Fig. 1. TLR4 deficiency aggravated TDI-induced airway hyperreactivity and inflammation. (A) Airway hyperresponsiveness was measured by RL. Results are shown as percentage of baseline (n = 4). (B) Numbers of total inflammatory cell in BALF. (C) Numbers of neutrophils and eosinophils in BALF (n = 6). (D) Representative H&E-stained lung sections of different groups. Original magnification was 200×. (E) Semi-quantification of airway inflammation was performed (n = 4–6). (F) Semi-quantification of epithelial denudation was performed (n = 4–6). (G) Analysis of ASM thickness was performed (n = 4–6). (H) Levels of Th2-related cytokines IL-4, IL-5 and IL-13 in BALF (n = 4–6). (I) Levels of Th17-related cytokines IL-17A, IL-17F, IL-6, IL-18 and in BALF (n = 4–6). (J) Levels of neutrophil chemoattractant CSF-3, CXCL1 and eosinophil chemoattractant CCL11 in BALF (n = 4–6).
WT, wild-type; TLR4, toll-like receptor 4; TDI, toluene diisocyanate; RL, lung resistance; H&E, hematoxylin and eosin; BALF, bronchoalveolar lavage fluid; NS, not significant; IL, interleukin; Th, T helper; CCL11, C-C motif chemokine 11; CXCL1, chemokine (C-X-C motif) ligand 1; CSF-3, colony-stimulating factor 3; ASM, airway smooth muscle.
*P < 0.05; †P < 0.01; ‡P < 0.001.