Airway Inflammation

  1. James H. Shelhamer;
  2. Stewart J. Levine;
  3. Tong Wu;
  4. David B. Jacoby;
  5. Michael A. Kaliner; and
  6. Stephen I. Rennard
  1. An edited summary of a Combined Clinical Staff Conference held on 27 April 1994 at the Clinical Center of the National Institutes of Health, Bethesda, Maryland. Authors who wish to cite a section of the conference and specifically indicate its author may use this example for the form of the reference: Levine SJ. Bronchial epithelial cell-cytokine interactions in airway inflammation, pp 288-291. In: Shelhamer JH, moderator. Airway inflammation. Ann Intern Med. 1995; 123:288-304. Requests for Reprints: James H. Shelhamer, MD, Building 10, Room 7-D-43, National Institutes of Health, Bethesda, MD 20892.

    Abstract

    Diseases characterized by airway inflammation, excessive airway secretion, and airway obstruction affect a substantial proportion of the population.These diseases include asthma, chronic bronchitis, bronchiectasis, and cystic fibrosis. Asthma and chronic bronchitis may affect 25 million persons in the United States. Much progress has been made in the last decade toward an understanding of the mechanisms underlying chronic airway inflammation; recent work has resulted in several new concepts of the initiation and maintenance of airway inflammation. Airway production of chemokines, cytokines, and growth factors in response to irritants, infectious agents, and inflammatory mediators may play an important role in the modulation of acute and chronic airway inflammation. Lipid mediators may be produced by resident airway cells and by inflammatory cells; production of these mediators may also be altered by inflammatory cytokines. Increased airway obstruction may be related to intercurrent viral respiratory infection and to the induction of airway inflammation and airway hyperreactivity that results from such infection. Furthermore, several models exist to explain the processes by which airway inflammation is perpetuated in diseases such as asthma and chronic bronchitis. These include neurogenic inflammation, the perpetuation of the acute inflammatory response, and cycles of airway epithelial cell-mediated and inflammatory cell-mediated recruitment and activation of inflammatory cells. An understanding of these mechanisms of airway inflammation may provide the clinician with new therapeutic approaches to the treatment of these common and chronic diseases.

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