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Alveolocapillary Cross-Talk*: Giles F. Filley Lecture

Jahar Bhattacharya, MD, DPhil
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*From the Lung Biology Laboratory, St. Luke’s-Roosevelt Hospital Center, and Department of Physiology & Cellular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY.

Correspondence to: Jahar Bhattacharya, MD, DPhil, St. Luke’s-Roosevelt Hospital Center, 1000 10th Ave, AJA 509, New York, NY 10019; e-mail: jb39@columbia.edu



Chest. 2005;128(6_suppl):553S-555S. doi:10.1378/chest.128.6_suppl.553S-a
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Host defense mechanisms fall in the categories of innate and adaptive immunity. The innate immune system deploys rapid-defense mechanisms, while the adaptive immune system activates a slower antigen-specific defense. In pulmonary alveoli that are continually exposed to airborne antigens, innate immune mechanisms are well developed and rapidly instituted. A large number of pathogenic substances including viruses, bacteria, and lipopolysaccharide, when introduced in the airway, induce leukocyte migration into the alveolus within 3 to 4 h, attesting to the efficacy of alveolar innate immunity.1 This time course is consistent with secretion of chemokines such as tumor necrosis factor (TNF)-α from alveolar macrophages, which provide the chemotactic signal for leukocyte recruitment. Ample evidence attests to this chemotactic effect, in that chemokines either directly instilled in the airspace or released on secretion by alveolar macrophages13 induce leukocyte influx into alveoli. It is clear that the chemotactic signal must vectorially cross the alveolar barrier to the site of leukocyte recruitment in adjoining capillaries. However, little attention has been paid to the role played by the alveolar wall epithelium in this inflammatory process.

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