Oral administration of bovine colostrum stimulates intestinal intraepithelial lymphocytes to polarize Th1-type in mice

2005 ◽  
Vol 5 (3) ◽  
pp. 581-590 ◽  
Author(s):  
Yasuko Yoshioka ◽  
Satsuki Kudo ◽  
Hitoshi Nishimura ◽  
Toshiki Yajima ◽  
Kenji Kishihara ◽  
...  
2003 ◽  
Vol 16 (2) ◽  
pp. 151-156 ◽  
Author(s):  
M.E. Roux ◽  
M.G. Marquez ◽  
S. Olmos ◽  
C.A. Frecha ◽  
A. Florin-Christensen

Compartmentalisation of mucosal immune response seems to be the result mainly of the preferential migration of activated cells back to their inductive sites. The aim of this report was to demonstrate, in a model of secondary immunodeficiency in Wistar rats (severely protein deprived at weaning and refed with casein 20 %; group R21), that the oral administration of Thymomodulin (group: R21TmB) has different effects on gut and BALT (Bronchus-associated lymphoid tissue). Tissue sections (5μ) were studied by immunohistochemistry 1). The oral administration of Thymomodulin restores only in gut Lamina propria (LP) the IgA B and CD4 T cell populations to control levels. The CD8a and CD25 subpopulations do not vary in gut as they return to control levels when refed with 20% casein diet. All the populations mentioned above remained decreased even after receiving Thymomodulin by the oral route. However, the same behaviour was observed for the TCRδ T cells that were decreased and return to normal levels in both mucosae by the effect of the immunomodulator; 2) when studying the iIEL (intestinal intraepithelial lymphocytes) CD8α, CD25 and TCRγδ T cells, that were increased in R21, return to control levels in R21TmB. In BALT intraepithelium CD8α and CD25 T cells remained decreased, while only TCRγδ T cells (increased in R21) return to control values. Conclusions: 1) there exists a compartmentalisation between both mucosae, as T CD4+ and IgA B+ cells are restored by TmB only in gut; 2) only those iIEL involved in inflammation (CD8α+/CD25+ and TCRγδ+/CD25+) are normalised by means of the Thymomodulin 3) however, in BALT, only TCRγδ+ T cells are restored 4) the oral administration of the present immunomodulator may be useful as a therapeutic agent, although the preferential survival in the tissue of initial stimulation is the major factor in the preferential distribution of activated cells.


1992 ◽  
Vol 22 (1) ◽  
pp. 159-164 ◽  
Author(s):  
Hiroaki Takimoto ◽  
Takao Nakamura ◽  
Makoto Takeuchi ◽  
Yukiko Sumi ◽  
Toshiyuki Tanaka ◽  
...  

2000 ◽  
Vol 24 (8) ◽  
pp. 783-795 ◽  
Author(s):  
Michael D Eisenbraun ◽  
R.Lee Mosley ◽  
Daniel H Teitelbaum ◽  
Richard A Miller

Nature ◽  
1989 ◽  
Vol 339 (6227) ◽  
pp. 712-714 ◽  
Author(s):  
Yohtaroh Takagaki ◽  
Amy DeCloux ◽  
Marc Bonneville ◽  
Susumu Tonegawa

2006 ◽  
Vol 74 (9) ◽  
pp. 5292-5301 ◽  
Author(s):  
Kyoko Inagaki-Ohara ◽  
Fitriya Nurannisa Dewi ◽  
Hajime Hisaeda ◽  
Adrian L. Smith ◽  
Fumiko Jimi ◽  
...  

ABSTRACT Eimeria spp. are intracellular protozoa that infect intestinal epithelia of most vertebrates, causing coccidiosis. Intestinal intraepithelial lymphocytes (IEL) that reside at the basolateral site of epithelial cells (EC) have immunoregulatory and immunoprotective roles against Eimeria spp. infection. However, it remains unknown how IEL are involved in the regulation of epithelial barrier during Eimeria sp. infection. Here, we demonstrated two distinct roles of IEL against infection with Eimeria vermiformis, a murine pathogen: production of cytokines to induce protective immunity and expression of junctional molecules to preserve epithelial barrier. The number of IEL markedly increased when oocyst production reached a peak. During infection, IEL increased production of gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) and decreased transforming growth factor β (TGF-β) production. Addition of IFN-γ and TNF-α or supernatants obtained from cultured IEL from E. vermiformis-infected mice reduced transepithelial electrical resistance (TER) in a confluent CMT93 cell monolayer, a murine intestine-derived epithelial line, but antibodies against these cytokines suppressed the decline of TER. Moreover, TGF-β attenuated the damage of epithelial monolayer and changes in TER caused by IFN-γ and TNF-α. The expression of junctional molecules by EC was decreased when IEL produced a high level of IFN-γ and TNF-α and a low level of TGF-β in E. vermiformis-infected mice. Interestingly, IEL constantly expressed junctional molecules and a coculture of EC with IEL increased TER. These results suggest that IEL play important multifunctional roles not only in protection of the epithelium against E. vermiformis-induced change by cytokine production but also in direct interaction with the epithelial barrier when intra-EC junctions are down-regulated.


1991 ◽  
Vol 10 (3-4) ◽  
pp. 302-305 ◽  
Author(s):  
Sabine Sarnacki ◽  
Bernadette Bègue ◽  
Anne Jarry ◽  
Nadine Cerf-Bensussan

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