• Sabrina M Heidemann and Maria Glibetic.
• Department of Pediatric Critical Care Medicine and Clinical Pharmacology, Wayne State University, Detroit, MI, USA. sheidema@med.wayne.edu
• J Inflamm Lond. 2007 Jan 1; 4: 7.

BackgroundNeutrophil infiltration commonly occurs in acute lung injury and may be partly responsible for the inflammatory response. However, acute lung injury still occurs in the neutropenic host. The objectives of this study are to determine if inflammation and acute lung injury are worse in neutropenic versus the normal host after endotoxemia.MethodsRats were divided into four groups: 1) control, 2) neutropenic, 3) endotoxemic and 4) endotoxemic and neutropenic. Tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MIP-2) were measured in the blood, lung lavage and for mRNA in the lung. Arterial blood gases were measured to determine the alveolar-arterial oxygen gradient which reflects on lung injury.ResultsIn endotoxemia, the neutropenic rats had lower plasma TNF-alpha (116 +/- 73 vs. 202 +/- 31 pg/ml) and higher plasma MIP-2 (26.8 + 11.9 vs. 15.6 + 6.9 ng/ml) when compared to non-neutropenic rats. The endotoxemic, neutropenic rats had worse lung injury than the endotoxemic, non-neutropenic rats as shown by increase in the alveolar-arterial oxygen gradient (24 +/- 5 vs. 12 +/- 9 torr). However, lavage concentrations of TNF-alpha and MIP-2 were similar in both groups.ConclusionNeutrophils may regulate TNF-alpha and MIP-2 production in endotoxemia. The elevation in plasma MIP-2 in the endotoxemic, neutropenic rat may be secondary to the lack of a neutrophil response to inhibit production or release of MIP-2. In endotoxemia, the severe lung injury observed in neutropenic rats does not depend on TNF-alpha or MIP-2 produced in the lung.

10 keywords...

hide…