• Hulya Babayigit, Can Kucuk, Erdogan Sozuer, Cevad Yazici, Kader Kose, and Hulya Akgun.
• Department of General Surgery, School of Medicine, Erciyes University, 38039 Kayseri, Turkey.
• Intensive Care Med. 2005 Jun 1; 31 (6): 865-70.

ObjectiveUnderstanding the biological mediators involved in the complex inflammatory response of sepsis and acute lung injury offers the possibility of future investigations targeting treatment based on these mediators. This study investigated whether macrophage activator beta-glucan has a protective effect on acute lung injury in an experimental model of sepsis.Design And SettingExperimental study in an experimental research center.Materials30 rats randomized into three groups (sham, sepsis, and beta-glucan).InterventionsCecal ligation and puncture were performed in the beta-glucan and sepsis groups. The beta-glucan group was given a single intraperitoneal dose of beta-glucan (4 mg/kg) following cecal ligation.Measurements And ResultsRats treated with beta-glucan had fewer circulating neutrophils, more blood monocytes, and higher serum interleukin 6 levels than septic animals. The percentages of neutrophils and lymphocytes from the bronchoalveolar lavage fluid and the myeloperoxidase activity measured in the lung tissue were lower in the beta-glucan group than in the sepsis group. Less alveolar hemorrhage and neutrophil infiltration were observed in lungs from animals in the beta-glucan group in the septic groups.ConclusionsIn this rat model of intra-abdominal sepsis beta-glucan treatment partially protected against secondary lung injury, decreased lung hemorrhages, and lung neutrophilia. These results suggest that beta-glucan protects against sepsis-associated lung damage.

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