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The tumor necrosis factor receptor family molecule 4-1BB (CD137) has diverse roles in adaptive and innate immune responses. However, little is known of its role in bacterial infections. Previously, we showed that 4-1BB-deficient mice have enhanced susceptibility toListeria monocytogenes infection, and mice pretreated with agonistic anti-4-1BB antibody (3E1) were much more resistant toL. monocytogenes infection than mice treated with control antibody. In this study, we report that stimulating 4-1BB by administering 3E1 in the early phase ofL. monocytogenes infection is critical for promoting the survival of mice by inducing rapid infiltration of neutrophils and monocytes intoL. monocytogenes -infected livers. The levels of tumor necrosis factor alpha, interleukin 6, and monocyte chemoattractant protein 1 in the livers of 3E1-treated mice increased as early as 30 min postinfection and peaked by 1 to 2 h, while those in mice treated with control antibody started to increase only at 16 h postinfection. Monocytes and neutrophils from the 3E1-treated mice had higher levels of activation markers, phagocytic activity, and reactive oxygen species than those from control mice. In vitro stimulation of 4-1BB induced the production of the inflammatory cytokines/chemokines of neutrophils, but not those of monocytes. These results suggest that 4-1BB stimulation of neutrophils in the early phase ofL. monocytogenes infection causes rapid production of inflammatory cytokines/chemokines and that the subsequent infiltration of neutrophils and monocytes is crucial for eliminating the infectingL. monocytogenes .

infection and immunity

Stimulation of the Molecule 4-1BB Enhances Host Defense against<i>Listeria monocytogenes</i>Infection in Mice by Inducing Rapid Infiltration and Activation of Neutrophils and Monocytes

Stimulation of the Molecule 4-1BB Enhances Host Defense againstListeria monocytogenesInfection in Mice by Inducing Rapid Infiltration and Activation of Neutrophils and Monocytes