Plcβ and Rac1 deficiency leads to reduced chemokine arrest and protects from LPS-induced lung injury. (A-B) WT mice transplanted with WT, Plcb2^−/−, Plcb3^−/−, Gnai2^−/−, and Rac1^−/− bone marrow cells were used to determine chemokine-induced arrest in the cremaster muscle. Arrested cells were counted after injection of 500 ng (A) CXCL1 or (B) LTB₄ over 15 minutes. (C) Chemokine-induced arrest of Plcb2^−/− mice pretreated with dimethylsulfoxide (DMSO) or with PLC inhibitor U73122. Arrested cells were determined before and after injection of 500 ng CXCL1 (n = 3). *P < .05. (D) WT, Plcb2^−/−, Plcb3^−/−, or Rac1^−/− mice were exposed to nebulized NaCl or LPS; 24 hours later, mice were euthanized and the bronchoalveolar fluid was collected and analyzed for neutrophil recruitment (n = 4). *P < .05 vs all other groups. (E) Representative images of hematoxylin and eosin (H&E)–stained formalin-fixed paraffin-embedded lung sections (slices 5 µm thick) from WT and Rac1^−/− mice, which were exposed to nebulized saline or LPS. Images were acquired by using a Zeiss LSM510 (×20 magnification).