Department of Physiology, College of Medicine, University of South Alabama, Mobile, Alabama 36688
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-1 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.
ARTICLE
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REFERENCES
and tumor
necrosis factor-
, 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.
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FOOTNOTES |
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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
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