Mesenteric lymph duct ligation attenuates lung injury and neutrophil activation after intraperitoneal injection of endotoxin in rats

Background: The release of injurious factors into the mesenteric lymph from the ischemic intestine has been shown to contribute to lung injury and systemic inflammation after shock and trauma. Since endotoxemia is also associated with gut injury, we tested the hypothesis that mesenteric lymph contributes to the lung injury seen in endotoxemia and that the ligation of the mesenteric lymph duct will attenuate this injury. Methods: To test this hypothesis, male Sprague-Dawley rats were given intraperitoneal injections (i.p.) of lipopolysaccharide (LPS) (10 mg/kg) with or without mesenteric lymph duct ligation (LDL). At 6 hours after injection of LPS, gut and lung injury, lung permeability, and neutrophil CD11b expression were measured. Lung permeability was quantified by calculating the percentage of Evan's Blue dye and the total protein concentration in the bronchoalveolar lavage fluid (BALF) when compared with the plasma and gut and lung injury were assessed morphologically. Results: LDL attenuated LPS-induced lung injury, lung permeability, and rat PMN CD11b expression but not villous injury. The magnitude of lung permeability as measured by Evan's Blue was approximately twofold greater in the LPS rats when compared with the LPS-treated rats with LDL. The expression of CD11b was greater in the LPS rats when compared with LPS rats with LDL or to sham controls (582 +/- 106 vs. 364 +/- 29 vs. 224 +/- 12 mean fluorescence intensity p < 0.001). C onclusion: Based on the attenuation of lung injury and CD11b expression, these results suggest that LPS-induced lung injury and neutrophil activation is partially mediated through the release of factors from the injured gut into mesenteric lymph.