Amphiregulin in infectious diseases: Role, mechanism, and potential therapeutic targets

doi:10.1016/j.micpath.2023.106463

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Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/34839

標題:	Amphiregulin in infectious diseases: Role, mechanism, and potential therapeutic targets
作者:	Hsu, Chou-Yi Mutee, Ahmed Faisal Porras, Sandra Pineda, Indira Mustafa, Mohammed Ahmed Saadh, Mohamed J. Adil, Mohaned Zainab, H. A.
貢獻者:	Chia Nan Univ Pharm & Sci, Dept Pharm Al Noor Univ Coll, Dept Pharm Escuela Super Politecn Chimborazo ESPOCH, Fac Mecan Escuela Super Politecn Chimborazo ESPOCH, Fac Salud Publ Imam Jaafar AL Sadiq Univ, Dept Med Lab Technol Univ Samarra, Coll Appl Sci, Dept Pathol Anal Middle East Univ, Fac Pharm Appl Sci Private Univ, Appl Sci Res Ctr Al Farahidi Univ, Pharm Coll Al Zahrawi Univ Coll, Dept Pharm
關鍵字:	AREG EGFR Treg Homeostasis Viral infection Bacterial infection Helminth infection
日期:	2024
上傳時間:	2024-12-25 11:04:20 (UTC+8)
出版者:	ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
摘要:	Amphiregulin (AREG) serves as a ligand for the epidermal growth factor receptor (EGFR) and is involved in vital biological functions, including inflammatory responses, tissue regeneration, and immune system function. Upon interaction with the EGFR, AREG initiates a series of signaling cascades necessary for several physiological activities, such as metabolism, cell cycle regulation, and cellular proliferation. Recent findings have provided evidence for the substantial role of AREG in maintaining the equilibrium of homeostasis in damaged tissues and preserving epithelial cell structure in the context of viral infections affecting the lungs. The development of resistance to influenza virus infection depends on the presence of type 1 cytokine responses. Following the eradication of the pathogen, the lungs are subsequently colonized by several cell types that are linked with type 2 immune responses. These cells contribute to the process of repairing and resolving the tissue injury and inflammation caused by infections. Following influenza infection, the activation of AREG promotes the regeneration of bronchial epithelial cells, enhancing the tissue's structural integrity and increasing the survival rate of infected mice. In the same manner, mice afflicted with influenza experience rapid mortality due to a subsequent bacterial infection in the pulmonary region when both bacterial and viral infections manifest concurrently inside the same host. The involvement of AREG in bacterial infections has been demonstrated. The gene AREG experiences increased transcriptional activity inside host cells in response to bacterial infections caused by pathogens such as Escherichia coli and Neisseria gonorrhea. In addition, AREG has been extensively studied as a mitogenic stimulus in epithelial cell layers. Consequently, it is regarded as a prospective contender that might potentially contribute to the observed epithelial cell reactions in helminth infection. Consistent with this finding, mice that lack the AREG gene exhibit a delay in the eradication of the intestinal parasite Trichuris muris. The observed delay is associated with a reduction in the proliferation rate of colonic epithelial cells compared to the infected animals in the control group. The aforementioned findings indicate that AREG plays a pivotal role in facilitating the activation of defensive mechanisms inside the epithelial cells of the intestinal tissue. The precise cellular sources of AREG in this specific context have not yet been determined. However, it is evident that the increased proliferation of the epithelial cell layer in infected mice is reliant on CD4+ T cells. The significance of this finding lies in its demonstration of the crucial role played by the interaction between immunological and epithelial cells in regulating the AREG-EGFR pathway. Additional research is necessary to delve into the cellular origins and signaling mechanisms that govern the synthesis of AREG and its tissue-protective properties, independent of infection.
關聯:	Microbial Pathogenesis, v.186, Article 106463
Appears in Collections:	[藥學系(所)] 期刊論文

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