. Modification of TLR2 and TLR4 expression may shape host susceptibility to inflammation.

frontiers in cellular and infection microbiology

Ureaplasma Species Differentially Modulate Pro- and Anti-Inflammatory Cytokine Responses in Newborn and Adult Human Monocytes Pushing the State Toward Pro-Inflammation