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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

(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.

(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.