Bronchial mucosal inflammation and upregulation of CXC chemoattractants and receptors in severe exacerbations of asthma
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BACKGROUND: A study was undertaken to test the hypothesis that severe exacerbations of asthma are characterised by increased bronchial mucosal neutrophilia associated with upregulation of neutrophil chemoattractant ligands and their specific cell surface receptors. METHODS: Immunohistology and in situ hybridisation were applied to endobronchial biopsy specimens from three groups: (1) 15 patients admitted to hospital with a severe exacerbation of asthma (E-asthma), (2) 15 with stable asthma (S-asthma) and (3) 15 non-atopic and non-smoker surgical controls (NSC). RESULTS: There were significantly more neutrophils and eosinophils in the epithelium and subepithelium of patients in the E-asthma group (median (range) neutrophils 7 (0-380) and 78 (10-898)/mm2, eosinophils 31 (0-167) and 60 (6-351)/mm2, p<or=0.01 compared with NSC: 0 (0-10, 0-7, 0-18 and 0-3)/mm2, respectively), resulting in similar final densities of eosinophils and neutrophils. With respect to neutrophil chemoattractants and receptors, counts of CXCL5, CXCL8, CXCR1 and CXCR2 mRNA-positive cells in the subepithelium of the E-asthma group were, respectively, 5, 4, 4 and 18 times greater (p<or=0.01) than those of the NSC group. In the E-asthma group, cells expressing CXCL5 or CXCR2 were eightfold and threefold more frequent than those expressing CXCL8 or CXCR1 mRNA, respectively (p<0.01). CXCL5 and CXCR2 in E-asthma were associated with the number of eosinophils (r=0.59 and 0.66, p<0.02 for both) rather than the number of neutrophils. CONCLUSION: In severe exacerbations of asthma there is a bronchial mucosal neutrophilia, eosinophilia and upregulation of CXC chemoattractants and their receptors. CXCL5 and CXCR2 have an association with eosinophila only, and these represent potentially new targets for treatment in exacerbations of asthma.
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By interfering with IFN production, respiratory viruses can block multiple antiviral pathways simultaneously, including IFN synthesis, ISG induction, and recruitment of inflammatory cells.
“By interfering with IFN production, respiratory viruses can block multiple antiviral pathways simultaneously, including IFN synthesis, ISG induction, and recruitment of inflammatory cells (71, 226).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [226]
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The airway epithelium: soldier in the fight against respiratory viruses
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- Authors
- Qiu, Y., Zhu, J., Bandi, V., Guntupalli, K. K., & Jeffery, P. K.
- Affiliations
- Royal Brompton Hospital (GB)
- Baylor College of Medicine (US)
- Corresponding author
- Jeffery, P. K
- Venue
- Thorax
- Publisher
- BMJ
- Published
- 2007-06-01
- Volume
- 62
- Issue
- 6
- Pages
- 475-482
- ISSN
- 0040-6376 (ISSN-L)
- PMC
- PMC2117215
- OpenAlex
- W2138425852
- Cited by
- 122
- References
- 52
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 5 · 2023: 6 · 2022: 2 · 2021: 2 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 7 · 2015: 9 · 2014: 17 · 2013: 9 · 2012: 9
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Thorax (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- severe asthma exacerbation, neutrophilia, eosinophilia, CXC chemokines, CXCL5, CXCR2, interleukin-8, CXCR1, chemokine receptors, neutrophil chemoattractants, airway epithelium, eosinophils, neutrophils, gene upregulation, bronchial biopsy, allergic asthma
- MeSH terms
- Acute Disease, Adult, Aged, Asthma, Biopsy, Bronchitis, Eosinophilia, Female, Humans, Immunohistochemistry, Male, Middle Aged, Neutropenia, Neutrophils, Up-Regulation, Chemokines, CXC, Respiratory Mucosa
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