Biology subjects

Chauvin, C.

Publications and source records attributed to Chauvin, C..

4 recordsLinked to original sources

bioRxiv2022

Antimicrobial resistance of Enterococcus cecorum: ECOFF determination

Enterococcus cecorum, a commensal Gram-positive bacterium of the chicken gut, has emerged as a worldwide cause of lameness in poultry, particularly in fast-growing broilers. It is responsible for osteomyelitis, spondylitis and femoral head necrosis, causing animal suffering, mortality and antimicrobial use. Research on the antimicrobial resistance of E. cecorum clinical isolates in France is scarce, and epidemiological cut-off (ECOFF) values unknown. To determine tentative ECOFF (COWT) values for E. cecorum and to investigate the antimicrobial resistance patterns of isolates from mainly French broilers, we tested the susceptibility of a collection of commensal and clinical isolates (n=208) to 29 antimicrobials by the disc diffusion (DD) method. We also determined the minimum inhibitory concentrations (MICs) of 23 antimicrobials by the broth micro-dilution method. To detect chromosomal mutations conferring antimicrobial resistance, we investigated the genomes of 118 E. cecorum isolates mainly obtained from infectious sites and previously described in the literature. We determined the COWT values for more than 20 antimicrobials and identified two chromosomal mutations explaining fluoroquinolone resistance. The DD method appears better suited for detecting E. cecorum antimicrobial resistance. Although tetracycline and erythromycin resistances were persistent in clinical and non-clinical isolates, we found little or no resistance to medically important antimicrobials.

microbiology↗

bioRxiv2022

Monocyte intrinsic NOD2 signalling inhibits pathogenic macrophage differentiation and its loss in inflammatory macrophages improves intestinal inflammation.

ObjectiveIt is believed that intestinal recruitment of monocytes from Crohns Disease (CD) patients who carry NOD2 risk alleles may repeatedly give rise to recruitment of pathogenic macrophages. We investigated an alternative possibility that NOD2 may rather inhibit their differentiation from intravasating monocytes. DesignThe monocyte fate decision was examined by using germ-free mice, mixed bone marrow chimeras and a culture system yielding macrophages and monocyte-derived dendritic cells (mo-DCs). We next asked whether Nod2 in either monocytes or tissue macrophages have distinct resolving properties in colitis. ResultsDespite a similar abundance of monocytes, the intestinal frequency of mo-DCs from Nod2-deficient mice was lowered independently of the changes in the gut microbiota that are caused by Nod2 deficiency. Similarly, the pool of mo-DCs was poorly reconstituted with mobilized bone marrow Nod2-deficient cells. The use of pharmacological inhibitors revealed that activated NOD2 at an early stage of development dominantly inhibits mTOR-mediated macrophage differentiation in a TNFalpha-dependent manner. These observations were supported by the identification of a TNFalpha-dependent response to MDP that is specifically lost in CD14-expressing blood cells bearing the frameshift mutation in NOD2. Accordingly, loss of NOD2 in monocytes lowers glycolytic reserve, CD115 expression and pro-resolving features. Dietary intake of aryl hydrocarbon receptor (AHR) agonists that promotes mo-DCs generation improves colitis in Nod2-deficient mice to the same extent as what is observed upon macrophage ablation of Nod2. ConclusionNOD2 negatively regulates a macrophage developmental program through a feed-forward loop that could be exploited for overcoming resistance to anti-TNF therapy in CD. Significance of this studyO_ST_ABSWhat is already known about this subject?C_ST_ABSO_LILoss of NOD2 function is predisposing to Crohns disease. C_LIO_LIRapamycin, a serine/THR kinase inhibitor of mammalian target (mTOR) has been reported as potentially effective treatment in discrete subset of CD patients with refractory colitis. C_LIO_LIThe NOD2 protein promotes the chemokine CCL2-dependent recruitment of inflammatory monocytes in response to tissue injury. C_LIO_LIAn accumulation of CCR2-expressing monocytes and inflammatory macrophages is observed within the intestinal mucosa of CD patients including those resistant to anti-TNF therapy. C_LIO_LIActivated NOD2 enhances proinflammatory activity of CX3CR1intLy6Chi effector monocytes. C_LIO_LIThe monocyte fate toward mo-DCs is orchestrated by the aryl hydrocarbon receptor. C_LI What are the new findings?O_LINOD2 has a hierarchically dominant negative role on the mTORC-driven monocyte conversion to inflammatory macrophages independently of the changes in the gut microbiota that are caused by Nod2 deficiency. C_LIO_LIA defect in monocytes fate at the early stage allow the expansion of pathogenic macrophages in Nod2-deficient mice at the expense of mo-DC. C_LIO_LIAdoptive transfer of Nod2-deficient monocytes into wild-type mice was sufficient to exacerbate DSS-induced intestinal damage. C_LIO_LIThe glycolytic reserve of monocytes and their ability to respond to M-CSF is lowered upon loss of NOD2 signalling. C_LIO_LIDeletion of NOD2 in macrophage improves colitis to the same extent as dietary supplementation of AHR agonist in mice. C_LIO_LIThe recognition of the gut microbiota by NOD2 is required for de novo reconstitution of mo-DCs in the lamina propria of the murine intestine, while having minimal effect on the mobilization of their precursors to the intestinal mucosa. C_LI How might it impact on clinical practice in the foreseeable future?This study might contribute to the development of novel mTORC-based therapeutic strategies for improving the response to biologics by restoring the ability of circulating monocytes to reconstitute the pool of mo-DCs during homeostatic turnover and upon tissue injury. It may thereby prevent the accumulation of pathogenic macrophages in patients with loss-of-function NOD2 alleles, which fail to respond to anti-TNF and are at greater risk of developing stricturing disease.

