| First Author | Ko HJ | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 4 | Pages | 2305-12 |
| PubMed ID | 19201885 | Mgi Jnum | J:144786 |
| Mgi Id | MGI:3831944 | Doi | 10.4049/jimmunol.0801980 |
| Citation | Ko HJ, et al. (2009) Innate immunity mediated by MyD88 signal is not essential for induction of lipopolysaccharide-specific B cell responses but is indispensable for protection against Salmonella enterica serovar Typhimurium infection. J Immunol 182(4):2305-12 |
| abstractText | 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. |
