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• W1871086124 abstract "Q fever is caused by Coxiella burnetii, an obligate intracellular bacterium, which survives in an acidic vacuole and escapes killing by preventing phagosome maturation [1Raoult D Marrie T Mege J.L. Natural history and pathophysiology of Q fever.Lancet Infect Dis. 2005; 5: 219-226Abstract Full Text Full Text PDF PubMed Scopus (519) Google Scholar]. In acute Q fever, granuloma formation is dependent on migration of leucocytes through the vascular endothelium. During chronic Q fever, granulomas are lacking and monocytes do not migrate across the endothelium [1Raoult D Marrie T Mege J.L. Natural history and pathophysiology of Q fever.Lancet Infect Dis. 2005; 5: 219-226Abstract Full Text Full Text PDF PubMed Scopus (519) Google Scholar], suggesting that host resistance against C. burnetii requires innate immune components. Toll-like receptors (TLRs) are pattern recognition receptors important in C. burnetii recognition. Although TLR4–/– and control mice have a similar pattern of tissue infection and clearance, granuloma formation and cytokine response are controlled, in part, by TLR4 [1Raoult D Marrie T Mege J.L. Natural history and pathophysiology of Q fever.Lancet Infect Dis. 2005; 5: 219-226Abstract Full Text Full Text PDF PubMed Scopus (519) Google Scholar]. TLR2 is also involved in granuloma formation but seems dispensable for bacterial clearance [2Meghari S Honstettre A Lepidi H Ryffel B Raoult D Mege JL TLR2 is necessary to inflammatory response in Coxiella burnetii infection.Ann N Y Acad Sci. 2005; 1063: 161-166Crossref PubMed Scopus (25) Google Scholar]. The obligate intracellular lifestyle of C. burnetii drew our attention to elucidate the contribution of another family of proteins implicated in microbial detection, the cytoplasmic nucleotide-binding oligomerization domain (Nod) proteins, and more specifically Nod2, in innate immunity to C. burnetii. Nod2 contains leucine-rich repeats similar to those found in TLRs and is thought to be responsible for recognition of peptidoglycans from Gram positive and Gram negative bacteria through direct or indirect interaction with muramyl dipeptide. Nod2 signalling contributes to inflammatory response via activation of the transcription factor NF-κB, which is necessary for clearing pathogens. The intracellular localisation of Nod2 and C. burnetii makes Nod2 a potential candidate for C. burnetii recognition through leaking into the cytoplasm of muramyl dipeptide-containing cell wall fragments. Bone marrow-derived macrophages (BMDM) from control and Nod2–/– mice [3Pauleau AL Murray PJ Role of Nod2 in the response of macrophages to Toll-like receptor agonists.Mol Cell Biol. 2003; 23: 7531-7539Crossref PubMed Scopus (222) Google Scholar] were incubated with C. burnetii for 4 h and cultured for 12 days. Infection was measured by determining the number of C. burnetii DNA copies as previously described [2Meghari S Honstettre A Lepidi H Ryffel B Raoult D Mege JL TLR2 is necessary to inflammatory response in Coxiella burnetii infection.Ann N Y Acad Sci. 2005; 1063: 161-166Crossref PubMed Scopus (25) Google Scholar]. Uptake and survival of C. burnetii in BMDM did not depend on Nod2 as DNA copy number was similar in control and Nod2–/– BMDM (data not shown). Next, we tested whether the production of cytokines/chemokines by C. burnetii-stimulated BMDM required Nod2. We assessed the expression of genes encoding pro-inflammatory (TNF) and immunoregulatory cytokines (IL-10). BMDM were stimulated for 8 h with C. burnetii and gene expression was monitored by quantitative RT-PCR [2Meghari S Honstettre A Lepidi H Ryffel B Raoult D Mege JL TLR2 is necessary to inflammatory response in Coxiella burnetii infection.Ann N Y Acad Sci. 2005; 1063: 161-166Crossref PubMed Scopus (25) Google Scholar]. In Nod2–/– BMDM, although TNF transcripts were induced, they were significantly reduced compared with control macrophages (Fig. 1a). This result agrees with other studies showing that TNF and IL-12p40 levels are reduced in the absence of Nod2 after stimulation with Mycobacterium tuberculosis [4Gandotra S Jang S Murray PJ Salgame P Ehrt S Nucleotide-binding oligomerization domain protein 2-deficient mice control infection with Mycobacterium tuberculosis.Infect Immun. 