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 Bacterial and Host Factors Implicated in Nasal Carriage of Methicillin-Resistant Staphylococcus aureus in Mice

2005 ◽  
Vol 73 (3) ◽  
pp. 1847-1851 ◽  
Author(s):  
Bruno González-Zorn ◽  
Jose P. M. Senna ◽  
Laurence Fiette ◽  
Spencer Shorte ◽  
Aurélie Testard ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Nasal Carriage ◽  
Transmembrane Conductance Regulator ◽  
Toll Like Receptor ◽  
Transmembrane Conductance ◽  
Methicillin Resistant ◽  
Toll Like Receptor 2 ◽  
Resistant Strains ◽  
Cystic Fibrosis Transmembrane ◽  
Deficient Mice

ABSTRACT Nasal carriage is a major risk factor for Staphylococcus aureus infection, especially for methicillin-resistant strains (MRSA). Using a mouse model of nasal carriage, we have compared several S. aureus strains and demonstrated increased colonization levels by MRSA in cystic fibrosis transmembrane conductance regulator-deficient mice and Toll-like receptor 2 (TLR2)-deficient mice but not TLR4-deficient mice.

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 Staphylococcus aureus Releases Proinflammatory Membrane Vesicles To Resist Antimicrobial Fatty Acids

mSphere ◽  
2020 ◽  
Vol 5 (5) ◽  
Author(s):  
Arnaud Kengmo Tchoupa ◽  
Andreas Peschel
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Membrane Vesicle ◽  
Membrane Vesicles ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Content Type ◽  
Healthy Humans ◽  
Toll Like Receptor 2

ABSTRACT Staphylococcus aureus is a major pathogen, which colonizes one in three otherwise healthy humans. This significant spread of S. aureus is largely due to its ability to circumvent innate immune responses, including antimicrobial fatty acids (AFAs) on the skin and in nasal secretions. In response to AFAs, S. aureus swiftly induces resistance mechanisms, which have yet to be completely elucidated. Here, we identify membrane vesicle (MV) release as a resistance strategy used by S. aureus to sequester host-specific AFAs. MVs protect S. aureus against a wide array of AFAs. Strikingly, beside MV production, S. aureus modulates MV composition upon exposure to AFAs. MVs purified from bacteria grown in the presence of linoleic acid display a distinct protein content and are enriched in lipoproteins, which strongly activate Toll-like receptor 2 (TLR2). Cumulatively, our findings reveal the protective capacities of MVs against AFAs, which are counteracted by an increased TLR2-mediated innate immune response. IMPORTANCE The nares of one in three humans are colonized by Staphylococcus aureus. In these environments, and arguably on all mucosal surfaces, bacteria encounter fatty acids with antimicrobial properties. Our study uncovers that S. aureus releases membrane vesicles (MVs) that act as decoys to protect the bacterium against antimicrobial fatty acids (AFAs). The AFA-neutralizing effects of MVs were neither strain specific nor restricted to one particular AFA. Hence, MVs may represent “public goods” playing an overlooked role in shaping bacterial communities in AFA-rich environments such as the skin and nose. Intriguingly, in addition to MV biogenesis, S. aureus modulates MV composition in response to exposure to AFAs, including an increased release of lipoproteins. These MVs strongly stimulate the innate immunity via Toll-like receptor 2 (TLR2). TLR2-mediated inflammation, which helps to fight infections, may exacerbate inflammatory disorders like atopic dermatitis. Our study highlights intricate immune responses preventing infections from colonizing bacteria.

scholarly journals Purified Streptococcus pneumoniae Endopeptidase O (PepO) Enhances Particle Uptake by Macrophages in a Toll-Like Receptor 2- and miR-155-Dependent Manner

