scholarly journals Adaptive Immunity Against Staphylococcus aureus

2016 ◽  
pp. 419-439 ◽  
Author(s):  
Hatice Karauzum ◽  
Sandip K. Datta
Keyword(s):  
Staphylococcus Aureus ◽  
Adaptive Immunity

scholarly journals Staphylococcus aureusImpairs the Function of and Kills Human Dendritic Cells via the LukAB Toxin

mBio ◽  
2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Evelien T. M. Berends ◽  
Xuhui Zheng ◽  
Erin E. Zwack ◽  
Mickaël M. Ménager ◽  
Michael Cammer ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Dendritic Cells ◽  
Adaptive Immunity ◽  
T Cell Activation ◽  
Antigen Presenting Cells ◽  
Infection Model ◽  
High Morbidity ◽  
Content Type ◽  
Human Dendritic Cells ◽  
Antigen Presenting

ABSTRACTStaphylococcus aureusis a human pathogen responsible for high morbidity and mortality worldwide. Recurrent infections with this bacterium are common, suggesting thatS. aureusthwarts the development of sterilizing immunity.S. aureusstrains that cause disease in humans produce up to five different bicomponent toxins (leukocidins) that target and lyse neutrophils, innate immune cells that represent the first line of defense againstS. aureusinfections. However, little is known about the role of leukocidins in blunting adaptive immunity. Here, we explored the effects of leukocidins on human dendritic cells (DCs), antigen-presenting cells required for the development of adaptive immunity. Using anex vivoinfection model of primary human monocyte-derived dendritic cells, we found thatS. aureus, including strains from different clonal complexes and drug resistance profiles, effectively kills DCs despite efficient phagocytosis. Although all purified leukocidins could kill DCs, infections with live bacteria revealed thatS. aureustargets and kills DCs primarily via the activity of leukocidin LukAB. Moreover, using coculture experiments performed with DCs and autologous CD4+T lymphocytes, we found that LukAB inhibits DC-mediated activation and proliferation of primary human T cells. Taken together, the data determined in the study reveal a novel immunosuppressive strategy ofS. aureuswhereby the bacterium blunts the development of adaptive immunity via LukAB-mediated injury of DCs.IMPORTANCEAntigen-presenting cells such as dendritic cells (DCs) fulfill an indispensable role in the development of adaptive immunity by producing proinflammatory cytokines and presenting microbial antigens to lymphocytes to trigger a faster, specific, and long-lasting immune response. Here, we studied the effect ofStaphylococcus aureustoxins on human DCs. We discovered that the leukocidin LukAB hinders the development of adaptive immunity by targeting human DCs. The ability ofS. aureusto blunt the function of DCs could help explain the high frequency of recurrentS. aureusinfections. Taken together, the results from this study suggest that therapeutically targeting theS. aureusleukocidins may boost effective innate and adaptive immune responses by protecting innate leukocytes, enabling proper antigen presentation and T cell activation.

scholarly journals Activation of Human Vδ2+ γδ T Cells by Staphylococcus aureus Promotes Enhanced Anti-Staphylococcal Adaptive Immunity

2020 ◽  
Vol 205 (4) ◽  
pp. 1039-1049 ◽  
Author(s):  
Andrew J. R. Cooper ◽  
Stephen J. Lalor ◽  
Rachel M. McLoughlin
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Adaptive Immunity ◽  
Γδ T Cells

scholarly journals Th1-Th17 Cells Mediate Protective Adaptive Immunity against Staphylococcus aureus and Candida albicans Infection in Mice

2009 ◽  
Vol 5 (12) ◽  
pp. e1000703 ◽  
Author(s):  
Lin Lin ◽  
Ashraf S. Ibrahim ◽  
Xin Xu ◽  
Joshua M. Farber ◽  
Valentina Avanesian ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Candida Albicans ◽  
Adaptive Immunity ◽  
Th17 Cells ◽  
Candida Albicans Infection

scholarly journals Omics Approaches for the Study of Adaptive Immunity to Staphylococcus aureus and the Selection of Vaccine Candidates

Proteomes ◽  
2016 ◽  
Vol 4 (1) ◽  
pp. 11 ◽  
Author(s):  
Silva Holtfreter ◽  
Julia Kolata ◽  
Sebastian Stentzel ◽  
Stephanie Bauerfeind ◽  
Frank Schmidt ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Adaptive Immunity ◽  
Vaccine Candidates ◽  
Selection Of

scholarly journals A Modulatory Interleukin-10 Response to Staphylococcal Peptidoglycan Prevents Th1/Th17 Adaptive Immunity to Staphylococcus aureus

