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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #162638
Title: UNIQUE STRUCTURAL FEATURES THAT INFLUENCE NEUTROPHIL EMIGRATION INTO THE LUNG

Author
item BURNS, ALAN - BAYLOR COLLEGE MED
item Smith, Wayne
item WALKER, DAVID - UNIV BRITISH COLUMBIA

Submitted to: Physiological Reviews
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/1/2003
Publication Date: 4/1/2003
Citation: BURNS, A.R., SMITH, W.C., WALKER, D.C. UNIQUE STRUCTURAL FEATURES THAT INFLUENCE NEUTROPHIL EMIGRATION INTO THE LUNG. PHYSIOLOGICAL REVIEWS. 2003.

Interpretive Summary: This review article deals with the anatomical features of the lung that are important to the effective function of the innate immunity in pulmonary tissue. The discussion focuses on unique features that allow white blood cell migration from the blood into the air sacs in cases of pneumonia. This paper is intended to provide researchers in the fields of nutrition and immunity with up to date concepts on basic mechanisms of inflammation in the lungs.

Technical Abstract: Neutrophil emigration in the lung differs substantially from that in systemic vascular beds where extravasation occurs primarily through postcapillary venules. Migration into the alveolus occurs directly from alveolar capillaries and appears to progress through a sequence of steps uniquely influenced by the cellular anatomy and organization of the alveolar wall. The cascade of adhesive and stimulatory events so critical to the extravasation of neutrophils from postcapillary venules in many tissues is not evident in this setting. Compelling evidence exists for unique cascades of biophysical, adhesive, stimulatory, and guidance factors that arrest neutrophils in the alveolar capillary bed and direct their movement through the endothelium, interstitial space, and alveolar epithelium. A prominent path accessible to the neutrophil appears to be determined by the structural interactions of endothelial cells, interstitial fibroblasts, as well as type I and type II alveolar epithelial cells.