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Asthma
Original research
Effect of obesity on airway and systemic inflammation in adults with asthma: a systematic review and meta-analysis
  1. Hayley A Scott1,2,
  2. Shawn HM Ng3,
  3. Rebecca F McLoughlin4,5,6,
  4. Sarah R Valkenborghs1,7,
  5. Parameswaran Nair8,
  6. Alexandra C Brown1,2,
  7. Olivia R Carroll1,2,
  8. Jay C Horvat1,2,
  9. Lisa G Wood1,2
  1. 1 School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, New South Wales, Australia
  2. 2 Immune Health Research Program, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
  3. 3 School of Medicine and Public Health, The University of Newcastle, Callaghan, New South Wales, Australia
  4. 4 School of Nursing and Midwifery, The University of Newcastle, Callaghan, New South Wales, Australia
  5. 5 National Health and Medical Research Council, Centre of Excellence in Treatable Traits, New Lambton Heights, New South Wales, Australia
  6. 6 Asthma and Breathing Research Program, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
  7. 7 Active Living Research Program, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
  8. 8 Division of Respirology, McMaster University and St Joseph's Healthcare, Hamilton, Ontario, Canada
  1. Correspondence to Dr Hayley A Scott, School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia; hayley.scott{at}newcastle.edu.au

Abstract

Background Obesity is associated with more severe asthma, however, the mechanisms responsible are poorly understood. Obesity is also associated with low-grade systemic inflammation; it is possible that this inflammation extends to the airways of adults with asthma, contributing to worse asthma outcomes. Accordingly, the aim of this review was to examine whether obesity is associated with increased airway and systemic inflammation and adipokines, in adults with asthma.

Methods Medline, Embase, CINAHL, Scopus and Current Contents were searched till 11 August 2021. Studies reporting measures of airway inflammation, systemic inflammation and/or adipokines in obese versus non-obese adults with asthma were assessed. We conducted random effects meta-analyses. We assessed heterogeneity using the I2 statistic and publication bias using funnel plots.

Results We included 40 studies in the meta-analysis. Sputum neutrophils were 5% higher in obese versus non-obese asthmatics (mean difference (MD)=5.0%, 95% CI: 1.2 to 8.9, n=2297, p=0.01, I2=42%). Blood neutrophil count was also higher in obesity. There was no difference in sputum %eosinophils; however, bronchial submucosal eosinophil count (standardised mean difference (SMD)=0.58, 95% CI=0.25 to 0.91, p<0.001, n=181, I2=0%) and sputum interleukin 5 (IL-5) (SMD=0.46, 95% CI=0.17 to 0.75, p<0.002, n=198, I2=0%) were higher in obesity. Conversely, fractional exhaled nitric oxide was 4.5 ppb lower in obesity (MD=−4.5 ppb, 95% CI=−7.1 ppb to −1.8 ppb, p<0.001, n=2601, I2=40%). Blood C reactive protein, IL-6 and leptin were also higher in obesity.

Conclusions Obese asthmatics have a different pattern of inflammation to non-obese asthmatics. Mechanistic studies examining the pattern of inflammation in obese asthmatics are warranted. Studies should also investigate the clinical relevance of this altered inflammatory response.

PROSPERO registeration number CRD42021254525.

  • asthma
  • pulmonary eosinophilia
  • neutrophil Biology

Data availability statement

Data are available upon reasonable request. The data that support the findings of this systematic review and meta-analysis are available from the corresponding author, HAS, upon reasonable request.

http://dx.doi.org/10.1136/thorax-2022-219268

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    Data availability statement

    Data are available upon reasonable request. The data that support the findings of this systematic review and meta-analysis are available from the corresponding author, HAS, upon reasonable request.

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    Footnotes

    • Twitter @DrHayleyScott

    • Contributors HAS and LGW conceived and designed the study. HAS, SHMN, RFM and LGW contributed to data acquisition, quality assessment and planning of the statistical analysis. HAS and SRV conducted the statistical analysis and assessed for compliance with reporting guidelines. HAS, PN, ACB, ORC and JCH wrote the first draft of the manuscript. All authors contributed to revision of the intellectual content of the manuscript and approved the final version for publication. HAS is the guarantor.

    • Funding This research was supported by a Thoracic Society of Australia and New Zealand (TSANZ)/National Asthma Council Australia Asthma and Airways Career Development Fellowship and a TSANZ/Astra-Zeneca Mid-Career Research Fellowship. PN is supported by the Frederick E. Hargreave Teva Innovation Chair in Airway Diseases.

    • Competing interests PN reports grants and personal fees from AZ, grants and personal fees from Teva, grants from Sanofi, personal fees from Equillium, grants from Foresee, personal fees from Arrowhead Pharma, grants from Cyclomedica, personal fees from GSK, outside the submitted work. LGW reports an Honorarium from Sanofi.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.