2007; 75: 5127-5134Crossref PubMed Scopus (83) Google Scholar]. Note that IL-10 was not affected by the absence of Nod2 (Fig. 1a). IL-10 is known to interfere with macrophage activation by stimulating the replication of C. burnetii through decreasing TNF production and blocking phagosomal maturation [1Raoult D Marrie T Mege J.L. Natural history and pathophysiology of Q fever.Lancet Infect Dis. 2005; 5: 219-226Abstract Full Text Full Text PDF PubMed Scopus (519) Google Scholar]. IL-10 is also associated with the chronic evolution of Q fever [1Raoult D Marrie T Mege J.L. Natural history and pathophysiology of Q fever.Lancet Infect Dis. 2005; 5: 219-226Abstract Full Text Full Text PDF PubMed Scopus (519) Google Scholar]. The absence of IL-10 modulation observed in Nod2–/– BMDM is consistent with these data, as we did not observe any increase in bacterial replication. We also measured the expression of RANTES and MCP-1, two chemokines modulated in response to C. burnetii [5Meghari S Desnues B Capo C Grau GE Raoult D Mege JL Coxiella burnetii stimulates production of RANTES and MCP-1 by mononuclear cells: modulation by adhesion to endothelial cells and its implication in Q fever.Eur Cytokine Netw. 2006; 17: 253-259PubMed Google Scholar]. RANTES expression was fourfold increased in Nod2–/– BMDM whereas MCP-1 expression was decreased by 40% (Fig. 1a). It is likely that RANTES and MCP-1 play a role in Q fever pathophysiology, as their production is dramatically increased in patients with chronic Q fever [5Meghari S Desnues B Capo C Grau GE Raoult D Mege JL Coxiella burnetii stimulates production of RANTES and MCP-1 by mononuclear cells: modulation by adhesion to endothelial cells and its implication in Q fever.Eur Cytokine Netw. 2006; 17: 253-259PubMed Google Scholar]. These data suggest that Nod2 is at least in part involved in BMDM activation and that Nod2 may be required for host defence against C. burnetii. We injected control and Nod2–/– mice with C. burnetii (5 × 105 organisms) by the intraperitoneal route, and monitored infection for 49 days. No sign of morbidity and mortality was observed. Host response to C. burnetii was assessed by measuring C. burnetii-specific circulating antibodies [2Meghari S Honstettre A Lepidi H Ryffel B Raoult D Mege JL TLR2 is necessary to inflammatory response in Coxiella burnetii infection.Ann N Y Acad Sci. 2005; 1063: 161-166Crossref PubMed Scopus (25) Google Scholar], which reached a maximal value at day 14 post-infection in control and Nod2–/– mice (Fig. 1b). Course of tissue infection was assessed by quantitative PCR. In the spleen from control and Nod2–/– mice (Fig. 1c), bacterial DNA copies were detectable at day 4 post-infection and maximal at day 7. In the liver from wt and Nod2–/– mice, a similar trend was observed, with a maximal value at day 14 (Fig. 1d). Hence, no difference in bacterial load was observed, and C. burnetii organisms were completely cleared after 42 days. In conclusion, these data suggest that Nod2 is dispensable for the control of C. burnetii infection. We cannot rule out synergistic host cell activation because C. burnetii possesses both TLR and Nod2 agonists. Indeed, TLR2 is required for granuloma formation while it is dispensable for C. burnetii clearance [2Meghari S Honstettre A Lepidi H Ryffel B Raoult D Mege JL TLR2 is necessary to inflammatory response in Coxiella burnetii infection.Ann N Y Acad Sci. 2005; 1063: 161-166Crossref PubMed Scopus (25) Google Scholar]. Further studies are required to address this hypothesis. It may be necessary to use mice lacking both Nod2 and Nod1, a closely related cytosolic protein also implicated in bacterial detection, to gain a full picture of C. burnetti cytoplasmic detection. The mechanism by which a cytosolic sensor such as Nod2 recognises phagosome-contained pathogens remains to be elucidated. M. Benoit was funded by a grant from ‘Fondation pour la Recherche Médicale’ and Y. Bechah was funded through ‘Crédits ministériels Programme Hospitalier de Recherche Clinique’. The authors thank Didier Raoult for critical reading of this manuscript." @default.
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• W1871086124 date "2009-12-01" @default.
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• W1871086124 title "Role of the cytoplasmic pattern recognition receptor Nod2 in Coxiella burnetii infection" @default.
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