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. Author manuscript; available in PMC: 2013 Aug 15.
Published in final edited form as: J Immunol. 2012 Jun 29;189(4):2006–2016. doi: 10.4049/jimmunol.1201065

Figure 5. Nlrp1b−/− mice are protected from lethal toxin-induced lung injury.

Figure 5

129 +/+ (black) and Nlrp1b −/− (white) mice were treated with 20 μg LT i.t. BAL fluid was collected at 0 h, 2 h, 6 h, 16 h, and 24 h after treatment. MIP-2 (A), KC (B), IL-1β (C), and CXCL15/lungkine (D) in the BAL fluid were detected by ELISA. (E) Western blot of HMGB1 protein in concentrated BAL fluid; GAPDH was used as a loading control, 20μg of protein per line. Results shown are representative of 3 independent experiments. (F) The total number of inflammatory cells in BAL fluid. (G) Cell death in BAL fluid assessed by LDH activity. (H) Vascular permeability evaluated as a concentration of albumin in the BAL fluid, measured by colorimetric assay. (I) Myeloperoxidase (MPO) level in BAL cell pellet collected from 129+/+ and Nlrp1b−/− mice 48 and 72 h after LT treatment. (J–N) FACS analysis of whole lung cell suspension from 129+/+ (J, L) and Nlrp1b−/− mice 16 h post-LT treatment (K,M). CD 45+ cells were gated and analyzed for Mac-1 and GR-1 epitope (J, K) or Mac-1 and CCR-2 epitope (L, M). (J–M) representative from 3 independent experiment, quantitative analysis of CD45+Mac-1+CCR2+ cells (N). n=2 per genotype at 0h, n=5 per genotype at 2h, n=6 per genotype at 6h, n=3 per genotype at 16h, n=7 per genotype at 24–72 h. * p < 0.05, ** p < 0.01, *** p < 0.001.