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mRNA in Gut-Associated Lymphoid Tissue Following Oral Cholera Toxin in Mice1
,
,
Departments of
*
Microbiology and Immunology and
Pharmacology, and
Center for Substance Abuse Research, Temple University School of Medicine, and
Department of Biology, University of Pennsylvania, Philadelphia, PA 19104
In this study, we investigated the effect of morphine on the
mucosal immune system using fragment cultures of ileal segments,
Peyer’s patches (PPs), and mesenteric lymph nodes. Mice were implanted
s.c. with a morphine slow release pellet. Control groups received a
naltrexone slow release pellet, a placebo pellet, or both a morphine
and a naltrexone pellet. After 48 h, mice were orally immunized
with cholera toxin (CT) and were boosted orally 1 wk later. Animals
were sacrificed 1 wk after the booster immunization, and PPs,
mesenteric lymph nodes, and ileal segments were cultured in 24-well
plates for 12 days. Morphine resulted in a highly significant
inhibition of CT-specific IgA and IgG production in fragment culture
supernatants of all three tissues compared with placebo. Naltrexone
blocked the reduction in Ab levels induced by morphine, indicating that
the effect is opioid receptor mediated. Morphine did not significantly
alter total IgA levels in any of the tissue culture supernatants.
Morphine also inhibited CT-specific IgA and IgG levels in serum. By
flow cytometry, morphine did not alter the lymphoid cell composition in
PPs compared with placebo. The effect of morphine on TGF-
, IL-5, and
IL-6 mRNA expression in PPs and ileal segments was determined following
oral immunization with CT. Morphine significantly decreased TGF-
mRNA compared with that in the placebo group, and naltrexone blocked
this effect. These results indicate that morphine inhibits Ag-specific
IgA responses in gut-associated lymphoid tissue at least partially
through the inhibition of TGF-, a putative IgA switch factor, in the
gastrointestinal tract.
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 H. Friedman, C. Newton, and T. W. Klein Microbial Infections, Immunomodulation, and Drugs of Abuse Clin. Microbiol. Rev., April 1, 2003; 16(2): 209 - 219. [Abstract] [Full Text] [PDF]
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