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On and Polymorphisms in Q Fever

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On and Polymorphisms in Q Fever Matrix metalloproteinase expression, produc3on and polymorphisms in Q fever Anne F.M. Jansen1,2, Teske Schoffelen1,2, Julien Textoris3, Jean Louis Mege3, Chantal P. Bleeker-Rovers1,2, Esther van de Vosse4, Hendrik Jan Roest5, Marcel van Deuren1,2 1. Department of Internal Medicine, Division of Experimental Medicine, Radboud university medical center, Nijmegen, The Netherlands 2. Radboud Expert Centre for Q fever, Radboud university medical center, Nijmegen, the Netherlands, 3. URMITE, CNRS UMR 7278, IRD 198, INSERM 1095 Aix-Marseille University, Marseille, France 4. Department of Infec3ous Diseases, Leiden University Medical Center, Leiden, The Netherlands 5. Department of Bacteriology and TSEs, Central Veterinary Instute, part of Wageningen UR, Lelystad, the Netherlands Background C. burnei induces MMP-1 and MMP-9 produc3on in PBMCs Chronic Q fever is a life threatening condi3on caused by the Gram-negave bacterium Coxiella burnei, manifes3ng as an infec3on of aneurysms, aor3c prosthesis or heart valves. Matrix metalloproteinases (MMPs) are proteoly3c enzymes that cleave extracellular matrix and are implicated in the pathology of aneurysms and endocardi3s. Currently, the contribu3on of MMPs to the pathogenesis of chronic Q fever is unknown. Methods We inves3gated the C. burnei specific gene expression of MMPs in PBMCs and protein produc3on by ELISA in chronic Q fever paents (n=6, n=10, respec3vely), cardiovascular paents with a history of Q fever (n=10) and healthy controls (n=4, n=10, respec3vely), in some experiments, the controls had vascular disease (n=10). Circulang MMP levels were assessed with Luminex technology and these groups were also genotyped for 20 SNPs in MMP and Tissue Inhibitor of MMP (TIMP) genes. MMP-7 serum levels are higher in chronic Q fever pa3ents Circulang MMP-2, MMP-7 and MMP-10 was C. burnei specifically upregulates MMP gene expression and induces MMP produc3on measured in serum using Luminex technology in Func3onal enrichment analysis revealed C. burnei specific upregulaon compared to LPS controls with vascular s3mulaon in healthy controls of 4 MMP genes: MMP1, MMP7, MMP10 and MMP19. This disease (n=10), encouraged us to look further into the role of MMPs in Q fever. cardiovascular paents with a history of Q fever Gene3c varia3on in MMP genes is associated with chronic Q fever (n=10) and chronic Q fever paents (n=27). We genotyped 139 chronic Q fever paents and 220 cardiovascular paents with a history of Q fever for 20 SNPs in MMP or TIMP genes. e Polymorphism Genotype distribuon P-valuea Conclusions Wild type Heterozygous Homozygous C. burnei: No (%) No (%) No (%) v upregulates MMP1, MMP7, MMP10 and MMP19 gene expression in PBMCs MMP2 CC CT TT rs243865 Controls 128 (58%) 84 (38%) 7 (3%) C>T v induces MMP produc3on in PBMCs Paents 80 (58%) 48 (35%) 11 (8%) 0.05* MMP7 AA AG GG In chronic Q fever: rs11568818 Controls 72 (33%) 97 (44%) 49 (22%) A>G v Polymorphisms in MMP2, MMP7 and MMP9 are more common in chronic Q fever Paents 32 (23%) 63 (46%) 43 (31%) 0.05** paents compared to cardiovascular paents with a history of Q fever MMP9 AA AG GG rs17576, Controls 106 (48%) 86 (39%) 27 (12%) A>G Paents 50 (36%) 71 (51%) 18 (13%) 0.02** v Serum levels of MMP-7 are higher in chronic Q fever paents compared to control a Logistic regression, * recessive model analysis, ** dominant model analysis groups Anne Jansen, MD Geert Grooteplein Zuid 8, 6525 GA Nijmegen, The Netherlands. ( +31-24-3619086 * [email protected] .
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