Fig. 6.
Mast cell (MC)-specific deficiency of calcium voltage-gated channel subunit alpha1 C (CaV1.2) ameliorates the antigen induced pulmonary inflammation (AIPI). (A) Construction strategy and verification of conditional knockout (CKO) mice. (B) Bone marrow MCs (BMMCs) were isolated from CaV1.2 CKO mice and wild type (WT) mice. The effect of CaV1.2 knockout on MCs activation (degranulation, upper left; Ca2+ influx, upper right; cytokines release (bottom). (C) Hematoxylin and eosin (H&E), Masson, and periodic acid-Schiff (PAS) stainings of lung sections of CaV1.2 CKO mice and CaV1.2fl/fl mice (used as WT) in AIPI (left) and negative control (NC, right). (D) Airway hyperreaction (AHR) of CKO mice and WT mice in AIPI (left) and NC (right) groups. (E) The numbers of eosinophils, neutrophils, and total cells as well as T helper 2 (Th2) cytokines release in bronchoalveolar lavage fluid (BALF) in CKO and WT mice in AIPI (left) and NC (right) groups. Experiments were repeated three times. Data are presented as the mean ± standard error of mean (SEM) and were analyzed using one-way analysis of variance (ANOVA) test. ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001, compared between experiment and CKO or WT groups; #P < 0.05 and ###P < 0.001, compared between experiment and WT groups. F1: forward primer 1; R1: reversed primer 1; IoxP: locus of X (cross)-overinP1; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; TNF-α: tumor necrosis factor; CCL-2: C–C motif chemokine ligand 2; Ach: acetylcholine; Rn: Newtonian resistance; Rrs: respiratory resistance; G: resistance of the peripheral lung; Cst: static compliance; IL: interleukin.