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. Author manuscript; available in PMC: 2010 Aug 9.
Published in final edited form as: Shock. 2009 Apr;31(4):376–381. doi: 10.1097/SHK.0b013e3181862279

Figure 3. Neutrophil recruitment to the lung after pulmonary contusion is dependent on the TLR4 pathway.

Figure 3

Figure 3

Figure 3

(A) The BAL from WT (closed) and TLR4 and MyD88 deficient (gray, KO) injured lungs were analyzed for neutrophil infiltration. Compared to uninjured (n=5), a significant increase in PMN in the BAL from WT mice is observed (**p≤.001) that is significantly decreased in KO mice (*p≤.001, n=6/genotype). (B) Lung homogenates from uninjured (open), WT (closed) and TLR4 and MyD88 deficient (gray) injured lungs were analyzed by immunoblot for neutrophil elastase (n=4). A significant increase in elastase in WT lung extracts is observed (**p≤.001) that is significantly decreased in KO mice (*p≤.01). (C) Immunostaining for neutrophil elastase in lungs from WT, and TLR4 or MyD88 deficient animals (100× magnification). Specimens are representative of immunohistochemistry for least 3 animals/genotype. Data shown are obtained at 24 hours after injury.