Abstract
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)-α 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-α (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-α and MIP-2 were similar in both groups.ConclusionNeutrophils may regulate TNF-α 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-α or MIP-2 produced in the lung.
Highlights
Neutrophil infiltration commonly occurs in acute lung injury and may be partly responsible for the inflammatory response
The first objective of this study is to determine if tumor necrosis factor (TNF)-α, IL-1β and macrophage inflammatory protein (MIP)-2 concentrations will be lower in the systemic circulation of neutropenic, endotoxemic rats compared to non-neutropenic, endotoxemic rats
Previous studies have shown that the early response to endotoxin would be an elevation in TNF-α and IL-1β followed by a rise in MIP-2 production [23,24]
Summary
Neutrophil infiltration commonly occurs in acute lung injury and may be partly responsible for the inflammatory response. 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. Improvements in the treatment of cancer have led to a growing population of immunocompromised patients with longer survival times and a propensity to develop sepsis and acute respiratory distress syndrome (ARDS) [1,2]. Neutropenia is commonly induced by cyclophosphamide in cancer-stricken patients. In these patients, white cells are markedly diminished in number but not absent. It is known that cyclophosphamide has effects on other cells (page number not for citation purposes)
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