4.7 Article

Race is associated with differences in airway inflammation in patients with asthma

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 140, Issue 1, Pages 257-+

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2016.10.024

Keywords

Asthma; race; eosinophil; airway inflammation; African American; body mass index; corticosteroid; induced sputum; clinical trial

Funding

  1. National Institutes of Health/National Heart, Lung, and Blood Institute Chicago Metropolitan AsthmaNet Consortium (CMAC) [U10HL098096]
  2. American Academy of Allergy, Asthma, & Immunology/Association of Specialty Professors T. Franklin Williams Scholar
  3. University of Illinois at Chicago (UIC) Center for Clinical and Translational Science (CCTS)
  4. National Center for Advancing Translational Sciences [KL2RR029878, UL1TR000050]
  5. [U10 HL074225]
  6. [U10 HLA074227]
  7. [U10 HLA074231]
  8. [U10 HLA074204]
  9. [U10 HLA074212]
  10. [U10 HLA074073]
  11. [U10 HLA074206]
  12. [U10 HLA074208]
  13. [U10 HLA074218]
  14. [R21 HL118588-01]

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Background: African American subjects have a greater burden from asthma compared with white subjects. Whether the pattern of airway inflammation differs between African American and white subjects is unclear. Objective: We sought to compare sputum airway inflammatory phenotypes of African American and white subjects treated or not with inhaled corticosteroids (ICSs; ICS+ and ICS-, respectively). Methods: We performed a secondary analysis of self-identified African American and white subjects with asthma enrolled in clinical trials conducted by the National Heart, Lung, and Blood Institute-sponsored Asthma Clinical Research Network and AsthmaNet. Demographics, clinical characteristics, and sputum cytology after sputum induction were examined. We used a sputum eosinophil 2% cut point to define subjects with either an eosinophilic (>= 2%) or noneosinophilic (<2%) inflammatory phenotype. Results: Among 1018 participants, African American subjects (n = 264) had a lower FEV1 percent predicted (80% vs 85%, P <.01), greater total IgE levels (197 vs 120 IU/mL, P <.01), and a greater proportion with uncontrolled asthma (43% vs 28%, P <.01) compared with white subjects (n = 754). There were 922 subjects in the ICS+ group (248 African American and 674 white subjects) and 298 subjects in the ICS- group (49 African American and 249 white subjects). Eosinophilic airway inflammation was not significantly different between African American and white subjects in either group (percentage with eosinophilic phenotype: ICS+ group: 19% vs 16%, P = .28; ICS- group: 39% vs 35%, P = .65; respectively). However, when adjusted for confounding factors, African American subjects were more likely to exhibit eosinophilic airway inflammation than white subjects in the ICS+ group (odds ratio, 1.58; 95% CI, 1.01-2.48; P = .046) but not in the ICS- group (P = .984). Conclusion: African American subjects exhibit greater eosinophilic airway inflammation, which might explain the greater asthma burden in this population.

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