Host Chemokines Bind to Staphylococcus aureus and Stimulate Protein A Release

Yung, Sunny C.; Parenti, David M.; Murphy, Philip M.

doi:10.1074/jbc.m110.195180

Cited by 24 publications

(26 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, researchers discovered that low concentrations of host chemokines, including CXCL9 and CXCL10, induce the release of SPA, while high concentrations of chemokines can also be antibacterial 70,71. This echoes findings from our previous research on the effects of the cytokine IL-1α.…”

Section: Discussionsupporting

confidence: 73%

Exoproteome ofStaphylococcus aureusReveals Putative Determinants of Nasal Carriage

Muthukrishnan¹,

Quinn²,

Lamers³

et al. 2011

J. Proteome Res.

View full text Add to dashboard Cite

SummaryDue to the increasing prevalence of nosocomial and community-acquired antibiotic resistant Staphylococcus aureus (SA), understanding the determinants of SA nasal carriage has become a major imperative. Previous research has revealed many host and bacterial factors that contribute to SA nasal carriage. To assess bacterial factors that facilitate nasal carriage, we compared the exoproteome of a nasal carrier strain of SA to a genetically similar non-carrier strain. Additionally, the carrier strain biofilm exoproteome was also compared against its planktonic counterpart. Using high throughput proteomics, it was observed that the carrier strain of SA secretes a greater number of proteins that may promote successful colonization of the human nose, including cell attachment and immunoevasive proteins, than the non-carrier strain. Similarly, SA carrier strain biofilm exoproteome contains a greater number of immunoevasive proteins than its planktonic counterpart. Analysis of the most abundant immunoevasive proteins revealed that Staphylococcal protein A was present at significantly higher levels in carrier than in non-carrier strains of SA, suggesting an association with nasal carriage. While further analyses of specific differences between carrier and non-carrier strains of SA are required, many of the differentially expressed proteins identified can be considered to be putative determinants of nasal carriage.

show abstract

Section: Discussionsupporting

confidence: 73%

Exoproteome ofStaphylococcus aureusReveals Putative Determinants of Nasal Carriage

Muthukrishnan¹,

Quinn²,

Lamers³

et al. 2011

J. Proteome Res.

View full text Add to dashboard Cite

show abstract

“…Both chemokines have previously been shown to have such antimicrobial activity against Staphylococcus aureus and Bacillus anthracis [43, 44]. …”

Section: Discussionmentioning

confidence: 99%

Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice

Bishop

Lionakis

Sassi

et al. 2015

Microbes and Infection

Self Cite

View full text Add to dashboard Cite

We examined gene expression levels of multiple chemokines and chemokine receptors during Pneumocystis murina infection in wild-type and immunosuppressed mice, using microarrays and qPCR. In wild-type mice, expression of chemokines that are ligands for Ccr2, Cxcr3, Cxcr6, and Cxcr2 increased at days 32 to 41 post-infection, with a return to baseline by day 75 to 150. Concomitant increases were seen in Ccr2 ,Cxcr3, and Cxcr6, but not in Cxcr2 expression. Induction of these same factors also occurred in CD40-ligand and CD40 knockout mice but only at a much later time-point, during uncontrolled Pneumocystis pneumonia (PCP). Expression of CD4 Th1 markers was increased in wild-type mice during clearance of infection. Ccr2 and Cx3cr1 knockout mice cleared Pneumocystis infection with kinetics similar to wild-type mice, and all animals developed anti-Pneumocystis antibodies. Upregulation of Ccr2, Cxcr3, and Cxcr6 and their ligands supports an important role for T helper cells and mononuclear phagocytes in the clearance of Pneumocystis infection. However, based on the current and prior studies, no single chemokine receptor appears to be critical to the clearance of Pneumocystis.

show abstract

“…For example, CXCL9 was recently reported to bind several surface proteins expressed by Chlamydophila pneumoniae, an activity that may promote antimicrobial activity against this organism (27). Also, S. aureus has been found to interact with numerous host chemokines; interestingly, these binding events are recognized by the bacteria and trigger the release of the virulence factor protein A (28). Indeed, it appears that host chemokines may be significantly involved in a previously unappreciated area of dynamic and, possibly, complex host-pathogen interaction that substantially influences bacterial pathogenesis and the outcome of infection.…”

Section: Discussionmentioning

confidence: 99%

Identification of the bacterial protein FtsX as a unique target of chemokine-mediated antimicrobial activity against Bacillus anthracis

Crawford

Lowe²,

Fisher

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Chemokines are a family of chemotactic cytokines that function in host defense by orchestrating cellular movement during infection. In addition to this function, many chemokines have also been found to mediate the direct killing of a range of pathogenic microorganisms through an as-yet-undefined mechanism. As an understanding of the molecular mechanism and microbial targets of chemokine-mediated antimicrobial activity is likely to lead to the identification of unique, broad-spectrum therapeutic targets for effectively treating infection, we sought to investigate the mechanism by which the chemokine CXCL10 mediates bactericidal activity against the Gram-positive bacterium Bacillus anthracis, the causative agent of anthrax. Here, we report that disruption of the gene ftsX, which encodes the transmembrane domain of a putative ATP-binding cassette transporter, affords resistance to CXCL10-mediated antimicrobial effects against vegetative B. anthracis bacilli. Furthermore, we demonstrate that in the absence of FtsX, CXCL10 is unable to localize to its presumed site of action at the bacterial cell membrane, suggesting that chemokines interact with specific, identifiable bacterial components to mediate direct microbial killing. These findings provide unique insight into the mechanism of CXCL10-mediated bactericidal activity and establish, to our knowledge, the first description of a bacterial component critically involved in the ability of host chemokines to target and kill a bacterial pathogen. These observations also support the notion of chemokine-mediated antimicrobial activity as an important foundation for the development of innovative therapeutic strategies for treating infections caused by pathogenic, potentially multidrug-resistant microorganisms.CXC chemokine | CXCR3 | innate immune system | transposon mutant library | ABC transporter

show abstract

Host Chemokines Bind to Staphylococcus aureus and Stimulate Protein A Release

Cited by 24 publications

References 49 publications

Exoproteome ofStaphylococcus aureusReveals Putative Determinants of Nasal Carriage

Exoproteome ofStaphylococcus aureusReveals Putative Determinants of Nasal Carriage

Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice

Identification of the bacterial protein FtsX as a unique target of chemokine-mediated antimicrobial activity against Bacillus anthracis

Contact Info

Product

Resources

About