Scholarlink

<p>Arsenic exposure poses a global health risk and is associated with numerous inflammatory diseases, such as asthma and skin lesions. C-C chemokine ligand 5 (CCL5) has been linked to the pathophysiology of asthma, dermatitis, and malignancies because of its role in migrating inflammatory cells to the site of inflammation. However, no research has been conducted on the relationship between arsenic exposure and CCL5 or CCL5’s role in arsenic-induced inflammatory disorders. Therefore, we designed this study to examine the association of arsenic exposure with serum CCL5 levels and its relations to allergic asthma and skin lesions. The participants (<i>n</i> = 461) were recruited from low- and high-arsenic exposure rural areas in Bangladesh. We found that the median of serum CCL5 levels of the participants in high-exposure areas was considerably (<i>p</i> &lt; 0.001) higher than that of the participants in low-exposure area. Serum CCL5 levels were increased dose-dependently with the increasing concentrations of arsenic in the participants’ drinking water, hair, and nails. Logistic regression analyses showed that serum CCL5 levels were significantly associated with the increased odds of airway obstruction, reversible airway obstruction, and asthma symptoms, the characteristic features of asthma. CCL5 levels were positively correlated with allergy-related type-2 mediators, such as IgE, IL-4, IL-5, IL-13, eotaxin, and periostin. In addition to the features of asthma, serum CCL5 levels were also associated with the progression of skin lesions. Taken together, these results suggest that elevated CCL5 may be implicated in the pathogenesis of allergic asthma and skin lesions in arsenic-exposed individuals through type-2-driven inflammatory immune responses.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Association between Arsenic Exposure and CCL5: its Implications in Asthma and Skin Lesions

  • 期刊论文

  • 发表日期：

    2025年12月9日

查看全文
  • Osman Goni,
  • Nesar Uddin,
  • Rajoana Karim Rimi,
  • Kamrun Nahar Rossi,
  • Faysal Abedin,
  • Sharmin Akter Beauty,
  • Sharon Jahan Sarder,
  • Junayed Sadi,
  • Mainul Islam,
  • Victor Mondal,
  • K M Ahsanul Kabir,
  • Abu Eabrahim Siddique,
  • Shakhawoat Hossain,
  • Md Ashraful Hoque,
  • Tetsuro Agusa,
  • Daigo Sumi,
  • Zahangir Alam Saud,
  • Seiichiro Himeno,
  • Khaled Hossain

摘要

Arsenic exposure poses a global health risk and is associated with numerous inflammatory diseases, such as asthma and skin lesions. C-C chemokine ligand 5 (CCL5) has been linked to the pathophysiology of asthma, dermatitis, and malignancies because of its role in migrating inflammatory cells to the site of inflammation. However, no research has been conducted on the relationship between arsenic exposure and CCL5 or CCL5’s role in arsenic-induced inflammatory disorders. Therefore, we designed this study to examine the association of arsenic exposure with serum CCL5 levels and its relations to allergic asthma and skin lesions. The participants (n = 461) were recruited from low- and high-arsenic exposure rural areas in Bangladesh. We found that the median of serum CCL5 levels of the participants in high-exposure areas was considerably (p < 0.001) higher than that of the participants in low-exposure area. Serum CCL5 levels were increased dose-dependently with the increasing concentrations of arsenic in the participants’ drinking water, hair, and nails. Logistic regression analyses showed that serum CCL5 levels were significantly associated with the increased odds of airway obstruction, reversible airway obstruction, and asthma symptoms, the characteristic features of asthma. CCL5 levels were positively correlated with allergy-related type-2 mediators, such as IgE, IL-4, IL-5, IL-13, eotaxin, and periostin. In addition to the features of asthma, serum CCL5 levels were also associated with the progression of skin lesions. Taken together, these results suggest that elevated CCL5 may be implicated in the pathogenesis of allergic asthma and skin lesions in arsenic-exposed individuals through type-2-driven inflammatory immune responses.