Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice

Abstract

It has been demonstrated that endogenous cytokines including Q interferon (IFN-Q), tumour necrosis factor-K (TNF-K), 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-K 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-K notably detected in the circulation in lethal infection were different from those in nonlethal infection. The maximum production of IFN-Q was observed before the peaks of TNF-K and IL-6, and IFN-Q almost disappeared from the bloodstreams and organs just before the mice died. No notable difference of IFN-Q 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-K and IL-6 during lethal infection, while IL-4 was never detected in the sera. The administration of monoclonal antibodies (mAbs) against TNF-K, IFN-Q, IL-6, IL-4 or IL-10 failed to rescue mice from lethal L. monocytogenes infection, whereas anti-TNF-K mAb and anti-IFN-Q 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. z

The adaptor ASC exacerbates lethal Listeria monocytogenes infection by mediating IL‐18 production in an inflammasome‐dependent and ‐independent manner

“…4D). A similar result has previously been shown with the same antibody at higher doses [28]. Therefore, it appears that the detrimental effect of IL-18 on host defense is not due to promotion of IFN-γ production.…”

Tumor Necrosis Factor-α, Interleukins-12(p40), 6, and 10 levels in cerebrospinal fluid and outcome prediction in Ossimi sheep with encephalitic listeriosis

“…It has been proved that IL-10 enhance the immunity during primary and secondary L. monocytogenes infection by up-regulating proinflammatory type 1 cytokine responses [36]. In mice, IL-10 was also detected in the bloodstreams earlier than the peaks of TNF-alpha and IL-6 during lethal infection [8]. However, in addition, in vitro stimulation of both IL-10-deficient peritoneal exudate cells and spleen cells with heat-killed Listeria resulted in a dramatically enhanced proinflammatory cytokine response [36].…”

“…TNF-a is essential for both control and survival of systemic listeriosis [8]. TNF is rapidly produced after systemic infection with L. monocytogenes by cells of the innate immune system including macrophages, granulocytes, and dendritic cells [9].…”

Comparison of Host Resistance to Primary and SecondaryListeria monocytogenesInfections in Mice by Intranasal and Intravenous Routes

“…TNF-␣ and IFN-␥ were determined by double sandwich enzyme linked immunosorbent assays (ELISAs) as described previously (22). Purified hamster anti-mouse TNF-␣ monoclonal antibody (Genzyme Co., Boston, Mass.)…”