Lung contusion (LC) and hemorrhagic shock (HS) result in early organ failure (lung and bone marrow [BM]), possibly through sequestration of mobilized BM hematopoietic progenitor cells (HPC) into the lung. Postinjury mesenteric lymph has been shown to cause early organ failure. Thus, we hypothesized that diversion of mesenteric lymph would improve early organ dysfunction through decreased mobilization of BM HPC to the lung. Rats were subjected to unilateral LC +/- lymph duct ligation (LDL). Additional groups underwent HS (mean arterial pressure of 35 mm Hg for 90 minutes) with and without LC +/- LDL. Controls were only cannulated. At 3 hours, both lungs and BM were harvested for growth of HPC (BFU-E, CFU-E, and CFU-GEMM). Additional rats were killed on day 14 and the lungs examined by histology. LC alone decreased BM HPC in all cell types and increased their number in the injured lung (all *p < 0.05 vs. control). Shock exacerbated these results and resulted in a further increase in BM cells in the injured lung and a decrease in BM HPC growth. LDL reversed the response to LC alone. In rats subjected to LC and HS, LDL restored BM HPC growth to levels observed after LC alone and decreased HPC recovered in the contused lung 50% compared with that in shocked rats without LDL. At day 14, all rats subjected to LC demonstrated healing of their injury. In contrast, all LC + LDL rats had evidence of pneumonia, thickened alveoli, and increased numbers of inflammatory cells. Diversion of the postinjury mesenteric lymph decreased early BM suppression after LC or LC with HS. However, this improved BM function occurred at the expense of impaired lung healing and an increased susceptibility to pulmonary infection. As mobilized BM cells differentiate into pneumocytes, these data indicate that mobilization of BM cells to the site of injury is an adaptive and necessary response for successful wound healing and tissue repair.