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Journal of Endotoxin Research
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Evidence for the requirement for CD40—CD154 interactions in resistance to infections with attenuated Salmonella

Maria J. Fernandez-Cabezudo

Department of Biochemistry, UAE University, Al Ain, United Arab Emirates

Azim Ullah

Department of Medical Microbiology, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates

Richard A. Flavell

Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA

Basel K. al-Ramadi

Department of Medical Microbiology, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates, ramadi.b{at}uaeu.ac.ae

Salmonella species include facultative intracellular pathogens which reside preferentially within cells of the host's reticulo-endothelial system. Resistance to Salmonella involves a collaboration between cells of the innate and adaptive immune systems, and protective immunity requires cell-mediated and humoral-immune responses. CD40—CD154 interactions are of central importance in the induction of cellular immune responses. In the present study, CD154-deficient (CD154—/—) mice were used to assess the role of CD40—CD154 interactions in immunity to Salmonella infection. Compared to C57BL/6 (CD154+/+) controls, CD154 —/—mice were hypersusceptible to infection by an attenuated strain of Salmonella enterica serovar Typhimurium (S. typhimurium), as evidenced by a significantly decreased survival rate. CD154—/— mice exhibited a defect in the production of IFN-{gamma} and NO in the acute phase of the disease, which resulted in a failure to control bacterial replication. We conclude that intercellular communications via the CD40—CD154 pathway play a critical role in the induction type-1 cytokine responses and protection against primary infections with attenuated Salmonella.

Key Words: Bacterial • co-stimulation • Th1/Th2 cells • cytokines • vaccination

Journal of Endotoxin Research, Vol. 11, No. 6, 395-399 (2005)
DOI: 10.1177/09680519050110060401
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