Oral immunization with the B subunit of the heat-labile enterotoxin of Escherichia coli induces early Th1 and late Th2 cytokine expression in Peyer’s

The B subunit of heat-labile toxin (LT-B) from enterotoxigenic Escherichia coli has been shown to be a powerful mucosal immunogen. Oral immunization of mice with LT-B revealed that BALBI c (H-2d) and C57BLl6 (H-2b) mice gave high serum IgG and mucosal IgA responsesspecificfor LT-B. However, ALY (H_2b) mice lacking intestinal Peyer's patches (PP) did not respond to oral LT-B with either serum or mucosal antibodies. These results indicate that PP lymphocytes supported both systemic and mucosal immune responses when the antigen was administered orally. Reverse transcription polymerasechain reaction analyses revealed that PP CD4 T cellsexpressed early Thl-type (interferon-y and interleukin [IL]-2) and late Th2-type (IL-4,-5, and-6) cytokine mRNA. These results suggest that the systemic and mucosal antibody responses induced by LT-B are regulated by a cooperation of PP Thl and Th2 cells. Heat-labile toxin (LT) of enterotoxigenic strains of Esche-richia coli is a major cause of severe, cramping diarrhea known as traveler's diarrhea [1]. LT is a heterohexameric protein that consists of two structurally and functionally distinct compo-nents (A and B subunits), and its structure and function ar