Scientific Section: Transplantation POST-BMT LUNG INJURY OCCURS INDEPENDENTLY OF THE EXPRESSION OF CCL2 OR ITS RECEPTOR, CCR2, ON HOST CELLS

Idiopathic pneumonia syndrome (IPS) is a significant cause of morbidity and mortality post-BMT in humans. In our murine IPS model, lethal pre-BMT conditioning and allogeneic T cells result in the recruitment of host antigen-presenting cells (APC) into the lung by day 3 and then donor T cells by day 7 post-BMT concomitant with development of severe lung dysfunction. CCL2 induction was found in bronchoalveolar lavage fluid (BALF) of these recipients prior to host monocyte influx. The major receptor for CCL2 is CCR2 present on monocytes and this interaction has been shown to play a crucial role in monocyte recruitment in inflammation. To determine whether blockade of the CCL2/CCR2 recruitment pathway could hinder host monocyte influx, lethally conditioned wild type (WT), CCL2-/-or CCR2-/-recipients were transplanted with allogeneic marrow and spleen cells. WT and-/-recipients exhibited equivalent lung dysfunction early post-BMT. The frequencies of host macrophages as well as donor CD4 + and CD8 + T cells in the lungs post-BMT did not differ between WT and-/-recipients. However, the T cell-dependency of the host CD11b