| Summary: | <i>Ureaplasma</i> species are common colonizers of the adult genitourinary tract and often considered as low-virulence commensals. Intraamniotic <i>Ureaplasma</i> infections, however, facilitate chorioamnionitis and preterm birth, and cases of <i>Ureaplasma</i>-induced neonatal sepsis, pneumonia, and meningitis raise a growing awareness of their clinical relevance. In vitro studies are scarce but demonstrate distinct <i>Ureaplasma</i>-driven impacts on immune mechanisms. The current study addressed cytokine and chemokine responses upon exposure of native or lipopolysaccharide (LPS) co-stimulated human brain microvascular endothelial cells (HBMEC) to <i>Ureaplasma urealyticum</i> or <i>U. parvum</i>, using qRT-PCR, RNA sequencing, multi-analyte immunoassay, and flow cytometry. <i>Ureaplasma</i> exposure in native HBMEC reduced monocyte chemoattractant protein (MCP)-3 mRNA expression (<i>p</i> < 0.01, vs. broth). In co-stimulated HBMEC, <i>Ureaplasma</i> spp. attenuated LPS-evoked mRNA responses for C-X-C chemokine ligand 5, MCP-1, and MCP-3 (<i>p</i> < 0.05, vs. LPS) and mitigated LPS-driven interleukin (IL)-1α protein secretion, as well as IL-8 mRNA and protein responses (<i>p</i> < 0.05). Furthermore, <i>Ureaplasma</i> isolates increased C-X-C chemokine receptor 4 mRNA levels in native and LPS co-stimulated HBMEC (<i>p</i> < 0.05). The presented results may imply immunomodulatory capacities of <i>Ureaplasma</i> spp. which may ultimately promote chronic colonization and long-term neuroinflammation.
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