Impaired CXCR1-dependent oxidative defence in active tuberculosis patients.
Author
Summary, in English
Much of the pronounced host inflammatory response that occurs in tuberculosis (TB) is related to failed immunity against the invading pathogen. The G-protein coupled receptors CXCR1 and CXCR2 are implicated in important signal transduction pathways in lung inflammatory responses. We investigated the expression and function of these receptors in a simple whole blood model from 24 patients with pulmonary TB and in subjects with latent TB infection (LTBI). Healthy controls were recruited from close contacts to the pulmonary index patients. We found that pulmonary TB patients had significantly increased CXCR1 expression on blood cells compared to LTBI subjects and controls (p < 0.001). In contrast, LTBI subjects had a significant increase in CXCR2 expression compared to pulmonary TB patients (p < 0.001) and controls (p < 0.01). Leukocyte function, measured as oxidative capacity, was decreased in pulmonary TB patients compared to LTBI and controls (p < 0.001) and correlated with the increased CXCR1 expression. Leukocyte recruitment, measured as the expression of microRNA-223 was increased in pulmonary TB patients compared to LTBI (p < 0.05). We found that variations in receptor expression are linked to disease progression and affect the immune response against Mycobacterium tuberculosis (Mtb).
Department/s
- Clinical Microbiology, Malmö
- Infectious Diseases Research Unit
- Infection Medicine (BMC)
- Division of Microbiology, Immunology and Glycobiology - MIG
Publishing year
2015
Language
English
Pages
744-750
Publication/Series
Tuberculosis
Volume
95
Issue
6
Links
Document type
Journal article
Publisher
Elsevier
Topic
- Immunology in the medical area
Status
Published
Research group
- Clinical Microbiology, Malmö
- Infectious Diseases Research Unit
ISBN/ISSN/Other
- ISSN: 1873-281X