7
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Club Cell Protein 16 (CC16) Augmentation: A Potential Disease-modifying Approach for Chronic Obstructive Pulmonary Disease (COPD)

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Introduction

          Club cell protein 16 (CC16) is the most abundant protein in bronchoalveolar lavage fluid. CC16 has anti-inflammatory properties in smoke-exposed lungs, and chronic obstructive pulmonary disease (COPD) is associated with CC16 deficiency. Herein, we explored whether CC16 is a therapeutic target for COPD.

          Areas Covered

          We reviewed the literature on the factors that regulate airway CC16 expression, its biologic functions and its protective activities in smoke-exposed lungs using PUBMED searches. We generated hypotheses on the mechanisms by which CC16 limits COPD development, and discuss its potential as a new therapeutic approach for COPD.

          Expert Opinion

          CC16 plasma and lung levels are reduced in smokers without airflow obstruction and COPD patients. In COPD patients, airway CC16 expression is inversely correlated with severity of airflow obstruction. CC16 deficiency increases smoke-induced lung pathologies in mice by its effects on epithelial cells, leukocytes, and fibroblasts. Experimental augmentation of CC16 levels using recombinant CC16 in cell culture systems, plasmid and adenoviral-mediated over-expression of CC16 in epithelial cells or smoke-exposed murine airways reduces inflammation and cellular injury. Additional studies are necessary to assess the efficacy of therapies aimed at restoring airway CC16 levels as a new disease-modifying therapy for COPD patients.

          Related collections

          Author and article information

          Journal
          101127833
          27020
          Expert Opin Ther Targets
          Expert Opin. Ther. Targets
          Expert opinion on therapeutic targets
          1472-8222
          1744-7631
          2 August 2016
          11 February 2016
          July 2016
          01 July 2017
          : 20
          : 7
          : 869-883
          Affiliations
          [1 ] Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
          [2 ] Pulmonary Care Service. University Hospital of Caracas, Caracas, Venezuela.
          [3 ] University of Parma, Parma, Italy.
          [4 ] Lovelace Respiratory Research Institute, Albuquerque, NM, USA.
          [5 ] Therabron Therapeutics, Inc. Rockville, MD, USA.
          Author notes
          [* ] Author for Correspondence Caroline A. Owen, MD, PhD, Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, HIM Building, Room 855B, Boston, MA 02115, mUSA. Telephone: 617-525-5408, Fax: 617-525-5413, cowen@ 123456bwh.harvard.edu
          Article
          PMC4977029 PMC4977029 4977029 nihpa802780
          10.1517/14728222.2016.1139084
          4977029
          26781659
          8641b207-e2e5-4e14-b308-3445be52ed88
          History
          Categories
          Article

          uteroglobin,Bronchoalveolar lavage fluid,CC10,CC16,chronic bronchitis,Club cells,COPD,emphysema,formyl peptide receptor-2,lipoxin A4 ,lung inflammation,nuclear factor kappa B,phospholipase A2 ,recombinant therapy,serum amyloid A,secretoglobin 1A1,small airway remodeling,toll-like receptor

          Comments

          Comment on this article