The Expression of Semaphorin3E in Vagal Ganglion and Lung Tissue Is Related to Airway Hyperresponsiveness in Murine Asthma Model

Figure 1

Sema3E ameliorated the airway hyperresponsiveness, collagen deposition and mucus production in AS model. (a) Protocol outline. Mice were sensitized intraperitoneally with 10 µg OVA (or NS as control) on Days 0, 7, and 14. On Days 21–23, mice were challenged i.n. with 200 µg OVA (or NS as control), mice were exposed intranasally to Sema3E 1 hr before challenge in AS + Sema3E group. (b) Lung resistance in response to inhaled methacholine 24 hr after the last OVA challenge. (c) The total inflammatory cell counts in the BALF of mice for all groups. (d) Representative lung sections stained with hematoxylin and eosin (HE), periodic acid–Schiff (PAS), and Masson staining. (e) Differential cell counts in BALF. (f) Scoring of leukocyte infiltration in HE-stained lung tissue sections. (g) Quantification of collagen deposition. (h) Quantification of mucus-producing goblet cells. Data in (b)–(h) were expressed as mean ± standard deviation (n = 5). Compared with the NS group, : ; : , : , compared with AS group, ^#: , ^##: , ^###: . HE staining: magnification = ×100, scale bar = 100 µm, PAS and Masson staining: magnification = ×200, scale bar = 100 µm. (NS: nasal saline group, AS: asthma group, EB: eosinophilic bronchitis group, DXM: dexamethasone group, Sema3E: Semaphorin3E, OVA: ovalbumin, MCh: methacholine, Eos: eosinophil, Neu: Neutrophil, Mac: macrophage, and Lym: lymphocyte).

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