title: Pseudomonas aeruginosa GroEL Stimulates Production of PTX3 by Activating the NF-κB Pathway and Simultaneously Downregulating MicroRNA-9.
abstract: As one of the first lines of host defense, monocytes play important roles in clearing infected microbes. The defensive response is triggered by recognition of diverse microbial moieties, including released factors, which modulate host immune responses to establish a harsh environment for clinically important bacterial pathogens. In this study, we found that the expression of PTX3, a soluble form of pattern recognition receptor, was induced by infection with livePseudomonas aeruginosaor treatment of cells with its supernatant.P. aeruginosaGroEL, a homolog of heat shock protein 60, was identified as one of the factors responsible for inducing the expression ofPTX3in host cells. GroEL inducedPTX3expression by activating the Toll-like receptor 4 (TLR4)-dependent pathway via nuclear factor-kappa B (NF-κB), while simultaneously inhibiting expression of microRNA-9, which targets thePTX3transcript. Finally, by acting as an opsonin, GroEL-induced PTX3 promoted the association and phagocytosis ofStaphylococcus aureusinto macrophages. These data suggest that the host defensive environment is supported by the production of PTX3 in response to GroEL, which thus has therapeutic potential for clearance of bacterial infections.
authors.affiliation: Department of Biotechnology and Bioinformatics, Korea University, Sejong, Republic of Korea.
authors.forename: Heesung
authors.initials: H
authors.lastname: Shin
authors.affiliation: Department of Biotechnology and Bioinformatics, Korea University, Sejong, Republic of Korea.
authors.forename: Jisu
authors.initials: J
authors.lastname: Jeon
authors.affiliation: Department of Biotechnology and Bioinformatics, Korea University, Sejong, Republic of Korea.
authors.forename: Jung-Hoon
authors.initials: JH
authors.lastname: Lee
authors.affiliation: State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Molecular Microbiology and Technology of the Ministry of Education, Department of Microbiology, College of Life Sciences, Nankai University, Tianjin, China.|Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, Florida, USA.
authors.forename: Shouguang
authors.initials: S
authors.lastname: Jin
authors.affiliation: Department of Biotechnology and Bioinformatics, Korea University, Sejong, Republic of Korea haunhwan@korea.ac.kr.
authors.forename: Un-Hwan
authors.initials: UH
authors.lastname: Ha
mesh_terms: D001426:Bacterial Proteins / Q000378:metabolism*; D002097:C-Reactive Protein / Q000096:biosynthesis* / Q000235:genetics; D002460:Cell Line; D002478:Cells, Cultured; D005786:Gene Expression Regulation; D006801:Humans; D035683:MicroRNAs / Q000235:genetics*; D016328:NF-kappa B / Q000378:metabolism; D010587:Phagocytosis; D011552:Pseudomonas Infections / Q000235:genetics* / Q000378:metabolism* / Q000382:microbiology; D011550:Pseudomonas aeruginosa / Q000502:physiology*; D000683:Serum Amyloid P-Component / Q000096:biosynthesis* / Q000235:genetics; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D000099153:Pentraxins
chemical_list: D001426:Bacterial Proteins; D002097:C-Reactive Protein; D035683:MicroRNAs; D016328:NF-kappa B; D000683:Serum Amyloid P-Component; D051197:Toll-Like Receptor 4; D000099153:Pentraxins; C541874:MIRN92 microRNA, human
keywords: GroEL; NF-κB; PTX3; Pseudomonas aeruginosa; microRNA-9