2017 ◽  
Vol 85 (4) ◽  
Author(s):  
Hua Yao ◽  
Hong Zhang ◽  
Kai Lan ◽  
Hong Wang ◽  
Yufeng Su ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Host Defense ◽  
Defense Response ◽  
Dependent Manner ◽  
Toll Like Receptor ◽  
Content Type ◽  
Host Defense Response ◽  
Toll Like Receptor 2 ◽  
In Cells

ABSTRACT Insights into the host-microbial virulence factor interaction, especially the immune signaling mechanisms, could provide novel prevention and treatment options for pneumococcal diseases. Streptococcus pneumoniae endopeptidase O (PepO) is a newly discovered and ubiquitously expressed pneumococcal virulence protein. A PepO-mutant strain showed impaired adherence to and invasion of host cells compared with the isogenic wild-type strain. It is still unknown whether PepO is involved in the host defense response to pneumococcal infection. Here, we demonstrated that PepO could enhance phagocytosis of Streptococcus pneumoniae and Staphylococcus aureus by peritoneal exudate macrophages (PEMs). Further studies showed that PepO stimulation upregulated the expression of microRNA-155 (miR-155) in PEMs in a time- and dose-dependent manner. PepO-induced enhanced phagocytosis was decreased in cells transfected with an inhibitor of miR-155, while it was increased in cells transfected with a mimic of miR-155. We also revealed that PepO-induced upregulation of miR-155 in PEMs was mediated by Toll-like receptor 2 (TLR2)–NF-κB signaling and that the increased expression of miR-155 downregulated expression of SHIP1. Taken together, these results indicate that PepO induces upregulation of miR-155 in PEMs, contributing to enhanced phagocytosis and host defense response to pneumococci and Staphylococcus aureus.

scholarly journals Toll-Like Receptor 2 Modulates the Proinflammatory Milieu in Staphylococcus aureus-Induced Brain Abscess

2005 ◽  
Vol 73 (11) ◽  
pp. 7428-7435 ◽  
Author(s):  
Tammy Kielian ◽  
Anessa Haney ◽  
Patrick M. Mayes ◽  
Sarita Garg ◽  
Nilufer Esen
Keyword(s):  
Staphylococcus Aureus ◽  
Brain Abscess ◽  
Complex Nature ◽  
Interleukin 17 ◽  
Immune Recognition ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Proinflammatory Mediators ◽  
Brain Abscesses ◽  
Toll Like Receptor 2

ABSTRACT Toll-like receptor 2 (TLR2) is a pattern recognition receptor (PRR) that plays an important role in innate immune recognition of conserved structural motifs on a wide array of pathogens, including Staphylococcus aureus. To ascertain the functional significance of TLR2 in the context of central nervous system (CNS) parenchymal infection, we evaluated the pathogenesis of S. aureus-induced experimental brain abscess in TLR2 knockout (KO) and wild-type (WT) mice. The expression of several proinflammatory mediators, including inducible nitric oxide synthase, tumor necrosis factor alpha, and macrophage inflammatory protein-2, was significantly attenuated in brain abscesses of TLR2 KO mice compared to WT mice during the acute phase of infection. Conversely, interleukin-17 (IL-17), a cytokine produced by activated and memory T cells, was significantly elevated in lesions of TLR2 KO mice, suggesting an association between innate and adaptive immunity in brain abscess. Despite these differences, brain abscess severity in TLR2 KO and WT animals was similar, with comparable mortality rates, bacterial titers, and blood-brain barrier permeability, implying a role for alternative PRRs. Expression of the phagocytic PRRs macrophage scavenger receptor type AI/AII and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) was increased in brain abscesses of both TLR2 KO and WT mice compared to uninfected animals. However, LOX-1 induction in brain abscesses of TLR2 KO mice was significantly attenuated compared to WT animals, revealing that the TLR2-dependent signal(s) influence LOX-1 expression. Collectively, these findings reveal the complex nature of gram-positive bacterial recognition in the CNS which occurs, in part, through engagement of TLR2 and highlight the importance of receptor redundancy for S. aureus detection in the CNS.

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