162
Views
3
CrossRef citations to date
0
Altmetric
Mechanisms

Serum IFNγ–induced protein 10 (IP10/CXCL10): association with asthma exacerbations and severity in children

, MD, , MD, , MSc & , MDORCID Icon
Pages 2135-2142 | Received 01 Mar 2021, Accepted 24 Oct 2021, Published online: 27 Dec 2021
 

Abstract

Objective

Asthma is a chronic disorder of the airways, in which chemokines coordinate airway inflammation and determine its severity. We aimed to study the chemokine interferonγ–inducible protein 10 kDa (IP10/CXCL10), a member of the CXC receptor 3 (CXCR3) ligand family, at the protein level in the serum of children, to evaluate the association between CXCL10 and exacerbations of childhood asthma.

Methods

Patients experiencing an asthma exacerbation (42 patients) and stable patients (43 patients) were investigated for serum CXCL10 levels.

Results

Patients with an asthma exacerbation expressed significantly higher CXCL10 levels in the serum than stable patients (p < 0.001). Additionally, CXCL10 values were elevated in severe asthma compared with moderate and mild disease (p < 0.001). In patients experiencing asthma exacerbations, higher values of CXCL10 were observed in atopic patients compared with non-atopic patients (p = 0.027) and in uncontrolled and partly controlled patients compared with controlled patients (p = 0.046).

Conclusions

CXCL10 is proposed as an inflammatory serum marker for asthma exacerbations and worsening asthma symptoms. The levels of CXCL10 are representative of the clinical severity of asthma.

Acknowledgements

We would like to thank Peter Basta, native speaker of English for proofreading the manuscript.

Declaration of interest

The authors report no conflicts of interest.

Funding

The author(s) reported there is no funding associated with the work featured in this article.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.