Fig 1.
Experimental procedure for establishing the OVA-induced asthma model.
(A) Low-dose-rate chronic irradiation equipment at Dongnam Institute of Radiological and Medical Sciences. (B) Schematic diagram of irradiation and experimental procedures.
Fig 2.
Inflammatory cell count of the bronchoalveolar lavage fluid (BALF) decreases after irradiation in OVA-sensitized/challenged mice.
(A) Representative pictures of Diff-quick staining of cytospin preparation. Changes in the number of eosinophils (B), macrophages (C), neutrophils (D), lymphocytes (E), and total cells (F) in the BALF of mice. The data are reported as means ± SE (n = 6 per group). *p < 0.05 vs. OVA-sensitized/challenged mice.
Fig 3.
Methylcholine responsiveness (PenH value) is decreased by irradiation in OVA-sensitized/challenged mice.
The methylcholine responsiveness was indirectly assessed 24 h after the last challenge using single-chamber, whole body plethysmography (Allmedicus, Seoul, Korea). Continuous exposure to low-dose-rate radiation reduced methylcholine responsiveness compared with that of the OVA-sensitized/challenged mice. The data are reported as means ± SE (n = 6 per group). *p < 0.05 vs. OVA-sensitized/challenged mice.
Fig 4.
IL-4 and IL-5 levels decreased in the BALF and OVA-specific IgE in the serum from OVA-sensitized/challenged mice after irradiation.
The OVA-sensitized/challenged mice showed significant increases in these cytokines. Continuous exposure to low-dose-rate radiation significantly reduced these cytokines compared with that in the OVA-sensitized/challenged mice. The data are reported as means ± SE (n = 6 per group). *p < 0.05 vs. OVA-sensitized/challenged mice.
Fig 5.
Airway inflammation was attenuated by irradiation in the lung tissue from OVA-sensitized/challenged mice.
(A) Histological examination of the airway inflammation (black arrow) stained with H&E (magnification ×200), (B) quantitative analysis for airway inflammation. Continuous exposure to low-dose-rate radiation reduced the airway inflammation in the lung tissue. The data are reported as means ± SE (n = 6 per group). *p < 0.05 vs. OVA-sensitized/challenged mice.
Fig 6.
Mucus production decreased following irradiation in the lung tissue from OVA-sensitized/challenged mice.
(A) Histological examination of mucus production (black arrow) in the lung tissue stained with PAS (magnification ×200), (B) western blot for Mucin-5, and (C) relative ratio vs. β-actin. Continuous exposure to low-dose-rate radiation showed marked reduction of mucus production and expression of Mucin-5 in the lung tissue. The data are reported as means ± SE (n = 6 per group). *p < 0.05 vs. OVA-sensitized/challenged mice.
Fig 7.
MMP-9 expression in the lung tissue from OVA-sensitized/challenged mice.
(A) Immunohistochemical examination of MMP-9 in the lung tissue, (B) western blot for MMP-9, and (C) relative ratio vs. β-actin. The OVA-sensitized/challenged mice exhibited a significant increase in MMP-9 activity and expression in the lung tissue. Continuous exposure to low-dose-rate radiation markedly reduced MMP-9 activity and expression in the lung tissue. The data are reported as means ± SE (n = 6 per group). *p < 0.05 vs. OVA-sensitized/challenged mice.
Fig 8.
ERK and JNK phosphorylation in the lung tissue from OVA-sensitized/challenged mice.
(A) Western blot for ERK and JNK, (B) phosphorylation of ERK (relative ratio vs. β-actin), and (C) phosphorylation of JNK (relative ratio vs. β-actin). The OVA-sensitized/challenged mice exhibited a significant increase in phosphorylation of ERK and JNK in the lung tissue. Continuous exposure to low-dose-rate radiation markedly reduced phosphorylation of ERK and JNK in the lung tissue. The data are reported as means ± SE (n = 6 per group). *p < 0.05 vs. OVA-sensitized/challenged mice.