Lee Se-Jin, Pak So-Won, Kim Woong-Il, Park Sin-Hyang, Cho Young-Kwon, Kim Tae-Won, Ko Je-Won, Kim Joong-Sun, Kim Jong-Choon, Kim In-Hyeon, Kim Sung-Hwan, Shin In-Sik
College of Veterinary Medicine and BK21 FOUR Program, Chonnam National University, 77 Yong-bong-ro, Buk-gu, Gwangju, 61186, Republic of Korea.
College of Health Sciences, Cheongju University, 298 Daesung-ro, Sangdang-gu, Cheongju-si, Chungbuk, 28503, Republic of Korea.
Lab Anim Res. 2025 May 9;41(1):13. doi: 10.1186/s42826-025-00243-9.
Asian sand dust (ASD), generated from the deserts of China and Mongolia, mainly affects the human health of several countries in Northeast Asia including China, Korea, and Japan. In this study, we investigated the toxic effects of ASD on respiratory tract and explored the effects of ASD exposure on allergic asthma using ovalbumin-induced asthma model. C57BL/6 male mice were used for both the toxicity and allergic asthma studies. ASD (10, 20, and 40 mg/kg) was administered intranasally on days 1, 3, and 5. For allergic asthma, mice were sensitized with OVA (20 µg/mouse) and aluminum hydroxide (2 mg) on days 1 and 15, followed by OVA inhalation (1%, w/v) on days 22, 24, and 26, with subsequent ASD instillation on days 21, 23, and 25.
ASD exposure showed the elevation of respiratory inflammation including inflammatory cell infiltration, cytokine production, and mucus secretion with the increase in phosphorylated (p)-nuclear factor-kappa B (NF-κB) p65 expression. In addition, ASD exposure to asthma model significantly increased airway responsiveness, inflammatory cell count and mucus secretion with the elevation of cytokines and immunoglobulin E, which were accompanied with the increases in p-NF-κB p65, p-p38 and cyclooxygenase 2 (COX2).
Therefore, ASD exposure induces respiratory inflammation and aggravates the progression of allergic asthma, which was closely associated with the phosphorylation of NF-κB. Respiratory exposure to ASD causes inflammation, upregulation of cytokines, p-NF-κB, and COX2, which can exacerbate asthma.
源自中国和蒙古沙漠的亚洲沙尘（ASD）主要影响包括中国、韩国和日本在内的东北亚几个国家的人类健康。在本研究中，我们调查了ASD对呼吸道的毒性作用，并使用卵清蛋白诱导的哮喘模型探索了ASD暴露对过敏性哮喘的影响。C57BL/6雄性小鼠用于毒性和过敏性哮喘研究。在第1、3和5天经鼻给予ASD（10、20和40mg/kg）。对于过敏性哮喘，在第1天和第15天用OVA（20μg/只小鼠）和氢氧化铝（2mg）使小鼠致敏，随后在第22、24和26天吸入OVA（1%，w/v），并在第21、23和25天随后滴注ASD。
ASD暴露显示呼吸道炎症升高，包括炎症细胞浸润、细胞因子产生和黏液分泌增加，同时磷酸化（p）-核因子-κB（NF-κB）p65表达增加。此外，ASD暴露于哮喘模型显著增加气道反应性、炎症细胞计数和黏液分泌，同时细胞因子和免疫球蛋白E升高，这伴随着p-NF-κB p65、p-p38和环氧化酶2（COX2）的增加。
因此，ASD暴露诱导呼吸道炎症并加重过敏性哮喘的进展，这与NF-κB的磷酸化密切相关。呼吸道暴露于ASD会导致炎症、细胞因子、p-NF-κB和COX2上调，从而加重哮喘。
