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1 Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA; Alcohol Research Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA
2 Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA; Department of Medicine - Section of Pulmonary Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA; Alcohol Research Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA
3 Department of Medicine - Section of Pulmonary Critical Care Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA; Alcohol Research Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA
4 Department of Medicine, Tulane University School of Medicine and the VA Medical Center, New Orleans, Louisiana, USA
* To whom correspondence should be addressed. E-mail: gbagby{at}lsuhsc.edu.
The CXC chemokines cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) are potent neutrophil chemoattractants in rats. We have previously shown that CINC, unlike MIP-2 and most other proinflammatory cytokines, is elevated in the systemic circulation in response to an intratracheal (i.t.) challenge. Therefore, we hypothesized that CINC generated within the lung selectively enters the vascular compartment in order to facilitate pulmonary neutrophil recruitment. Rats were administered i.t. LPS, and plasma CINC and MIP-2 levels were measured 90 minutes and 4h after injection, along with mRNA expression in lung, spleen, liver, and kidney. Ninety minutes and 4h after i.t. LPS, CINC and MIP-2 mRNA expression were largely confined to lung homogenate, but of the two chemokines, only CINC was present in plasma. In separate experiments, rats received i.t. injections of recombinant (r) CINC and/or MIP-2. Here, plasma levels of CINC, but not MIP-2, were significantly increased throughout the 4h observation period. This finding was verified by individually administering 125I-labelled forms of each chemokine. Instillation of recombinant MIP-2 or CINC into the lung increased the number of neutrophils recovered in BALF at 4h, and this effect was enhanced when both chemokines were administered together. In addition, i.v. CINC, but not i.v. MIP-2, increased pulmonary neutrophil recruitment in response to i.t. MIP-2. Our results show that CINC, in contrast to MIP-2, is selectively transported from the lung to the systemic circulation, where it promotes neutrophil migration into the lung in response to a chemotactic stimulus.
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