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Airborne fungi induce nasal polyp epithelial cell activation and Toll-like receptor expression

Seung-Heon Shin1, Young-Ho Lee

  • 1Department of Otorhinolaryngology, School of Medicine, Catholic University of Daegu, Daegu, South Korea. hsseung@cu.ac.kr

International Archives of Allergy and Immunology
|April 2, 2010
PubMed
Abstract

Insights

Fungal proteases and Toll-like receptor 4 (TLR4) activation drive airway inflammation. This study shows fungi stimulate nasal epithelial cells to produce cytokines like interleukin-8 (IL-8) and granulocyte macrophage colony-stimulating factor (GM-CSF).

Area of Science:

  • Immunology
  • Microbiology
  • Rhinology

Background:

  • Nasal epithelium acts as a primary defense against airborne allergens and contributes to airway inflammation.
  • Fungi are increasingly implicated as significant pathogens in sinusitis and other airway diseases.

Purpose of the Study:

  • To investigate fungal protease activity in relation to cytokine production by nasal polyp epithelial cells.
  • To determine the expression of Toll-like receptor (TLR) mRNA in response to fungal stimulation.

Main Methods:

  • Nasal polyp epithelial cells were stimulated with fungal species (Alternaria, Aspergillus).
  • Interleukin-8 (IL-8) and granulocyte macrophage colony-stimulating factor (GM-CSF) levels were measured.
  • Reverse transcriptase polymerase chain reaction (RT-PCR) was used to assess TLR mRNA expression.
  • Protease inhibitors and anti-human TLR antibodies were employed to block cytokine production.

Main Results:

  • Fungal exposure significantly increased IL-8 and GM-CSF production by nasal epithelial cells.
  • Activation of nasal epithelial cells by fungi led to enhanced expression of TLR2, TLR3, and TLR4 mRNA.
  • Cytokine production was successfully inhibited by protease inhibitors and anti-human TLR4 antibodies.

Conclusions:

  • Fungi interact with nasal epithelial cells, augmenting cytokine production and TLR mRNA expression.
  • Fungal protease activity and TLR4 signaling are key mechanisms involved in this inflammatory response.

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