Microbiome modulates intestinal homeostasis against inflammatory diseases

被引:31
作者
Sun, Xiaolun [1 ]
Jia, Zhenquan [2 ]
机构
[1] Univ Arkansas, Ctr Excellence Poultry Sci, Fayetteville, AR 72701 USA
[2] Univ N Carolina, Dept Biol, Greensboro, NC 27402 USA
关键词
Intestinal microbiome; Animal; Intestinal diseases; Inflammation; Metabolites; ARYL-HYDROCARBON RECEPTOR; REGULATORY T-CELLS; INNATE LYMPHOID-CELLS; CHAIN FATTY-ACIDS; ANTIBIOTIC-RESISTANCE CRISIS; GROWTH-FACTOR-BETA; BILE-ACID; GUT MICROBIOTA; CLOSTRIDIUM-DIFFICILE; FECAL MICROBIOTA;
D O I
10.1016/j.vetimm.2018.10.014
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Eliminating prophylactic antibiotics in food animal production has exerted pressure on discovering antimicrobial alternatives (e.g. microbiome) to reduce elevated intestinal diseases. Intestinal tract is a complex ecosystem coupling host cells with microbiota. The microbiota and its metabolic activities and products are collectively called microbiome. Intestinal homeostasis is reached through dynamic and delicate crosstalk between host immunity and microbiome. However, this balance can be occasionally broken, which results in intestinal inflammatory diseases such as human Inflammatory Bowel Diseases, chicken necrotic enteritis, and swine post weaning diarrhea. In this review, we introduce the intestinal immune system, intestinal microbiome, and microbiome modulation of inflammation against intestinal diseases. The purpose of this review is to provide updated knowledge on host-microbe interaction and to promote using microbiome as new antimicrobial strategies to reduce intestinal diseases.
引用
收藏
页码:97 / 105
页数:9
相关论文
共 174 条
[11]   The immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) is caused by mutations of FOXP3 [J].
Bennett, CL ;
Christie, J ;
Ramsdell, F ;
Brunkow, ME ;
Ferguson, PJ ;
Whitesell, L ;
Kelly, TE ;
Saulsbury, FT ;
Chance, PF ;
Ochs, HD .
NATURE GENETICS, 2001, 27 (01) :20-21
[12]   TLR-signaling Networks: An Integration of Adaptor Molecules, Kinases, and Cross-talk [J].
Brown, J. ;
Wang, H. ;
Hajishengallis, G. N. ;
Martin, M. .
JOURNAL OF DENTAL RESEARCH, 2011, 90 (04) :417-427
[13]   Cellular plasticity of CD4+T cells in the intestine [J].
Brucklacher-Waldert, Verena ;
Carr, Edward J. ;
Linterman, Michelle A. ;
Veldhoen, Marc .
FRONTIERS IN IMMUNOLOGY, 2014, 5
[14]   Precision microbiome reconstitution restores bile acid mediated resistance to Clostridium difficile [J].
Buffie, Charlie G. ;
Bucci, Vanni ;
Stein, Richard R. ;
McKenney, Peter T. ;
Ling, Lilan ;
Gobourne, Asia ;
No, Daniel ;
Liu, Hui ;
Kinnebrew, Melissa ;
Viale, Agnes ;
Littmann, Eric ;
van den Brink, Marcel R. M. ;
Jenq, Robert R. ;
Taur, Ying ;
Sander, Chris ;
Cross, Justin R. ;
Toussaint, Nora C. ;
Xavier, Joao B. ;
Pamer, Eric G. .
NATURE, 2015, 517 (7533) :205-U207
[15]   Use of natural AhR ligands as potential therapeutic modalities against inflammatory disorders [J].
Busbee, Philip B. ;
Rouse, Michael ;
Nagarkatti, Mitzi ;
Nagarkatti, Prakash S. .
NUTRITION REVIEWS, 2013, 71 (06) :353-369
[16]   Microbiota-Mediated Inflammation and Antimicrobial Defense in the Intestine [J].
Caballero, Silvia ;
Pamer, Eric G. .
ANNUAL REVIEW OF IMMUNOLOGY VOL 33, 2015, 33 :227-256
[17]   Unraveling intestinal stem cell behavior with models of crypt dynamics [J].
Carulli, Alexis J. ;
Samuelson, Linda C. ;
Schnell, Santiago .
INTEGRATIVE BIOLOGY, 2014, 6 (03) :243-257
[18]   The European ban on growth-promoting antibiotics and emerging consequences for human and animal health [J].
Casewell, M ;
Friis, C ;
Marco, E ;
McMullin, P ;
Phillips, I .
JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, 2003, 52 (02) :159-161
[19]   Autoinflammatory granulomatous diseases: from Blau syndrome and early-onset sarcoidosis to NOD2-mediated disease and Crohn's disease [J].
Caso, Francesco ;
Galozzi, Paola ;
Costa, Luisa ;
Sfriso, Paolo ;
Cantarini, Luca ;
Punzi, Leonardo .
RMD OPEN, 2015, 1 (01)
[20]  
CDC, 2018, NEWL REP GEN MCR 1 T