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Sepsis is one of the most important risk factors in acute respiratory distress syndrome (ARDS). β-Glucan is a potent reticuloendothelial modulating agent, the immunobiological activity of which is mediated in part by an increase in the number and function of macrophages. In this study, we investigated the putative protective role of β-glucan against sepsis-induced lung injury. Sepsis was induced by cecal ligation and puncture (CLP) in Wistar rats. The control group received saline, and the treatment groups received β-glucan or β-glucan + β-1,3-D-glucanase. Five hours thereafter, plasma tumor necrosis factor (TNF) α, interleukin (IL) 1β, and IL-6 levels were determined. Presence of lung injury was determined via lung tissue myeloperoxidase (MPO) activity, intercellular adhesion molecule (ICAM) 1 levels, and histopathological examination at 18 h after CLP. In a separate set of experiments, survival was monitored for 7 days after CLP. β-Glucan treatment led to a significant increase in survival rate (63% in glucan-treated rats vs 38% in saline-treated rats). Administration of the β-glucan inhibitor abrogated β-glucan's survival benefit (50%). After CLP, plasma TNF-α, IL-1β, and IL-6 concentrations were increased in control animals. When β-glucan was administered, it completely blocked the elevation of TNF-α, IL-1β, and IL-6. Administration of β-1,3-D-glucanase suppressed glucan-induced decrease in cytokines. Animals treated with β-glucan showed a significant reduction in lung injury score, a marked decrease in ICAM-1 expression, and a significant decrease in MPO levels. In contrast, β-1,3-D-glucanase caused a significantly increased MPO and ICAM-1 levels in the lung. These data reveal that β-glucan treatment improved the course of CLP-induced peritonitis and attenuated the lung injury. Administration of β-glucanase inhibited the β-glucan activity and resulted in enhanced lung injury.