Affiliation:
1. Pathogenic Biology Institute, University of South China, Hengyang, China 421001
Abstract
ABSTRACT
Mycoplasma genitalium
is a leading pathogen of nongonoccocal chlamydia-negative urethritis, which has been implicated directly in numerous other genitourinary and extragenitourinary tract pathologies. The pathogenesis of infection is attributed in part to excessive immune responses.
M. genitalium
-derived lipid-associated membrane proteins (LAMPs) are a mixture of bacterial lipoproteins, exposed at the surface of mycoplasma, that are potent inducers of the host innate immune system. However, the interaction of
M. genitalium
-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-κB activation have not been fully elucidated. In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in a dose-dependent manner. Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-α and IL-6 in THP-1 cells. Furthermore, LAMP-induced NF-κB activation was increased in 293T cells transfected with TLR2 plasmid. The activity of NF-κB was synergically augmented by cotransfected TLR1, TLR6, and CD14. Additionally, LAMPs were shown to inhibit NF-κB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids. These results suggest that
M. genitalium
-derived LAMPs activate NF-κB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway.
Publisher
American Society for Microbiology
Subject
Microbiology (medical),Clinical Biochemistry,Immunology,Immunology and Allergy
Cited by
52 articles.
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