IFN-gamma-induced protein 10 is a novel biomarker of rhinovirus-induced asthma exacerbations

J Allergy Clin Immunol. 2007 Sep;120(3):586-93. doi: 10.1016/j.jaci.2007.04.046. Epub 2007 Jul 12.


Background: Rhinovirus-induced acute asthma is the most frequent trigger for asthma exacerbations.

Objective: We assessed which inflammatory mediators were released from bronchial epithelial cells (BECs) after infection with rhinovirus and then determined whether they were also present in subjects with acute virus-induced asthma, with the aim to identify a biomarker or biomarkers for acute virus-induced asthma.

Methods: BECs were obtained from bronchial brushings of steroid-naive asthmatic subjects and healthy nonatopic control subjects. Cells were infected with rhinovirus 16. Inflammatory mediators were measured by means of flow cytometry with a cytometric bead array. Subjects with acute asthma and virus infection were recruited; they were characterized clinically by using lung function tests and had blood taken to measure the inflammatory mediators identified as important by the BEC experiments.

Results: IFN-gamma-induced protein 10 (IP-10) and RANTES were released in the greatest quantities, followed by IL-6, IL-8, and TNF-alpha. Dexamethasone treatment of BECs only partially suppressed IP-10 and TNF-alpha but was more effective at suppressing RANTES, IL-6, and IL-8. In acute clinical asthma serum IP-10 levels were increased to a greater extent in those with acute virus-induced asthma (median of 604 pg/mL compared with 167 pg/mL in those with non-virus-induced acute asthma, P < .01). Increased serum IP-10 levels were predictive of virus-induced asthma (odds ratio, 44.3 [95% CI, 3.9-100.3]). Increased serum IP-10 levels were strongly associated with more severe airflow obstruction (r = -0.8; P < .01).

Conclusions: IP-10 release is specific to acute virus-induced asthma.

Clinical implications: Measurement of serum IP-10 could be used to predict a viral trigger to acute asthma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Anti-Inflammatory Agents / pharmacology
  • Asthma / blood*
  • Asthma / virology*
  • Biomarkers / blood*
  • Cells, Cultured
  • Chemokine CCL5 / biosynthesis
  • Chemokine CXCL10
  • Chemokines, CXC / blood*
  • Dexamethasone / pharmacology
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism
  • Flow Cytometry
  • Humans
  • Interleukin-6 / biosynthesis
  • Interleukin-8 / biosynthesis
  • Lung / drug effects
  • Lung / immunology
  • Lung / virology
  • Middle Aged
  • Picornaviridae Infections / complications*
  • Rhinovirus / immunology
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / drug effects


  • Anti-Inflammatory Agents
  • Biomarkers
  • CXCL10 protein, human
  • Chemokine CCL5
  • Chemokine CXCL10
  • Chemokines, CXC
  • Interleukin-6
  • Interleukin-8
  • Tumor Necrosis Factor-alpha
  • Dexamethasone