Neutrophil recruitment by allergens contribute to allergic sensitization and allergic inflammation

Koa Hosoki, Toshiko Itazawa, Istvan Boldogh, Sanjiv Sur

Research output: Contribution to journalReview articlepeer-review

59 Scopus citations


Purpose of review To discuss the presence and role of neutrophils in asthma and allergic diseases, and outline the importance of pollen and cat dander-induced innate neutrophil recruitment in induction of allergic sensitization and allergic inflammation. Recent findings Uncontrolled asthma is associated with elevated numbers of neutrophils, and levels of neutrophil-attracting chemokine IL-8 and IL-17 in bronchoalveolar lavage fluids. These parameters negatively correlate with lung function. Pollen allergens and cat dander recruit neutrophils to the airways in a toll-like receptor 4, myeloid differentiation protein-2, and chemokine (C-X-C motif) receptor (CXCR) 2-dependent manner. Repeated recruitment of activated neutrophils by these allergens facilitates allergic sensitization and airway inflammation. Inhibition of neutrophil recruitment with CXCR2 inhibitor, disruption of toll-like receptor 4, or small interfering RNA against myeloid differentiation protein-2 also inhibits allergic inflammation. The molecular mechanisms by which innately recruited neutrophils contribute to shifting the airway inflammatory response induced by allergens from neutrophilic to an eosinophilic-allergic is an area of active research. Summary Recent studies have revealed that neutrophil recruitment is important in the development of allergic sensitization and inflammation. Inhibition of neutrophils recruitment may be a strategy to control allergic inflammation.

Original languageEnglish (US)
Pages (from-to)45-50
Number of pages6
JournalCurrent opinion in allergy and clinical immunology
Issue number1
StatePublished - 2016


  • Cat dander
  • Myeloid differentiation protein-2
  • Neutrophils
  • Pollens
  • Toll-like receptor 4

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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