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* Mucosal Immunology Section, Laboratory Science Division, International Vaccine Institute, Seoul, Korea; and
Center for Infectious Diseases and Vaccinology, The Biodesign Institute, Arizona State University, Tempe, AZ 85287
Salmonella organisms are Gram negative and facultative anaerobic bacteria that cause typhoid fever in humans. In this study, we evaluated LPS-specific adaptive immunity in innate immune-deficient mice after oral administration of attenuated Salmonella enterica serovar Typhimurium (S. Typhimurium) strains. Of interest, identical levels of LPS-specific IgG and IgA Abs were elicited in the systemic (i.e., serum and spleen) and mucosal (i.e., fecal extract and small intestine) compartments of wild-type, TLR4–/–, and MyD88–/– mice following oral vaccination with recombinant attenuated S. Typhimurium (RASV). Depletion of CD4+ T cells during RASV vaccination completely abrogated the generation of LPS-specific Abs in MyD88–/– mice. In addition, mRNA expression levels of a B cell-activating factor of the TNF family were significantly increased in the spleens of MyD88–/– mice after oral administration, implying that T cell-independent B cell switching might be also enhanced in the MyD88 signal-deficient condition. Of most interest, orally vaccinated MyD88–/– mice that possessed high levels of LPS-specific IgG and IgA, which had a neutralizing effect against Salmonella, died earlier than nonvaccinated wild-type mice following lethal oral challenge with virulent Salmonella species. These results suggest that innate immunity mediated by MyD88 signal is dispensable for induction of LPS-specific Ab responses following oral administration of attenuated Salmonella strains but indispensable for efficient protection.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by The Bill & Melinda Gates Foundation (Grant 37863), National Institutes of Health Grant R01-AI056289, and a Korea Science and Engineering Foundation grant funded by the Korean government (Grants 2007-04213 and R01-2008-000-10649-0).
2 H.-J.K. and J.-Y.Y. contributed equally to this work.
3 Address correspondence and reprint requests to Dr. Mi-Na Kweon, Mucosal Immunology Section, International Vaccine Institute, Seoul National University Research Park, Kwanak-Gu, Seoul, Korea 151-818. E-mail address: mnkweon{at}ivi.int
4 Abbreviations used in this paper: SIgA, secretory IgA; RASV, recombinant attenuated S. enterica serovar Typhimurium vaccine; BAFF, a B cell-activating factor of the TNF family; pIgR, polymeric Ig receptor; PP, Peyer’s patches; DC, dendritic cell; ASC, Ab-secreting cell; MLN, mesenteric lymph node; WT, wild type; SI-LP, lamina propria of the small intestine.
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