Abstract

The relationships between Listeria monocytogenes (LM) pathogenesis, based on bacterial load, and serum levels of IL-6, IFNγ, and corticosterone (CORT) were quantified. Serum IFNγ levels increased along with the LM burden; however, with LM burdens ≥3 × 106 CFU per spleen, the serum IFNγ level decreased along with a decrease in splenic weight. Serum IL-6 levels exponentially increased with increases of LM, and the CORT level positively correlated with the increase in IL-6 and LM. The serum level of IFNγ appeared to be a good biomarker of the host's ability to combat the infection only when the LM burden did not exceed a critical level (>3 × 106 CFU per spleen). Interestingly, the LM load at which the IFNγ level began to decline was near the dose at which the IL-6 concentration exponentially increased, suggesting a transition point shift from stress (assessed as CORT level) being immunoenhancing to becoming immunosuppressive. The IL-6:IFNγ ratio may be a good indicator of disease severity and/or the ability to cope with an infection.

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