关键词: allergic rhinitis benzo[α]pyrene mucus nasal mucosa remodeling

来  源:   DOI:10.1177/00034894241275449

Abstract:
UNASSIGNED: Exposure to benzo[α]pyrene (BaP) increases the incidence and severity of allergic rhinitis (AR), but the underlying mechanisms remain unclear. Thus, we investigated the in vivo effects of BaP exposure on mucus hypersecretion and tissue remodeling in a rat model of AR.
UNASSIGNED: Female Sprague-Dawley rats were randomly divided into 4 groups: a negative control group, a group of healthy rats exposed to BaP, a group of rats with ovalbumin (OVA)-induced AR, and a group of AR model rats exposed to BaP. Nasal symptoms and levels of OVA-specific serum immunoglobulin E (IgE) were measured in each individual rat. Moreover, examination of goblet cell hyperplasia and collagen deposition was carried out with periodic acid-Schiff (PAS) staining and Masson trichrome (MT) staining. Mucin 5AC (MUC5AC) expression was assessed by immunohistochemistry.
UNASSIGNED: BaP significantly increased the number of sneezes, the number of nasal rubs and the levels of OVA-specific serum IgE in rats with AR. Statistically significant differences in goblet cell hyperplasia and collagen deposition were observed between the BaP-exposed AR model group and the AR model group. Immunohistochemical results showed that the nasal mucosa of AR model rats displayed markedly elevated MUC5AC expression after BaP exposure.
UNASSIGNED: Our data indicate that mucus hypersecretion and the development of nasal remodeling might be pathophysiologic mechanisms underlying increased susceptibility to AR after exposure to BaP.
摘要:
暴露于苯并[α]芘(BaP)会增加过敏性鼻炎(AR)的发生率和严重程度,但潜在的机制仍不清楚。因此,我们在AR大鼠模型中研究了BaP暴露对粘液高分泌和组织重塑的体内影响。
雌性Sprague-Dawley大鼠随机分为4组:阴性对照组,一组暴露于BaP的健康大鼠,一组卵清蛋白(OVA)诱导的AR大鼠,和一组暴露于BaP的AR模型大鼠。在每只大鼠中测量鼻部症状和OVA特异性血清免疫球蛋白E(IgE)的水平。此外,用高碘酸希夫(PAS)染色和马森三色(MT)染色检查杯状细胞增生和胶原蛋白沉积。通过免疫组织化学评估粘蛋白5AC(MUC5AC)表达。
BaP显著增加了打喷嚏的次数,AR大鼠的鼻擦次数和OVA特异性血清IgE水平。BaP暴露AR模型组与AR模型组之间杯状细胞增生和胶原沉积差异有统计学意义。免疫组织化学结果显示,BaP暴露后,AR模型大鼠鼻黏膜MUC5AC表达明显升高。
我们的数据表明,粘液分泌过多和鼻重塑的发展可能是暴露于BaP后对AR易感性增加的病理生理机制。
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