Figure 5.

RelB overexpression reduces cigarette smoke–induced proinflammatory cytokine production in mouse lungs. Mice received either the control or RelB virus (two doses of 5 × 10⁸ plaque-forming units per mouse delivered 24 hours apart) and either air or smoke (two 1-hour exposures per day for 3 days). Cytokine production was detected in the BAL fluids by either enzyme-linked immunosorbent assay (A–E) or cytokine multiplex assay (F–H). Cigarette smoke exposure significantly increased production of each cytokine, whereas RelB overexpression reduced the production of IL-6 (A), MIP-2 (B), KC (C), JE (D), TNF-α (E), granulocyte-macrophage colony-stimulating factor (F), LIX (G), IFN-γ (H), and IL-10 (I). Only MIP-2 (B) and LIX (G) did not achieve statistical significance. Basal production of JE was also significantly reduced on RelB overexpression (D). *P < 0.05, **P < 0.01, and ***P < 0.001 (two-way analysis of variance with a Bonferroni posttest; n = 5 to 6 per group).