JCI - Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice

Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice

Min-Jong Kang, Chun Geun Lee, Jae-Young Lee, Charles S. Dela Cruz, Zhijian J. Chen, Richard Enelow, Jack A. Elias

Published in Volume 118, Issue 8

J Clin Invest. 2008; 118(8):2771–2784 doi:10.1172/JCI32709

Abstract | Full text | PDF | Supplemental material

Options: View larger image (or click on image)

Figure 9

Effects of CS and poly(I:C) on cellular apoptosis.

Mice were exposed to CS or RA (CS–) for 2 weeks and then given 4 doses of poly(I:C) (50 μg) or vehicle control. The effects of these interventions on the percentage of alveolar structural cells that were TUNEL stained (+) can be seen in A. Double-label IHC was used to define the percentage of pro–SP-C–positive alveolar type II cells, CD31-positive endothelial cells, and CCSP-positive airway epithelial cells that were TUNEL stained, respectively (B). The effects of CS and poly(I:C) on caspase-3 activation, PARP accumulation and activation, and eIF2α accumulation and activation were also assessed (C). The role of MAVS was assessed by comparing the levels of TUNEL staining, phosphorylation of eIF2α, and caspase-3 activation in WT mice (+/+) and mice with null (–/–) mutations of MAVS (D and E). The roles of IL-18Rα, IFN-γ, and PKR were assessed by comparing these responses in WT mice (+/+) and mice with null (–/–) mutations of IL-18Rα, IFN-γ, or PKR (F and G). The data in each row in parts C, E, and G were generated from blots of individual gels that were run at the same time. Parts C, E, and G are representative of a minimum of 3 similar evaluations. The values in parts A, B, D, and F represent the mean ± SEM of evaluations in a minimum of 5 mice. *P < 0.05; **P < 0.01; ***P < 0.001.