ArticleBMC pulmonary medicine2014
Inflammatory cytokine response to exercise in alpha-1-antitrypsin deficient COPD patients 'on' or 'off' augmentation therapy.
Article in BMC pulmonary medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Pulmonary Rehabilitation for Chronic Obstructive Pulmonary Disease Patients with Underlying Alpha-1 Antitrypsin Deficiency: A Systematic Review and Practical Recommendations.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2024Article
- Immunological and homeostatic pathways of alpha -1 antitrypsin: a new therapeutic potential.Frontiers in immunology · 2024Review
- Augmentation Therapy Modulates Systemic Inflammation in Individuals with Alpha-1 Antitrypsin Deficiency and Chronic Obstructive Pulmonary Disease.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2023Article
- Physical Activity, Exercise Capacity and Sedentary Behavior in People with Alpha-1 Antitrypsin Deficiency: A Scoping Review.International journal of chronic obstructive pulmonary disease · 2023Article
- Possible Mechanisms for the Effects of Sound Vibration on Human Health.Healthcare (Basel, Switzerland) · 2021Review
- Home-Based Multicomponent Intervention Increases Exercise Activity and Improves Body Mass Index: Results of a 5-Year Randomized Trial Among Individuals with Alpha-1 Antitrypsin Deficiency-Associated Lung Disease.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2021Article
- Alpha-1 antitrypsin deficient individuals have circulating extracellular vesicles with profibrogenic cargo.Cell communication and signaling : CCS · 2020Article
- Acute Effects of Whole-Body Vibration on Inflammatory Markers in People with Chronic Obstructive Pulmonary Disease: A Pilot Study.Rehabilitation research and practice · 2018Article
- Gene and miRNA expression profiles in PBMCs from patients with severe and mild emphysema and PiZZ alpha1-antitrypsin deficiency.International journal of chronic obstructive pulmonary disease · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThere is still limited information on systemic inflammation in alpha-1-antitrypsin-deficient (AATD) COPD patients and what effect alpha-1-antitrypsin augmentation therapy and/or exercise might have on circulating inflammatory cytokines. We hypothesized that AATD COPD patients on augmentation therapy (AATD + AUG) would have lower circulating and skeletal muscle inflammatory cytokines compared to AATD COPD patients not receiving augmentation therapy (AATD-AUG) and/or the typical non-AATD (COPD) patient. We also hypothesized that cytokine response to exercise would be lower in AATD + AUG compared to AATD-AUG or COPD subjects.
methodsArterial and femoral venous concentration and skeletal muscle expression of TNFα, IL-6, IL-1β and CRP were measured at rest, during and up to 4-hours after 50% maximal 1-hour knee extensor exercise in all COPD patient groups, including 2 additional groups (i.e. AATD with normal lung function, and healthy age-/activity-matched controls).
resultsCirculating CRP was higher in AATD + AUG (4.7 ± 1.6 mg/dL) and AATD-AUG (3.3 ± 1.2 mg/dL) compared to healthy controls (1.5 ± 0.3 mg/dL, p < 0.05), but lower in AATD compared to non-AATD-COPD patients (6.1 ± 2.6 mg/dL, p < 0.05). TNFα, IL-6 and IL-1β were significantly increased by 1.7-, 1.7-, and 4.7-fold, respectively, in non-AATD COPD compared to AATD COPD (p < 0.05), and 1.3-, 1.7-, and 2.2-fold, respectively, compared to healthy subjects (p < 0.05). Skeletal muscle TNFα was on average 3-4 fold greater in AATD-AUG compared to the other groups (p < 0.05). Exercise showed no effect on these cytokines in any of our patient groups.
conclusionThese data show that AATD COPD patients do not experience the same chronic systemic inflammation and exhibit reduced inflammation compared to non-AATD COPD patients. Augmentation therapy may help to improve muscle efflux of TNFα and reduce muscle TNFα concentration, but showed no effect on IL-6, IL-1β or CRP.
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