Contribution of phagocytosis and intracellular sensing for cytokine production by Staphylococcus aureus-activated macrophages

Kapetanovic, Ronan, Nahori, Marie-Anne, Balloy, ViViane, Fitting, Catherine, Philpott, Dana J., Cavaillon, Jean-Marc and Adib-Conquy, Minou (2007) Contribution of phagocytosis and intracellular sensing for cytokine production by Staphylococcus aureus-activated macrophages. Infection and Immunity, 75 2: 830-837. doi:10.1128/IAI.01199-06

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Author Kapetanovic, Ronan
Nahori, Marie-Anne
Balloy, ViViane
Fitting, Catherine
Philpott, Dana J.
Cavaillon, Jean-Marc
Adib-Conquy, Minou
Title Contribution of phagocytosis and intracellular sensing for cytokine production by Staphylococcus aureus-activated macrophages
Formatted title
Contribution of phagocytosis and intracellular sensing for cytokine production by Staphylococcus aureus-activated macrophages
Journal name Infection and Immunity   Check publisher's open access policy
ISSN 1098-5522
1070-6313
Publication date 2007-02
Sub-type Article (original research)
DOI 10.1128/IAI.01199-06
Open Access Status File (Publisher version)
Volume 75
Issue 2
Start page 830
End page 837
Total pages 8
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Abstract Toll-like receptors (TLRs) are involved in the sensing of microbially derived compounds. We analyzed the contribution of these receptors to cytokine production by macrophages following stimulation with whole bacteria. Using knockout mice, we confirmed that the TLR4 and TLR2 contribution was predominant in the induction of tumor necrosis factor alpha and interleukin-10 by gram-negative bacteria. In contrast, the absence of TLR2 and/or TLR4 or TLR9 did not affect the response to gram-positive bacteria. In the absence of TLR2, phagocytosis was essential for cytokine production in response to heat-killed Staphylococcus aureus (HKSA). Because intracellular sensing was important in the absence of TLR2, we evaluated the contribution of Nodi and Nod2, intracytoplasmic sensors of peptidoglycan-derived muropeptides, to the response to HKSA. By transfecting RAW 264.7 macrophages with dominant negative (DN) forms of Nodi and Nod2, we showed that both molecules inhibited NF-κB activation in response to HKSA. The unexpected interference of DN Nod1 in the response of macrophages to gram-positive bacteria was confirmed with a Nod2 agonist (muramyl dipeptide) in transfection experiments with HEK293T cell. Taken together, these results show the contribution of phagocytosis and Nod molecules to the response to HKSA in macrophages and also identify possible cross talk between Nod1 and Nod2.
Keyword TLR
HKSA
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Institute for Molecular Bioscience - Publications
 
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