Modulation of adherence invasion and tumor necrosis factor alpha secretion during the early stages of infection by Strepococcus pneumoniae ClpL

Simple item page
dc.contributor.authorTu, L.
dc.contributor.authorJeong, H.
dc.contributor.authorKwon, H.
dc.contributor.authorOgunniyi, A.
dc.contributor.authorPaton, J.
dc.contributor.authorPyo, S.
dc.contributor.authorRhee, D.
dc.date.issued2007
dc.description.abstractHeat shock proteins (HSPs) play a pivotal role as chaperones in the folding of native and denatured proteins and can help pathogens penetrate host defenses. However, the underlying mechanism(s) of modulation of virulence by HSPs has not been fully determined. In this study, the role of the chaperone ClpL in the pathogenicity of Streptococcus pneumoniae was assessed. A clpL mutant adhered to and invaded nasopharyngeal or lung cells much more efficiently than the wild type adhered to and invaded these cells in vitro, as well as in vivo, although it produced the same amount of capsular polysaccharide. However, the level of secretion of tumor necrosis factor alpha (TNF-{alpha}) from macrophages infected with the clpL mutant was significantly lower than the level of secretion elicited by the wild type during the early stages of infection. Interestingly, treatment of the human lung epithelial carcinoma A549 and murine macrophage RAW 264.7 cell lines with cytochalasin D, an inhibitor of actin polymerization, increased adherence of the mutant to the host cells. In contrast, cytochalasin D treatment of RAW 264.7 cells decreased TNF-{alpha} secretion after infection with either the wild type or the mutant. However, pretreatment of cell lines with the actin polymerization activator jasplakinolide reversed these phenotypes. These findings indicate, for the first time, that the ClpL chaperone represses adherence of S. pneumoniae to host cells and induces secretion of TNF-{alpha} via a mechanism dependent upon actin polymerization during the initial infection stage.
dc.description.statementofresponsibilityLe Nhat Tu, Hye-Yoon Jeong, Hyog-Young Kwon, Abiodun D. Ogunniyi, James C. Paton, Suhk-Neung Pyo, and Dong-Kwon Rhee
dc.identifier.citationInfection and Immunity, 2007; 75(6):2996-3005
dc.identifier.doi10.1128/IAI.01716-06
dc.identifier.issn0019-9567
dc.identifier.issn1098-5522
dc.identifier.orcidOgunniyi, A. [0000-0001-9308-5629]
dc.identifier.orcidPaton, J. [0000-0001-9807-5278]
dc.identifier.urihttp://hdl.handle.net/2440/43770
dc.language.isoen
dc.publisherAmer Soc Microbiology
dc.source.urihttps://doi.org/10.1128/iai.01716-06
dc.subjectTumor Cells, Cultured
dc.subjectMacrophages
dc.subjectStreptococcus pneumoniae
dc.subjectPneumococcal Infections
dc.subjectEndopeptidase Clp
dc.subjectTumor Necrosis Factor-alpha
dc.subjectBacterial Adhesion
dc.subjectVirulence
dc.titleModulation of adherence invasion and tumor necrosis factor alpha secretion during the early stages of infection by Strepococcus pneumoniae ClpL
dc.typeJournal article
pubs.publication-statusPublished

Files

Collections

Molecular and Biomedical Science publications