FIGURE 1.

Histological and biochemical evidence from patients for pathologic involvement of endocannabinoid/CB₁R and iNOS systems in HPSPF. Masson trichrome staining sections from HPSPF patients and controls without fibrotic lung disease (A). CB₁R and iNOS immunohistochemistry from the same subjects (B). AEA (C) and 2‐AG (D) levels in BALF from normal volunteers (NV), HPS‐1 patients without fibrosis, patients with HPSPF and HPS‐3 patients. Pulmonary function tests (PFTs) in the same groups (E). Abbreviations: DLCO, diffusion capacity; FVC, forced vital capacity; TLC, total lung capacity. Correlation between PFTs and AEA in BALF in NV, HPS‐1, and HPSPF (F). NV: empty black symbol, HPS1: blue symbol, HPSPF: red filled symbol, HPS3: empty yellow symbol. Correlation was calculated by using Pearson correlation coefficients. Data represent mean ± SEM from five subjects for histology in each group, and 16 NV, 6 HPS‐1, 10 HPSPF, and 3 HPS‐3 subjects for BALF and PFTs. Data were analyzed by t‐test for comparison of histological scoring and by one‐way ANOVA followed by Dunnett's multiple comparisons test for endocannabinoids and PFT. * (p < 0.05) indicates significant difference from the NV group