- Author:
Hirokazu KINOSHITA
1
;
Jun ABE
;
Kenji AKADEGAWA
;
Hideaki YURINO
;
Tetsuya UCHIDA
;
Shigaku IKEDA
;
Kouji MATSUSHIMA
;
Sho ISHIKAWA
Author Information
- Publication Type:Journal Article
- Keywords: IgA; TCDD; allergy; mucosal immunity; oral tolerance
- From:Environmental Health and Preventive Medicine 2006;11(5):256-263
- CountryJapan
- Language:English
-
Abstract:
OBJECTIVESMucosal immunity plays a pivotal role for body defense against infection and allergy. The aim of this study was to clarify the effects of 2,3,7,8-tetraclorodibenzo-p-dioxin (TCDD) on mucosal immunity in the gut.
METHODSFecal IgA level and oral tolerance induction were examined in TCDD-treated mice. Flow cytometric and histological analyses were also performed.
RESULTSSingle oral administration of low dose 2,3,7,8-TCDD resulted in a marked decrease in IgA secretion in the gut without any effects on the cellular components of gut-associated lymphoid tissues (GALT) including Peyer's patches (PPs) and mesenteric lymph nodes (LNs). Decressed IgA secretion by TCDD was not observed in aryl hydrocarbon receptor (AhR)-deficient mice. Flow cytometric analysis revealed that IgA B cells in PPs and the mesenteric LNs remained unchanged in the TCDD-treated mice. An immunofluorescence study also demonstrated that a significant number of cytoplasmic IgA cells were present in the lamina propria of the gut in the TCDD-treated mice. Furthermore, oral tolerance induction by ovalbumin (OVA) was impaired in the TCDD-treated mice and OVA-specific T cell proliferation occurred in the peripheral lymphoid tissues including the spleen and LNs.
CONCLUSIONSThese results suggest that a relatively low dose of TCDD impairs mucosal immunity in the gut and induces systemic sensitization by oral antigens.