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Physiology Program, Harvard School of Public Health, Boston, MA 02115
The early response cytokines, TNF and IL-1, have overlapping
biologic effects that may function to propagate, amplify, and
coordinate host responses to microbial challenges. To determine whether
signaling from these early response cytokines is essential to
orchestrating innate immune responses to intrapulmonary bacteria, the
early inflammatory events induced by instillation of Escherichia
coli into the lungs were compared in wild-type (WT) mice and
mice deficient in both TNF receptor 1 (TNFR1) and the type I IL-1
receptor (IL1R1). Neutrophil emigration and edema accumulation induced
by E. coli were significantly compromised by TNFR1/IL1R1
deficiency. Neutrophil numbers in the circulation and within alveolar
septae did not differ between WT and TNFR1/IL1R1 mice, suggesting that
decreased neutrophil emigration did not result from decreased
sequestration or delivery of intravascular neutrophils. The nuclear
translocation of NF-
B and the expression of the chemokine macrophage
inflammatory protein-2 did not differ between WT and TNFR1/IL1R1 lungs.
However, the concentration of the chemokine KC was significantly
decreased in the bronchoalveolar lavage fluids of TNFR1/IL1R1 mice
compared with that in WT mice. Thus, while many of the molecular and
cellular responses to E. coli in the lungs did not
require signaling by either TNFR1 or IL1R1, early response cytokine
signaling was critical to KC expression in the pulmonary air spaces and
neutrophil emigration from the alveolar septae.
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