scholarly journals Divergent roles of Toll-like receptor 2 in response to lipoteichoic acid and Staphylococcus aureus in vivo

2010 ◽  
Vol 40 (6) ◽  
pp. 1639-1650 ◽  
Author(s):  
Mark R. Gillrie ◽  
Lori Zbytnuik ◽  
Erin McAvoy ◽  
Roxna Kapadia ◽  
Kristine Lee ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Lipoteichoic Acid ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
And Staphylococcus Aureus

scholarly journals Response to Staphylococcus aureus requires CD36-mediated phagocytosis triggered by the COOH-terminal cytoplasmic domain

2005 ◽  
Vol 170 (3) ◽  
pp. 477-485 ◽  
Author(s):  
Lynda M. Stuart ◽  
Jiusheng Deng ◽  
Jessica M. Silver ◽  
Kazue Takahashi ◽  
Anita A. Tseng ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mutational Analysis ◽  
Scavenger Receptor ◽  
Lipoteichoic Acid ◽  
Cytoplasmic Domain ◽  
Toll Like Receptor ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

Phagocyte recognition and clearance of bacteria play essential roles in the host response to infection. In an on-going forward genetic screen, we identify the Drosophila melanogaster scavenger receptor Croquemort as a receptor for Staphylococcus aureus, implicating for the first time the CD36 family as phagocytic receptors for bacteria. In transfection assays, the mammalian Croquemort paralogue CD36 confers binding and internalization of Gram-positive and, to a lesser extent, Gram-negative bacteria. By mutational analysis, we show that internalization of S. aureus and its component lipoteichoic acid requires the COOH-terminal cytoplasmic portion of CD36, specifically Y463 and C464, which activates Toll-like receptor (TLR) 2/6 signaling. Macrophages lacking CD36 demonstrate reduced internalization of S. aureus and its component lipoteichoic acid, accompanied by a marked defect in tumor necrosis factor-α and IL-12 production. As a result, Cd36−/− mice fail to efficiently clear S. aureus in vivo resulting in profound bacteraemia. Thus, response to S. aureus requires CD36-mediated phagocytosis triggered by the COOH-terminal cytoplasmic domain, which initiates TLR2/6 signaling.

scholarly journals Staphylococcus aureus –derived lipoteichoic acid induces temporary T-cell paralysis independent of Toll-like receptor 2

2016 ◽  
Vol 138 (3) ◽  
pp. 780-790.e6 ◽  
Author(s):  
Susanne Kaesler ◽  
Yuliya Skabytska ◽  
Ko-Ming Chen ◽  
Wolfgang E. Kempf ◽  
Thomas Volz ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
T Cell ◽  
Lipoteichoic Acid ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Staphylococcus aureus Peptidoglycan Is a Toll-Like Receptor 2 Activator: a Reevaluation

2005 ◽  
Vol 73 (8) ◽  
pp. 5212-5216 ◽  
Author(s):  
Roman Dziarski ◽  
Dipika Gupta
Keyword(s):  
Staphylococcus Aureus ◽  
Sodium Dodecyl ◽  
Lipoteichoic Acid ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Phenol Extraction ◽  
Tlr2 Activation ◽  
Toll Like Receptor 2 ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Since the ability of peptidoglycan (PGN) to activate Toll-like receptor 2 (TLR2) was recently questioned, we reevaluated activation of TLR2 by PGN. Polymeric soluble or insoluble Staphylococcus aureus PGN, repurified by sodium dodecyl sulfate or phenol extraction, activated TLR2 at 0.1 to 1 or 10 μg/ml, respectively, and induced tumor necrosis factor alpha production. The TLR2 activation by PGN, but not by lipoteichoic acid, was abolished by muramidase digestion. We conclude that polymeric S. aureus PGN is a TLR2 activator.

scholarly journals Heterozygous Toll-Like Receptor 2 Polymorphism Does Not Affect Lipoteichoic Acid-Induced Chemokine and Inflammatory Responses

2004 ◽  
Vol 72 (3) ◽  
pp. 1828-1831 ◽  
Author(s):  
Sonja von Aulock ◽  
Nicolas W. J. Schröder ◽  
Stephanie Traub ◽  
Katja Gueinzius ◽  
Eva Lorenz ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Lipoteichoic Acid ◽  
Cytokine Response ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Functional Allele ◽  
Polymorphic Gene ◽  
Toll Like Receptor 2

ABSTRACT While transfection of tlr2 conveyed responsiveness to lipoteichoic acid (LTA), the Arg753Gln polymorphic gene could not. LTA induced a stronger chemokine and anti-inflammatory response than lipopolysaccharides did. Blood from heterozygous polymorphic and wild-type donors reacted uniformly to LTA and Staphylococcus aureus. Thus, one functional allele for Toll-like receptor 2 suffices for full cytokine response.

