Early Response Cytokines and Innate Immunity: Essential Roles for TNF Receptor 1 and Type I IL-1 Receptor During Escherichia coli Pneumonia in Mice

摘要: The early response cytokines, TNF and IL-1, have overlapping biologic effects that may function to propagate, amplify, coordinate host responses microbial challenges. To determine whether signaling from these cytokines is essential orchestrating innate immune intrapulmonary bacteria, the inflammatory events induced by instillation of Escherichia coli into lungs were compared in wild-type (WT) mice deficient both receptor 1 (TNFR1) type I IL-1 (IL1R1). Neutrophil emigration edema accumulation E. significantly compromised TNFR1/IL1R1 deficiency. numbers circulation within alveolar septae did not differ between WT mice, suggesting decreased neutrophil result sequestration or delivery intravascular neutrophils. nuclear translocation NF-κB expression chemokine macrophage protein-2 lungs. However, concentration KC was bronchoalveolar lavage fluids with mice. Thus, while many molecular cellular require either TNFR1 IL1R1, cytokine critical pulmonary air spaces septae.