immunology↗

bioRxiv2019

Dynamics of Livestock-Associated Methicillin Resistant Staphylococcus aureus in pig farms networks: insight from mathematical modeling and French data

Livestock-associated methicillin resistant Staphylococcus aureus (LA-MRSA) colonizes livestock animals worldwide, especially pigs and calves. Although frequently carried asymptomatically, LA-MRSA can cause severe infections in humans. It is therefore important to better understand LA-MRSA spreading dynamics within pig farms and over pig farms networks, and to compare different strategies of control and surveillance. For this purpose, we propose a stochastic meta-population model of LA-MRSA spread along the French pig-farm network (n=10,542 farms), combining within- and between-farms dynamics, based on detailed data on breeding practices and pig exchanges between holdings. We calibrate the model using French epidemiological data. We then identify farm-level factors associated with the spreading potential of LA-MRSA in the network. We also show that, assuming control measures applied in a limited (n=100) number of farms, targeting farms depending on their centrality in the network is the only way to significantly reduce LA-MRSA global prevalence. Finally, we investigate the scenario of emergence of a new LA-MRSA strain, and find that the farms with the highest indegree would be the best sentinels for a targeted surveillance of such a strains introduction.

microbiology↗

bioRxiv2017

Abundance and diversity of the fecal resistome in slaughter pigs and broilers in nine European countries

EFFORT groupHaitske Graveland, Alieda van Essen, Bruno Gonzalez-Zorn, Gabriel Moyano, Pascal Sanders, Claire Chauvin, Julie David, Antonio Battisti, Andrea Caprioli, Jeroen Dewulf, Thomas Blaha, Katharina Wadepohl, Maximiliane Brandt, Dariusz Wasyl, Magdalena Skarzynska, Magdalena Zajac, Hristo Daskalov, Helmut W Saatkamp, Katharina D.C. Stark.\n\nAbstractAntimicrobial resistance (AMR) in bacteria and associated human morbidity and mortality is increasing. Use of antimicrobials in livestock selects for AMR that can subsequently be transferred to humans. This flow of AMR between reservoirs demands surveillance in livestock as well as in humans. As part of the EFFORT project (www.effort-against-amr.eu), we have quantified and characterized the acquired resistance gene pools (resistomes) of 181 pig and 178 poultry farms from nine European countries, generating more than 5,000 gigabases of DNA sequence, using shotgun metagenomics. We quantified acquired AMR using the ResFinder database and a database constructed for this study, consisting of AMR genes identified through screening environmental DNA. The pig and poultry resistomes were very different in abundance and composition. There was a significant country effect on the resistomes, more so in pigs than poultry. We found higher AMR loads in pigs, while poultry resistomes were more diverse. We detected several recently described, critical AMR genes, including mcr-1 and optrA, the abundance of which differed both between host species and countries. We found that the total acquired AMR level, was associated with the overall country-specific antimicrobial usage in livestock and that countries with comparable usage patterns had similar resistomes. Novel, functionally-determined AMR genes were, however, not associated with total drug use.

microbiology↗