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Defensins couple dysbiosis to primary immunodeficiency in Crohn's disease

World Journal of Gastroenterology 2011年第5期17卷 567-571页

作者： Mathias Chamaillard Rodrigue Dessein Institut Pasteur de Lille Center for Infection and Immunity of LilleF-59019 LilleFrance Mathias ChamaillardRodrigue DesseinCNRSUMR 8204F-59021 LilleFrance Institut National de la Santé et de la Recherche Médicale U1019Team 7Equipe FRMF-59019 LilleFrance Univ Lille Nord de France F-59000 LilleFrance C.H.R.U.de Lille F-59000 LilleFrance

Antimicrobial peptides,including defensins,are essential effectors in host defence and in the maintenance of immune homeostasis.Clinical studies have linked the defective expression of both α-and β-defensin to the reduced killing of certain microorganisms by the intestinal mucosa of patients suffering from ileal and colonic Crohn's disease(CD),respectively.Only recently have the events leading to defective expression of defensins in CD been further elucidated,and are discussed herein.These events may account for CD-associated alterations in the microbiome and may subsequently precipitate the development of granulomatous inflammatory lesions in genetically-predisposed patients.We also address how these discoveries may pave the way for the development of a molecular medicine aimed at restoring gut barrier function in CD.

关键词：免疫缺陷防御素 TiAl基宿主防御肠道黏膜分子医学屏障功能微生物

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Caspase-1 activation by NLRP3 inflammasome dampens IL-33-dependent house dust mite-induced allergic lung inflammation

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分子细胞生物学报:英文版 2015年第4期7卷 351-365页

作者： Fahima Madouri Noelline Guillou Louis Fauconnier Tiffany Marchiol Nathalie Rouxel Pauline Chenuet Aurelie Ledru Lionel Apetoh Franc¸ois Ghiringhelli Mathias Chamaillard Song Guo Zheng Fabrice Trovero Valerie F.J.Quesniaux Bernhard Ryffel Dieudonnee Togbe Laboratory of Experimental and Molecular Immunology and Neurogenetics(INEM) UMR 7355 CNRS-University of OrleansF-45071 Orleans-Cedex2France Artimmune SAS 45100 Orle´ansFrance Faculte´de Me´decine University of BourgogneDijonFrance INSERM U866DijonFrance Centre Georges Franc¸ois Leclerc DijonFrance CIIL–Center for Infection and Immunity of Lille INSERM U1019Institut PasteurLilleFrance Division of Rheumatology Penn State Milton S.Hershey Medical CenterHersheyPA 17033USA Clinical Immunology Section Third Affiliated Hospital at Sun Yat-Sen UniversityGuangzhou 510630China

The cysteine protease caspase-1(Casp-1)contributes to innate immunity through the assembly of NLRP3,NLRC4,AIM2,and NLRP6 inflammasomes.Here we ask whether caspase-1 activation plays a regulatory role in house dust mite(HDM)-induced experimental allergic airway inflammation.We report enhanced airway inflammation in caspase-1-deficient mice exposed toHDMwith a marked eosinophil recruitment,increased expression of IL-4,IL-5,IL-13,aswell as full-length and bioactive IL-33.Furthermore,mice deficient for NLRP3 failed to control eosinophil influx in the airways and displayed augmented Th2 cytokine and chemokine levels,suggesting that the NLPR3 inflammasome complex controls HDM-induced inflammation.IL-33 neutralization by administration of soluble ST2 receptor inhibited the enhanced allergic inflammation,while administration of recombinant IL-33 during challenge phase enhanced allergic inflammation in caspase-1-deficient mice.Therefore,we show that caspase-1,NLRP3,and ASC,but not NLRC4,contribute to the upregulation of allergic lung inflammation.Moreover,we cannot exclude an effect of caspase-11,because caspase-1-deficient mice are deficient for both caspases.Mechanistically,absence of caspase-1 is associated with increased expression of IL-33,uric acid,and spleen tyrosine kinase(Syk)production.This study highlights acritical role of caspase-1 activation andNLPR3/ASCinflammasomecomplex in the down-modulation of IL-33 in vivo and in vitro,thereby regulating Th2 response in HDM-induced allergic lung inflammation.

关键词： house dust mite allergic asthma caspase-1 inﬂammasomes IL-33 spleen tyrosine kinase(Syk) uric acid

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