Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 Dec;67(12):1061-6.
doi: 10.1136/thoraxjnl-2012-201634. Epub 2012 Sep 26.

Epithelial eotaxin-2 and eotaxin-3 expression: relation to asthma severity, luminal eosinophilia and age at onset

John M Coleman  1 , Chetan Naik, Fernando Holguin, Anuradha Ray, Prabir Ray, John B Trudeau, Sally E Wenzel
Affiliations

Epithelial eotaxin-2 and eotaxin-3 expression: relation to asthma severity, luminal eosinophilia and age at onset

John M Coleman et al. Thorax. 2012 Dec.

Abstract

Background: Eosinophilic inflammation is implicated in asthma. Eotaxin 1-3 regulate eosinophil trafficking into the airways along with other chemotactic factors. However, the epithelial and bronchoalveolar lavage (BAL) cell expression of these chemokines in relation to asthma severity and eosinophilic phenotypes has not been addressed.

Objective: To measure the expression of the three eotaxin isoforms in bronchoscopically obtained samples and compare them with clinically relevant parameters between normal subjects and patients with asthma.

Methods: Normal subjects and patients with asthma of varying severity recruited through the Severe Asthma Research Program underwent clinical assessment and bronchoscopy with airway brushing and BAL. Eotaxin 1-3 mRNA/protein were measured in epithelial and BAL cells and compared with asthma severity, control and eosinophilic inflammation.

Results: Eotaxin-2 and eotaxin-3 mRNA and eotaxin-2 protein were increased in airway epithelial brushings from patients with asthma and were highest in cases of severe asthma (p values 0.0155, 0.0033 and 0.0006, respectively), with eotaxin-2 protein increased with age at onset. BAL cells normally expressed high levels of eotaxin-2 mRNA/protein but BAL fluid levels of eotaxin-2 were lowest in severe asthma. Epithelial eotaxin-2 and eotaxin-3 mRNA/protein was associated with sputum eosinophilia, lower forced expiratory volume in 1 s and more asthma exacerbations. Airway epithelial cell eotaxin-2 protein differed by asthma severity only in those with late onset disease, and tended to be highest in those with late onset eosinophilic asthma.

Conclusions: Epithelial eotaxin-2 and 3 are increased in asthma and severe asthma. Their expression may contribute to luminal migration of eosinophils, especially in later onset disease, asthma control and severity.

PubMed Disclaimer

Figures

Figure 1
Figure 1
(A) Eotaxin-2 mRNA expression in cells obtained by epithelial brushings from patients with asthma and normal controls. (bB) Eotaxin-2 protein levels among the subject groups. Data represent the values of the median, 25th and 75th percentiles with maximum/minimum whiskers. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; ICS inhaled corticosteroid.
Figure 2
Figure 2
Eotaxin-3 mRNA levels in cells obtained by epithelial brushings from patients with asthma and normal controls (NCs). Data represent the values of the median, 25th and 75th percentiles with maximum/minimum whiskers. GAPDH, glyceraldehyde 3-phosphate dehydrogenase; ICS inhaled corticosteroid.
Figure 3
Figure 3
Bronchoalveolar lavage fluid eotaxin-2 levels from patients with asthma and normal controls. Data represent medians with 25th–75th percentiles and maximum/minimum whiskers. BALF, bronchoalveolar lavage fluid; ICS inhaled corticosteroid.
See this image and copyright information in PMC

Comment in

References

    1. American Thoracic Society. Proceedings of the ATS workshop on refractory asthma: current understanding, recommendations, and unanswered questions. Am J Respir Crit Care Med. 2000;162:2341–2351. - PubMed
    1. Wenzel SE, Schwartz LB, Langmack EL, et al. Evidence that severe asthma can be divided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics. Am J Respir Crit Care Med. 1999;160:1001–1008. - PubMed
    1. Haldar PBC, Hargadon B, Gupat S, et al. Mepolizumab (anti-IL 5) and exacerbations of refractory eosinophilic asthma. N Engl J Med. 2009;360:973–984. - PMC - PubMed
    1. Miranda C, Busacker A, Balzar S, et al. Distinguishing severe asthma phenotypes: role of age at onset and eosinophilic inflammation. J Allergy Clin Immunol. 2004;113:101–108. - PubMed
    1. ten Brinke A, Zwinderman AH, Sterk PJ, et al. Factors associated with persistent airflow limitation in severe asthma. Am J Respir Crit Care Med. 2001;164:744–748. - PubMed

Publication types