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      Cigarette smoke augments MUC5AC production via the TLR3-EGFR pathway in airway epithelial cells.

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          Abstract

          Viral infections are a major cause of chronic obstructive pulmonary disease (COPD) exacerbations. Toll-like receptor 3 (TLR3) reacts with double-stranded RNA (dsRNA) and participates in the immune response after viral infection. In the present study, we examined whether cigarette smoke, which is involved in the pathogenesis of COPD, enhances mucin production via the TLR3-epidermal growth factor receptor (EGFR) pathway in airway epithelial cells.

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          Author and article information

          Journal
          Respir Investig
          Respiratory investigation
          Elsevier BV
          2212-5353
          2212-5345
          Jul 2015
          : 53
          : 4
          Affiliations
          [1 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: kanaik@wakayama-med.ac.jp.
          [2 ] Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. Electronic address: koarai@rm.med.tohoku.ac.jp.
          [3 ] Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. Electronic address: Yutaka.Sisikura@mc2.seikyou.ne.jp.
          [4 ] Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. Electronic address: sugiura@rm.med.tohoku.ac.jp.
          [5 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: 1kawa@wakayama-med.ac.jp.
          [6 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: kikuchi@wakayama-med.ac.jp.
          [7 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: akamatsu@wakayama-med.ac.jp.
          [8 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: tsuna@wakayama-med.ac.jp.
          [9 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: masa-n@wakayama-med.ac.jp.
          [10 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: kazmatsu@wakayama-med.ac.jp.
          [11 ] Third Department of Internal Medicine, Wakayama Medical University, Wakayama, Japan. Electronic address: minakaty@wakayama-med.ac.jp.
          [12 ] Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan. Electronic address: ichinose@rm.med.tohoku.ac.jp.
          Article
          S2212-5345(15)00011-8
          10.1016/j.resinv.2015.01.007
          26100173
          46452906-5db7-4c14-8c96-98077d00a108
          History

          Mucin,Oxidative stress,Toll-like receptor 3,COPD,Exacerbation

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