2011 ◽  
Vol 204 (2) ◽  
pp. 253-262 ◽  
Author(s):  
Vanessa Frodermann ◽  
Thu A. Chau ◽  
Samar Sayedyahossein ◽  
Judit M. Toth ◽  
David E. Heinrichs ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Adaptive Immunity ◽  
Interleukin 10

scholarly journals Microbiota-Driven Immune Cellular Maturation Is Essential for Antibody-Mediated Adaptive Immunity to Staphylococcus aureus Infection in the Eye

2014 ◽  
Vol 82 (8) ◽  
pp. 3483-3491 ◽  
Author(s):  
Tanweer Zaidi ◽  
Tauqeer Zaidi ◽  
Colette Cywes-Bentley ◽  
Roger Lu ◽  
Gregory P. Priebe ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Adaptive Immunity ◽  
Protective Efficacy ◽  
Intercellular Adhesion Molecule ◽  
Interleukin 17 ◽  
Tissue Destruction ◽  
Intercellular Adhesion Molecule 1 ◽  
Corneal Surface ◽  
Content Type

ABSTRACTAs an immune-privileged site, the eye, and particularly the outer corneal surface, lacks resident mature immune effector cells. Physical barriers and innate mediators are the best-described effectors of immunity in the cornea. When the barriers are breached, infection can result in rapid tissue destruction, leading to loss of visual acuity and frank blindness. To determine the cellular and molecular components needed for effective adaptive immunity on the corneal surface, we investigated which immune system effectors were required for protection againstStaphylococcus aureuscorneal infections in mice, which are a serious cause of human eye infections. Both systemically injected and topically applied antibodies to the conserved cell surface polysaccharide poly-N-acetylglucosamine (PNAG) were effective at mediating reductions in corneal pathology and bacterial levels. Additional host factors impacting protection included intercellular adhesion molecule 1 (ICAM-1)-dependent polymorphonuclear leukocyte (PMN) recruitment, functional CD4+T cells, signaling via the interleukin-17 (IL-17) receptor, and IL-22 production. In germfree mice, there was no protective efficacy of antibody to PNAG due to the lack of LY6G+inflammatory cell coeffector recruitment to the cornea. Protection was manifest after 3 weeks of exposure to conventional mice and acquisition of a resident microbiota. We conclude that in the anterior eye, ICAM-1-mediated PMN recruitment to the infected cornea along with endogenous microbiota-matured CD4+T cells producing both IL-17 and IL-22 is required for antibody to PNAG to protect againstS. aureusinfection.

scholarly journals Meta-Analysis of Human Molecular Responses to Staphylococcus aureus

2020 ◽  
Vol 1 (4) ◽  
pp. 11
Author(s):  
Sidra Younis ◽  
Farah Deeba ◽  
Qamar Javed ◽  
Miroslav Blumenberg
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Staphylococcus Aureus ◽  
Adaptive Immunity ◽  
Microarray Data ◽  
Immune Cell ◽  
Meta Analysis ◽  
Protein Catabolism ◽  
Transcriptional Responses ◽  
Aureus Infection

Objective: To compare the local and systematic transcriptional responses of human body to S. aureus or its components. Study Design: Meta-analysis of microarray data. Place and Duration of Study: The study was conducted at R.O. Perelman Department of Dermatology, The NYU Cancer Institute, NYU Langone Medical Center, New York, USA, from March 2015 to May 2015. Materials and Methods: Public repository “GEO Datasets” was searched using key term “Staphylococcus aureus” for data sets covering effects of S. aureus infection in Homo sapiens cells. The microarray data for immune cell responses to S. aureus was analyzed using Rank Prod, RMA Express and DAVID software. Results: The analysis has shown that S. aureus infection was responsible for inducing immunity, platelet activation, vasodilation, MyD88 dependent gene expression and cell cycle. It suppressed gene expression of normal cell processes, protein catabolism and apoptosis. Heat-inactivated S. aureus challenged the cell induced immunity, cell cycle, growth regulators, anti-apoptosis and anticoagulant genes, while suppressed the genes for adaptive immunity, carbohydrate synthesis and Myd88 dependent pathway. Furthermore, in the S. aureus-infected patients the genes for defense, innate immunity, solute receptors and anti-apoptotic processes were upregulated, whereas adaptive immunity and positive regulators of apoptosis were downregulated. Conclusion: MyD88 signaling pathway, ubiquitin mediated protein catabolism and IFNγ mediated cell death processes can be targeted for treatment against virulent S. aureus infections.

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