Bronchoalveolar lavage fluid cytokines and chemokines changesafter bronchial thermoplasty in severe asthma
Nophol Leelayuwatanakul,1,4 Pimpayao Sodsai,2,5 Ketsupar Jirakran,3 Vorawut Thanthitaweewat,1
Virissorn Wongsrichanalai,1 Thitiwat Sriprasart1
Affiliations:
1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
2 Immunology Division, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
3 Center of Excellence for Maximizing Children’s Developmental Potential, Department of Pediatrics, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
4 Excellence Chulalongkorn Comprehensive Cancer Center, Department of Medicine, King Chulalongkorn Memorial Hospital, The Thai Red Cross Society, Bangkok, Thailand
5 Center of Excellence in Immunology and Immune-mediated Diseases, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
Abstract
Background: Bronchial thermoplasty (BT) is a non-pharmacological intervention in severe asthma with a well-known mechanism of reducing airway smooth muscle. However, its effect on airway inflammation remains uncertain.
Objectives: To investigate the effect of BT on bronchoalveolar lavage fluid (BALF) cytokines and chemokines in severe asthma patients before BT, after the first BT, and 12 weeks after BT
Methods: Ten severe asthma patients were recruited, and BALF was obtained from right lower lobe before BT, after the first BT, and 12 weeks after BT. BALF analytes were measured and values were compared among the time points. Lung function, asthma control test (ACT), and asthma quality of life questionnaire (AQLQ) were also measured.
Results: Tumor necrosis factor (TNF)-α concentration was significantly decreased after the first BT and significantly increased at 12 weeks after BT. Interleukin-6 (IL-6) and TNF-related apoptosis inducing ligand (TRAIL) concentration were significantly increased at 12 weeks after BT. There were no significant changes in Regulated upon activation, normal T-cell expressed and secreted (RANTES) and transforming growth factor-beta1 (TGF-β1) concentration over time after BT. At 12 weeks after BT, there were significantly greater improvements in the scores on AQLQ (3.93 ± 0.88 to 5.3 ± 0.99, p = 0.002) and ACT (13.6 ± 3.27 to 19 ± 4.44, p = 0.002). The lung function did not differ significantly between pre- and post-BT.
Conclusions: BT has limited effect on TNF-α, IL-6, TRAIL, RANTES, and TGF- β1 in BALF suggesting that its clinical benefit is not primarily related to this local airway inflammation. The effect on long-term airway inflammation probably needs further studies.
Key words: Severe asthma, Bronchial thermoplasty, Airway inflammation, Airway smooth muscle cells, Airway remodeling