scholarly journals Relationship between toll-like receptor 2 R753Q and T16934A polymorphisms and Staphylococcus aureus nasal carriage

2017 ◽  
Vol 49 (2) ◽  
pp. 110-115
Author(s):  
Maciej Żukowski ◽  
Olga Taryma-Leśniak ◽  
Mariusz Kaczmarczyk ◽  
Katarzyna Kotfis ◽  
Łukasz Szydłowski ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Nasal Carriage ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
And Staphylococcus Aureus

scholarly journals Targeting Toll-Like Receptor 2: Polarization of Porcine Macrophages by a Mycoplasma-Derived Pam2cys Lipopeptide

Vaccines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 692
Author(s):  
Giulia Franzoni ◽  
Antonio Anfossi ◽  
Chiara Grazia De Ciucis ◽  
Samanta Mecocci ◽  
Tania Carta ◽  
...  
Keyword(s):  
Mhc Class Ii ◽  
Macrophage Polarization ◽  
Surface Protein ◽  
Antimicrobial Activities ◽  
Toll Like Receptor ◽  
Activation Markers ◽  
Class I Mhc ◽  
Toll Like Receptor 2

Toll-like receptor 2 (TLR2) ligands are attracting increasing attention as prophylactic and immunotherapeutic agents against pathogens and tumors. We previously observed that a synthetic diacylated lipopeptide based on a surface protein of Mycoplasma agalactiae (Mag-Pam2Cys) strongly activated innate immune cells, including porcine monocyte-derived macrophages (moMΦ). In this study, we utilized confocal microscopy, flow cytometry, multiplex cytokine ELISA, and RT-qPCR to conduct a comprehensive analysis of the effects of scalar doses of Mag-Pam2Cys on porcine moMΦ. We observed enhanced expression of activation markers (MHC class I, MHC class II DR, CD25), increased phagocytotic activity, and release of IL-12 and proinflammatory cytokines. Mag-Pam2Cys also upregulated the gene expression of several IFN-α subtypes, p65, NOS2, and molecules with antimicrobial activities (CD14, beta defensin 1). Overall, our data showed that Mag-Pam2Cys polarized porcine macrophages towards a proinflammatory antimicrobial phenotype. However, Mag-Pam2Cys downregulated the expression of IFN-α3, six TLRs (TLR3, -4, -5, -7, -8, -9), and did not interfere with macrophage polarization induced by the immunosuppressive IL-10, suggesting that the inflammatory activity evoked by Mag-Pam2Cys could be regulated to avoid potentially harmful consequences. We hope that our in vitro results will lay the foundation for the further evaluation of this diacylated lipopeptide as an immunopotentiator in vivo.

Cefotaxime and amikacin: results of in vitro and in vivo studies against Gram-negative bacteria and Staphylococcus aureus

1980 ◽  
Vol 6 (suppl A) ◽  
pp. 55-61 ◽  
Author(s):  
J. Klastersky ◽  
H. Gaya ◽  
S. H. Zinner ◽  
C. Bernard ◽  
J-C. Ryff ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
In Vivo Studies ◽  
Gram Negative Bacteria ◽  
Gram Negative ◽  
And Staphylococcus Aureus

scholarly journals The Synergistic Effect of Nicotine and Staphylococcus aureus on Peri-Implant Infections

2021 ◽  
Vol 9 ◽  
Author(s):  
Yao Hu ◽  
Wen Zhou ◽  
Chengguang Zhu ◽  
Yujie Zhou ◽  
Qiang Guo ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Synergistic Effects ◽  
Protein A ◽  
Treated Group ◽  
Combination Group ◽  
Staphylococcal Protein A ◽  
Receptor Activator ◽  
And Staphylococcus Aureus

Smoking is considered a key risk factor for implant survival; however, how it interacts with the pathogens in peri-implant infections is not clear. Here, we identified that nicotine, the key component of cigarette smoking, can interact with Staphylococcus aureus and synergistically induce peri-implant infections in a rat osteolysis model. The nicotine–S. aureus combination group increased the gross bone pathology, osteolysis, periosteal reactions, and bone resorption compared to the nicotine or S. aureus single treated group (p < 0.05). Nicotine did not promote the proliferation of S. aureus both in vitro and in vivo, but it can significantly upregulate the expression of staphylococcal protein A (SpA), a key virulence factor of S. aureus. The nicotine–S. aureus combination also synergistically activated the expression of RANKL (receptor activator of nuclear factor-kappa B ligand, p < 0.05) to promote the development of peri-implant infections. The synergistic effects between nicotine and S. aureus infection can be a new target to reduce the peri-implant infections.

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