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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Microbiota-Dependent Sequelae of Acute Infection Compromise Tissue-Specific Immunity

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Author(s):
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da Fonseca, Denise Morais [1, 2, 3] ; Hand, Timothy W. [2, 3] ; Han, Seong-Ji [2, 3] ; Gerner, Michael Y. [4] ; Zaretsky, Arielle Glatman [2, 3] ; Byrd, Allyson L. [2, 3, 5, 6] ; Harrison, Oliver J. [2, 3] ; Ortiz, Alexandra M. [7, 8] ; Quinones, Mariam [9] ; Trinchieri, Giorgio [10] ; Brenchley, Jason M. [7, 8] ; Brodsky, Igor E. [11] ; Germain, Ronald N. [4] ; Randolph, Gwendalyn J. [12] ; Belkaid, Yasmine [2, 3]
Total Authors: 15
Affiliation:
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[1] Univ Sao Paulo, Ribeirao Preto Sch Med, Dept Biochem & Immunol, BR-14049900 Ribeirao Preto - Brazil
[2] NIAID, Mucosal Immunol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 - USA
[3] NIAID, Immun Barrier Sites Initiat, NIH, Bethesda, MD 20892 - USA
[4] NIAID, Lymphocyte Biol Sect, Lab Syst Biol, NIH, Bethesda, MD 20892 - USA
[5] NHGRI, Translat & Funct Genom Branch, NIH, Bethesda, MD 20892 - USA
[6] Boston Univ, Dept Bioinformat, Boston, MA 02215 - USA
[7] NIAID, Program Tissue Immun & Repair, NIH, Bethesda, MD 20892 - USA
[8] NIAID, Immunopathogenesis Sect, NIH, Bethesda, MD 20892 - USA
[9] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 - USA
[10] NCI, Canc & Inflammat Program, Ctr Canc Res, Bethesda, MD 20892 - USA
[11] Univ Penn, Sch Vet Med, Dept Pathobiol, Philadelphia, PA 19104 - USA
[12] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 - USA
Total Affiliations: 12
Document type: Journal article
Source: Cell; v. 163, n. 2, p. 354-366, OCT 8 2015.
Web of Science Citations: 98
Abstract

Infections have been proposed as initiating factors for inflammatory disorders; however, identifying associations between defined infectious agents and the initiation of chronic disease has remained elusive. Here, we report that a single acute infection can have dramatic and long-term consequences for tissue-specific immunity. Following clearance of Yersinia pseudotuberculosis, sustained inflammation and associated lymphatic leakage in the mesenteric adipose tissue deviates migratory dendritic cells to the adipose compartment, thereby preventing their accumulation in the mesenteric lymph node. As a consequence, canonical mucosal immune functions, including tolerance and protective immunity, are persistently compromised. Post-resolution of infection, signals derived from the microbiota maintain inflammatory mesentery remodeling and consequently, transient ablation of the microbiota restores mucosal immunity. Our results indicate that persistent disruption of communication between tissues and the immune system following clearance of an acute infection represents an inflection point beyond which tissue homeostasis and immunity is compromised for the long-term. (AU)

FAPESP's process: 12/14669-7 - Dendritic cells and pattern recognition receptors in the activation and plasticity of T lymphocytes subpopulations during intestinal mucosal inflammation
Grantee:Denise Morais da Fonseca
Support type: Scholarships abroad - Research Internship - Post-doctor