EDITORIAL FOCUS
The time has finally arrived: use of intravital microscopy in the airway circulation

Aubrey E. Taylor, Timothy Moore, and Peyton Paisley

Department of Physiology, College of Medicine, University of South Alabama, Mobile, Alabama 36688


    ARTICLE
TOP
ARTICLE
REFERENCES

THE STUDY by Lim et al., one of this issue's articles in focus (Ref. 6a, see p. L959), provides important new information on the potential use of intravital microscopy in evaluating the inflammatory response in postcapillary venules of the rat trachea. The pulmonary, mesentery, cheek pouch, and renal blood vessels have been studied for many years using this technique, but this is the first paper using intravital microscopy to study inflammation in the airway circulation.

The inflammatory response in the lung's circulation has been extensively studied using biophysical measures of endothelial damage and incorporating immunological techniques to evaluate the role of cytokines as well as plasma and tissue cells involved in producing the ischemia-reperfusion injury of microvessels in isolated or in situ lungs (1, 9). Ischemia-reperfusion has been and still remains an important model to evaluate and define the inflammatory system when either the lung or other organs, remote from the lung, are subjected to periods of ischemia and the resulting inflammatory response in the lung evaluated following reperfusion (2, 4). It is well known that asthma is an inflammatory disease associated with airway smooth muscle, yet it has been extremely difficult to study the airway circulation's contribution to the tissue accumulation of neutrophils, monocytes, and their release of inflammatory mediators in asthma. An experimental model that can evaluate inflammation in the airway circulation will prove to be an extremely useful addition to our experimental inflammation model repertoire.

The present study clearly shows that the airway circulation can be studied in inflammation caused by challenges with either N-formyl-methionyl-leucyl-phenylalanine or lipopolysaccharide, and the mechanisms responsible for producing the inflammation were evaluated in a quantitative fashion. Although the inflammatory response in airways is well defined in asthma (3, 8), and the inflammatory response to interleukin-1beta and tumor necrosis factor-alpha , important inflammatory cytokines, has also been studied in isolated airway smooth muscle cells (7), the paper by Lim et al. (6a) is the first to use intravital microscopy. There is absolutely no doubt that the techniques presented by Lim et al. provide a new model in which the inflammatory response can be evaluated in the airway circulation relative to monocyte and neutrophil activation, infiltration of leukocytes into the tissues, and the ways by which various cytokines and chemokines are involved in the phenomena. The airway circulation's response to inflammation is definitely an area in need of new techniques, and we believe that Lim et al. provide a new and valuable method in a research area that has previously relied on either histological or tissue staining techniques to define inflammatory responses in the airways.

Although Landis et al. (6) popularized the mesentery technique to evaluate capillary filtration in the 1930s as they worked in Krogh's laboratory, their technique has been used to provide substantial new information about the inflammatory response in many organs over the last decade (5). Applying these same experimental principles to the airway circulation will greatly extend our knowledge of the airway circulation and provide the necessary information to understand the mechanisms involved in the airway inflammatory process. We can hardly wait to see the data resulting from this technique to evaluate the inflammatory responses in the airway circulation, not just with ischemia-reperfusion but also with the evaluation of experimental rhinitis and the effect of various oligonucleotides and dust mite allergies on the airway microcirculation. Future studies using the techniques outlined by Lim et al. may allow us not only to open the black box of asthma development in the airways but also to accelerate the development of new therapies to use in patients subjected to various forms of inflammation. For the first time we will be able to observe how neutrophils roll, adhere, and migrate across the airway endothelial barrier during inflammation. The time course of various monocytes adhering in the process can also be evaluated in response to challenges with various cytokines and chemokines and their specific antibodies in portions of the airway circulation under study. There is absolutely no doubt that this technique will be rapidly adapted to determine the mechanisms associated with the inflammatory response because it definitely provides quantitative assessments of how various inflammatory cells respond in the airway circulation during a defined inflammatory stress.


    FOOTNOTES

Address for reprint requests and other correspondence: A. E. Taylor, Dept. of Physiology, College of Medicine, Univ. of South Alabama, Mobile, AL 36688 (E-mail: ataylor{at}jaguar1.usouthal.edu).

10.1152/ajplung.00441.2001


    REFERENCES
TOP
ARTICLE
REFERENCES

1.   Adkins, WK, and Taylor AE. Role of xanthine oxidase and neutrophils in ischemia-reperfusion injury in the rabbit lung. J Appl Physiol 69: 2012-2018, 1990[Abstract/Free Full Text].

2.   Carden, DL, Young JA, and Granger DN. Pulmonary microvascular injury following intestinal ischemia-reperfusion: role of P-selectin. J Appl Physiol 75: 2529-2534, 1993[Abstract].

3.   Cohn, L. Food for thought: can immunological tolerance be induced to treat asthma? Am J Respir Cell Mol Biol 24: 509-512, 2001[Free Full Text].

4.   Eppinger, MJ, Deeb GM, Bolling SF, and Ward PA. Mediators of ischemia-reperfusion injury of rat lung. Am J Pathol 150: 1773-1784, 1997[Abstract].

5.   Granger, DN, and Kubes P. The microcirculation and inflammation: modulation of leukocyte-endothelial cell adhesion. J Leukoc Biol 55: 662-675, 1994[Abstract].

6.   Landis, EM, Jonas L, Angevine M, and Erb W. The passage of fluid and protein through the human capillary wall during venous congestion. J Clin Invest 11: 717-734, 1932.

6a.   Lim, LHK, Bochner BS, and Wagner EM. Leukocyte recruitment in the airways: an intravital microscopic study of rat tracheal microcirculation. Am J Physiol Lung Cell Mol Physiol 282: L959-L967, 2002[Abstract/Free Full Text].

7.   Moore, PE, Lahiri T, Laporte J, Church T, Panettieri RA, Jr, and Shore SA. Selected contribution: synergism between TNF-alpha and IL-1beta in airway smooth muscle cells: implication for beta -adrenergic responsiveness. J Appl Physiol 91: 1467-1474, 2001[Abstract/Free Full Text].

8.   Stirling, RG, and Chung KF. New immunological approaches and cytokine targets in asthma and allergy. Eur Respir J 16: 1158-1174, 2000[Abstract/Free Full Text].

9.   Taylor, A, Khimenko P, Moore T, and Rippe B. Overview of lung ischemia/reperfusion experimental models. In: Proceedings of 20th European Conference on Microcirculation, edited by Carpenter P, Vicaut E, and Guilmot J-L.. Bologna, Italy: Monduzzi Editore, 1998, p. 95-103.


Am J Physiol Lung Cell Mol Physiol 282(5):L957-L958
1040-0605/02 $5.00 Copyright © 2002 the American Physiological Society




This Article
Full Text (PDF)
Alert me when this article is cited
Alert me if a correction is posted
Citation Map
Services
Email this article to a friend
Similar articles in this journal
Similar articles in ISI Web of Science
Similar articles in PubMed
Alert me to new issues of the journal
Download to citation manager
Google Scholar
Articles by Taylor, A. E.
Articles by Paisley, P.
Articles citing this Article
PubMed
PubMed Citation
Articles by Taylor, A. E.
Articles by Paisley, P.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online