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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Immunology
2016 ; 148
(3
): 304-14
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Transient activation of mucosal effector immune responses by resident intestinal
bacteria in normal hosts is regulated by interleukin-10 signalling
#MMPMID27147411
Wu C
; Sartor RB
; Huang K
; Tonkonogy SL
Immunology
2016[Jul]; 148
(3
): 304-14
PMID27147411
show ga
Interleukin-10 (IL-10) is a key regulator of mucosal homeostasis. In the current
study we investigated the early events after monoassociating germ-free (GF)
wild-type (WT) mice with an Escherichia coli strain that we isolated previously
from the caecal contents of a normal mouse housed under specific pathogen-free
conditions. Our results show that interferon-? (IFN-?) secreted by mesenteric
lymph node (MLN) cells from both IL-10 deficient mice and WT mice, stimulated
ex vivo with E. coli lysate, was dramatically higher at day 4 after
monoassociation compared with IFN-? secreted by cells from GF mice without
E. coli colonization. Production of IFN-? rapidly and progressively declined
after colonization of WT but not IL-10-deficient mice. The E. coli
lysate-stimulated WT MLN cells also produced IL-10 that peaked at day 4 and
subsequently declined, but not as precipitously as IFN-?. WT cells that express
CD4, CD8 and NKp46 produced IFN-?; WT CD4-positive cells and B cells produced
IL-10. Recombinant IL-10 added to E. coli-stimulated MLN cell cultures inhibited
IFN-? secretion in a dose-dependent fashion. MLN cells from WT mice treated
in vivo with neutralizing anti-IL-10 receptor antibody produced more IFN-?
compared with MLN cells from isotype control antibody-treated mice. These
findings show that a resident E. coli that induces chronic colitis in
monoassociated IL-10-deficient mice rapidly but transiently activates the
effector immune system in normal hosts, in parallel with induction of protective
IL-10 produced by B cells and CD4(+) cells that subsequently suppresses this
response to mediate mucosal homeostasis.