Advertisement

Inflammation Research

, Volume 53, Issue 12, pp 644–652 | Cite as

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

  • R. SchrammEmail author
  • H. Thorlacius
Review

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.

Keywords

Rheumatoid Arthritis Arthritis Mast Cell Glucocorticoid Hypersensitivity Reaction 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations.

CD

cluster of differenciation

ENA

epithelial-cell derived neutrophil activating peptide

GCP

granulocyte chemotactic protein

GRO

growth-related oncogene

HCC

hemofiltrate CC chemokine

IL

interleukin

IP

interferon-gamma inducible protein

I-TAC

IFN-inducible T cell alpha chemoattractant

LEC

liver-expressed chemokine

LFA

lymphocyte function-associated antigen

LTC4

leukotriene C4

MDC

macrophage-derived chemokine

MIG

monokine induced by interferon-gamma

NAP

neutrophil-activating protein

PF

platelet factor

RANTES

regulated on activation, normal T-cells expressed and secreted

SDF

stromal-derived factor

SLC

secondary lymphoid tissue chemokine

TARC

thymus and activation-regulated chemokine

TECK

thymus–expressed chemokine

TNF

tumor necrosis factor

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

Copyright information

© Birkhäuser Verlag, Basel 2004

Authors and Affiliations

  1. 1.Department of Thoracic and Cardiovascular Surgery, University Hospital Homburg/SaarUniversity of SaarlandGermany
  2. 2.Institute for Clinical and Experimental Surgery, University Hospital Homburg/SaarUniversity of SaarlandGermany
  3. 3.Department of Surgery, Malmö University HospitalLund UniversitySweden

Personalised recommendations