CX3CR1+ macrophages support IL-22 production by innate lymphoid cells during infection with Citrobacter rodentium

被引:103
作者
Manta, C. [1 ]
Heupel, E. [2 ]
Radulovic, K. [1 ]
Rossini, V. [1 ]
Garbi, N. [3 ,4 ]
Riedel, C. U. [2 ]
Niess, J. H. [1 ]
机构
[1] Univ Ulm, Dept Internal Med 1, Ulm, Germany
[2] Univ Ulm, Inst Microbiol & Biotechnol, Ulm, Germany
[3] Inst Mol Med, Dept Mol Immunol, Bonn, Germany
[4] Inst Expt Immunol IMMEI, Bonn, Germany
关键词
INFLAMMATORY-BOWEL-DISEASE; DENDRITIC CELLS; HOST-DEFENSE; INTESTINAL HOMEOSTASIS; FLUORESCENT PROTEIN; CROHNS-DISEASE; FRACTALKINE; IMMUNITY; EXPRESSION; RESPONSES;
D O I
10.1038/mi.2012.61
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Innate immune cells, such as intestinal epithelial cells, dendritic cells (DCs), macrophages, granulocytes, and innate lymphoid cells provide a first line of defence to enteric pathogens. To study the role of CX(3)CR1(+) DCs and macrophages in host defence, we infected CX(3)CR1-GFP animals with Citrobacter rodentium. When transgenic CX(3)CR1-GFP animals are infected with the natural mouse pathogen C. rodentium, CX(3)CR1(-/-) animals showed a delayed clearance of C. rodentium as compared with (age- and sex-matched) wild-type B6 animals. The delayed clearance of C. rodentium is associated with reduced interleukin (IL)-22 expression. In C. rodentium-infected CX(3)CR1-GFP animals, IL-22 producing lymphoid-tissue inducer cells (LTi cells) were selectively reduced in the absence of CX(3)CR1. The reduced IL-22 expression correlates with decreased expression of the antimicrobial peptides RegIII beta and RegIII gamma The depletion of CX(3)CR1(+) cells by diphtheria toxin injection in CX(3)CR1-GFPxCD11c.DOG animals confirmed the role of CX(3)CR1(+) phagocytes in establishing IL-22 production, supporting the clearance of a C. rodentium infection.
引用
收藏
页码:177 / 188
页数:12
相关论文
共 44 条
[1]   Salmonella Induces Flagellin- and MyD88-Dependent Migration of Bacteria-Capturing Dendritic Cells Into the Gut Lumen [J].
Arques, Juan L. ;
Hautefort, Isabelle ;
Ivory, Kamal ;
Bertelli, Eugenio ;
Regoli, Mari ;
Clare, Simon ;
Hinton, Jay C. D. ;
Nicoletti, Claudio .
GASTROENTEROLOGY, 2009, 137 (02) :579-587
[2]   IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia [J].
Aujla, Shean J. ;
Chan, Yvonne R. ;
Zheng, Mingquan ;
Fei, Mingjian ;
Askew, David J. ;
Pociask, Derek A. ;
Reinhart, Todd A. ;
McAllister, Florencia ;
Edeal, Jennifer ;
Gaus, Kristi ;
Husain, Shahid ;
Kreindler, James L. ;
Dubin, Patricia J. ;
Pilewski, Joseph M. ;
Myerburg, Mike M. ;
Mason, Carol A. ;
Iwakura, Yoichiro ;
Kolls, Jay K. .
NATURE MEDICINE, 2008, 14 (03) :275-281
[3]   Utility of the Citrobacter rodentium infection model in laboratory mice [J].
Borenshtein, Diana ;
McBee, Megan E. ;
Schauer, David B. .
CURRENT OPINION IN GASTROENTEROLOGY, 2008, 24 (01) :32-37
[4]   IL-22 is increased in active Crohn's disease and promotes proinflammatory gene expression and intestinal epithelial cell migration [J].
Brand, S ;
Beigel, F ;
Olszak, T ;
Zitzmann, K ;
Eichhorst, ST ;
Otte, JM ;
Diepolder, H ;
Marquardt, A ;
Jagla, W ;
Popp, A ;
Leclair, S ;
Herrmann, K ;
Seiderer, J ;
Ochsenkühn, T ;
Göke, B ;
Auernhammer, CJ ;
Dambacher, J .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2006, 290 (04) :G827-G838
[5]   Increased expression of the chemokine fractalkine in Crohn's disease and association of the fractalkine receptor T280M polymorphism with a fibrostenosing disease phenotype [J].
Brand, S ;
Hofbauer, K ;
Dambacher, J ;
Schnitzler, F ;
Staudinger, T ;
Pfennig, S ;
Seiderer, J ;
Tillack, C ;
Konrad, A ;
Göke, B ;
Ochsenkühn, T ;
Lohse, P .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2006, 101 (01) :99-106
[6]   Fractalkine-mediated signals regulate cell-survival and immune-modulatory responses in intestinal epithelial cells [J].
Brand, S ;
Sakaguchi, T ;
Gu, XB ;
Colgan, SP ;
Reinecker, HC .
GASTROENTEROLOGY, 2002, 122 (01) :166-177
[7]   A human natural killer cell subset provides an innate source of IL-22 for mucosal immunity [J].
Cella, Marina ;
Fuchs, Anja ;
Vermi, William ;
Facchetti, Fabio ;
Otero, Karel ;
Lennerz, Jochen K. M. ;
Doherty, Jason M. ;
Mills, Jason C. ;
Colonna, Marco .
NATURE, 2009, 457 (7230) :722-725
[8]   Vasoactive intestinal peptide ameliorates intestinal barrier disruption associated with Citrobacter rodentium-induced colitis [J].
Conlin, V. S. ;
Wu, X. ;
Nguyen, C. ;
Dai, C. ;
Vallance, B. A. ;
Buchan, A. M. J. ;
Boyer, L. ;
Jacobson, K. .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2009, 297 (04) :G735-G750
[9]   EspJ is a prophage-carried type III effector protein of attaching and effacing pathogens that modulates infection dynamics [J].
Dahan, S ;
Wiles, S ;
La Ragione, RM ;
Best, A ;
Woodward, MJ ;
Stevens, MP ;
Shaw, RK ;
Chong, YW ;
Knutton, S ;
Phillips, A ;
Frankel, G .
INFECTION AND IMMUNITY, 2005, 73 (02) :679-686
[10]   Animal models of inflammatory bowel disease - Lessons from enteric infections [J].
Eckmann, Lars .
INFLAMMATORY BOWEL DISEASE: GENETICS, BARRIER FUNCTION, IMMUNOLOGIC MECHANISMS, AND MICROBIAL PATHWAYS, 2006, 1072 :28-38