Pathophysiology of allergic inflammation

Immunol Rev. 2011 Jul;242(1):31-50. doi: 10.1111/j.1600-065X.2011.01020.x.

Abstract

Allergic inflammation is due to a complex interplay between several inflammatory cells, including mast cells, basophils, lymphocytes, dendritic cells, eosinophils, and sometimes neutrophils. These cells produce multiple inflammatory mediators, including lipids, purines, cytokines, chemokines, and reactive oxygen species. Allergic inflammation affects target cells, such as epithelial cells, fibroblasts, vascular cells, and airway smooth muscle cells, which become an important source of inflammatory mediators. Sensory nerves are sensitized and activated during allergic inflammation and produce symptoms. Allergic inflammatory responses are orchestrated by several transcription factors, particularly NF-κB and GATA3. Inflammatory genes are also regulated by epigenetic mechanisms, including DNA methylation and histone modifications. There are several endogenous anti-inflammatory mechanisms, including anti-inflammatory lipids and cytokines, which may be defective in allergic disease, thus amplifying and perpetuating the inflammation. Better understanding of the pathophysiology of allergic inflammation has identified new therapeutic targets but developing effective novel therapies has been challenging. Corticosteroids are highly effective with a broad spectrum of anti-inflammatory effects, including epigenetic modulation of the inflammatory response and suppression of GATA3.

Publication types

  • Review

MeSH terms

  • Adrenal Cortex Hormones / pharmacology
  • Allergens / immunology
  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • B-Lymphocytes / immunology
  • B-Lymphocytes / metabolism
  • Child
  • Cytokines / biosynthesis*
  • DNA Methylation
  • Dendritic Cells / immunology
  • Dendritic Cells / metabolism
  • Eosinophils / immunology
  • Eosinophils / metabolism
  • Epigenomics
  • Epithelial Cells / immunology
  • Epithelial Cells / metabolism
  • Fibroblasts / cytology
  • Fibroblasts / immunology
  • Fibroblasts / metabolism
  • GATA3 Transcription Factor / biosynthesis*
  • Histones / metabolism
  • Humans
  • Hypersensitivity / drug therapy
  • Hypersensitivity / genetics
  • Hypersensitivity / immunology
  • Hypersensitivity / physiopathology*
  • Inflammation / drug therapy
  • Inflammation / genetics
  • Inflammation / immunology
  • Inflammation / physiopathology*
  • Mast Cells / immunology
  • Mast Cells / metabolism
  • NF-kappa B / biosynthesis*
  • Neutrophils / immunology
  • Neutrophils / metabolism
  • Superantigens / immunology
  • Th2 Cells / immunology
  • Th2 Cells / metabolism

Substances

  • Adrenal Cortex Hormones
  • Allergens
  • Anti-Inflammatory Agents
  • Cytokines
  • GATA3 Transcription Factor
  • GATA3 protein, human
  • Histones
  • NF-kappa B
  • Superantigens