Original article: general thoracicβ-chemokine function in experimental lung ischemia-reperfusion injury
Section snippets
Reagents
Polyclonal rabbit antibodies to rat MIP-1α, MCP-1, RANTES, and nonspecific IgG were purchased from Peprotech Industries (Rocky Hills, NJ). All other reagents were purchased from Sigma Chemical (St. Louis, MO) unless otherwise specified.
Animal model
Pathogen-free Long-Evans rats (Simonsen Labs, Gilroy, CA) weighing 280 to 320 g were used for all experiments. The University of Washington Animal Care Committee approved all experimental protocols. All animals received humane care in accordance with the Guide
Lung vascular permeability
The PI in animals undergoing thoracotomy alone (0.18 ± 0.02) was double that seen in unmanipulated, negative control lungs (0.09 ± 0.006). The increase in permeability seen with thoracotomy and ventilation was statistically significant (p < 0.04). The difference in permeability between thoracotomy-alone animals and those that underwent 90 minutes of ischemia without reperfusion (0.22 ± 0.005) was not statistically significant (p = 0.2). However, a significant increase in permeability was seen
Comment
MIP-1α is unique among the β-chemokines in that it is also chemotactic for neutrophils. Initial studies indicated that MIP-1α was a potent chemoattractant for both CD4 and CD8 lymphocytes [11]. Subsequently, other investigators demonstrated in vitro that MIP-1α was a potent macrophage chemoattractant and activator [12]. These activities of MIP-1α are currently being investigated in human trials, where a genetically engineered analogue of MIP-1α has demonstrated safety in clinically relevant
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