期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 165, 期 6, 页码 2187-2196出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)63268-3
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- NIGMS NIH HHS [R01 GM029507, GM-029507, R37 GM029507] Funding Source: Medline
Blood neutrophils (PMN) are usually unresponsive to CC chemokines such as monacyte chemotactic protein-1 and macrophage inflammatory protein-la. In rodents, the lung buildup of PMN as determined by myeloperoxidase (MPO) activity after airway instillation of bacterial lipopolysaccharide (LPS) was independent of MCP-1 and MIP-1alpha. In striking contrast, during sepsis following cecal ligation and puncture (CLP), blood PAIN demonstrated mRNA for CC chemokine receptors. Furthermore, PMN from CLP, but not from sham rodents, bound MCP-1 and MIP-1alpha and responded chemotactically in vitro to both MCP-1 and MIP-1alpha. In CCR2(-/-) mice or WT mice treated in vivo with antibodies to either MCP-1 or MIP-1alpha, MPO activity was greatly attenuated in CLP animals. In CLP mice, increased serum IL-6 levels were found to be dependent on CCR2, MCP-1, and MIP-1alpha. When PMN from CLP rodents were incubated in vitro with either MCP-1 or MIP-1alpha, release of IL-6 was also shown. These findings suggest that sepsis fundamentally alters the trafficking of PMN into the lung in a manner that now engages functional responses to CC chemokines.
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