Endogenous cytokines during a lethal infection withListeria monocytogenesin mice

Publisher Website
Google Scholar
Abstract
It has been demonstrated that endogenous cytokines including γ interferon (IFN-γ), tumour necrosis factor-α (TNF-α), and interleukin-6 (IL-6) play protective roles but that IL-4 and IL-10 play detrimental roles in nonlethal Listeria monocytogenes infection in mice. In this paper, we studied the roles of endogenous cytokines in a lethal infection with L. monocytogenes in mice. TNF-α and IL-6 titres in the bloodstreams, spleens and livers paralleled bacterial numbers in the organs, and both these cytokines and the bacterial numbers peaked just before the mice died. The high titres of TNF-α notably detected in the circulation in lethal infection were different from those in nonlethal infection. The maximum production of IFN-γ was observed before the peaks of TNF-α and IL-6, and IFN-γ almost disappeared from the bloodstreams and organs just before the mice died. No notable difference of IFN-γ titres between lethal infection and nonlethal infection in the specimens obtained from mice was observed. IL-10 was also detected in the bloodstreams earlier than the peaks of TNF-α and IL-6 during lethal infection, while IL-4 was never detected in the sera. The administration of monoclonal antibodies (mAbs) against TNF-α, IFN-γ, IL-6, IL-4 or IL-10 failed to rescue mice from lethal L. monocytogenes infection, whereas anti-TNF-α mAb and anti-IFN-γ mAb prevented mice from lethality by high-dose endotoxin shock. These results suggest that lethality in L. monocytogenes infection might not be determined solely by these cytokines.