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Neutrophil recruitment in mast cell-dependent inflammation: inhibitory mechanisms of glucocorticoids

Schramm, R and Thorlacius, Henrik LU (2004) In Inflammation Research 53(12). p.644-652
Abstract
Mast cells are strategically localized along the microvasculature in tissues in close contact with the external environment, such as the skin, lung and intestines. By releasing a multi-faceted spectrum of proinflammatory mediators, such as cytokines and chemokines, mast cells have the capacity to coordinate trafficking of leukocytes. Mast cells play a pathophysiological role in numerous inflammatory diseases as diverse as hypersensitivity reactions, ischemia/reperfusion injury and rheumatoid arthritis. On the other hand, mast cells act also as tissue sentinels and are critically involved in the host defensive response against microbial infection by stimulating neutrophil recruitment. Glucocorticoids are powerful agents frequently used in... (More)
Mast cells are strategically localized along the microvasculature in tissues in close contact with the external environment, such as the skin, lung and intestines. By releasing a multi-faceted spectrum of proinflammatory mediators, such as cytokines and chemokines, mast cells have the capacity to coordinate trafficking of leukocytes. Mast cells play a pathophysiological role in numerous inflammatory diseases as diverse as hypersensitivity reactions, ischemia/reperfusion injury and rheumatoid arthritis. On the other hand, mast cells act also as tissue sentinels and are critically involved in the host defensive response against microbial infection by stimulating neutrophil recruitment. Glucocorticoids are powerful agents frequently used in mast cell-dependent diseases, although the anti-inflammatory mechanisms of these compounds are not completely understood at present. In order to circumvent steroid-associated side-effects and develop more specific therapeutics, numerous studies have examined the mechanisms underlying glucocorticoid inhibition of mast cell-dependent neutrophil recruitment. Based on recent findings, it may be suggested that glucocorticoids selectively inhibit the expression and function of certain adhesion molecules and chemokines. This review summarizes current insights into the underlying mechanisms of mast cell-regulated tissue accumulation of neutrophils and the inhibitory effects of glucocorticoids. (Less)
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author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Inflammation Research
volume
53
issue
12
pages
644 - 652
publisher
Birkhäuser Verlag
external identifiers
  • wos:000226061300001
  • pmid:15654511
  • scopus:12944278742
ISSN
1420-908X
DOI
10.1007/s00011-004-1307-8
language
English
LU publication?
yes
id
26822957-63ab-42ba-a619-485d74514c5e (old id 257963)
date added to LUP
2016-04-01 12:28:16
date last changed
2022-01-27 05:32:07
@article{26822957-63ab-42ba-a619-485d74514c5e,
  abstract     = {{Mast cells are strategically localized along the microvasculature in tissues in close contact with the external environment, such as the skin, lung and intestines. By releasing a multi-faceted spectrum of proinflammatory mediators, such as cytokines and chemokines, mast cells have the capacity to coordinate trafficking of leukocytes. Mast cells play a pathophysiological role in numerous inflammatory diseases as diverse as hypersensitivity reactions, ischemia/reperfusion injury and rheumatoid arthritis. On the other hand, mast cells act also as tissue sentinels and are critically involved in the host defensive response against microbial infection by stimulating neutrophil recruitment. Glucocorticoids are powerful agents frequently used in mast cell-dependent diseases, although the anti-inflammatory mechanisms of these compounds are not completely understood at present. In order to circumvent steroid-associated side-effects and develop more specific therapeutics, numerous studies have examined the mechanisms underlying glucocorticoid inhibition of mast cell-dependent neutrophil recruitment. Based on recent findings, it may be suggested that glucocorticoids selectively inhibit the expression and function of certain adhesion molecules and chemokines. This review summarizes current insights into the underlying mechanisms of mast cell-regulated tissue accumulation of neutrophils and the inhibitory effects of glucocorticoids.}},
  author       = {{Schramm, R and Thorlacius, Henrik}},
  issn         = {{1420-908X}},
  language     = {{eng}},
  number       = {{12}},
  pages        = {{644--652}},
  publisher    = {{Birkhäuser Verlag}},
  series       = {{Inflammation Research}},
  title        = {{Neutrophil recruitment in mast cell-dependent inflammation: inhibitory mechanisms of glucocorticoids}},
  url          = {{http://dx.doi.org/10.1007/s00011-004-1307-8}},
  doi          = {{10.1007/s00011-004-1307-8}},
  volume       = {{53}},
  year         = {{2004}},
}