Responsiveness to pulmonary rehabilitation in people with COPD is associated with changes in microbiota

Abstract

Abstract Rationale: Pulmonary Rehabilitation (PR) is one of the most cost-effective therapies for chronic obstructive pulmonary disease (COPD) management. There are, however, people who do not respond to PR and reasons for non-response are mostly unknown. PR is likely to change the airway microbiota and this could play a role in its responsiveness. Objectives: In this study we have explored the association between PR effectiveness and specific alterations in oral microbiota and inflammation. Methods: A prospective longitudinal study was conducted. Data on exercise capacity, dyspnoea, impact of disease and 418 saliva samples were collected from 76 patients, half of whom participated in a 12-weeks PR programme. Responders and non-responders to PR (dyspnoea, exercise-capacity and impact of disease) were defined based on minimal clinically important differences. Measurements and Main Results: Changes in microbiota, including Prevotella melaninogenica and Streptococcus were observed upon PR. Prevotella, previously found to be depleted in severe COPD, increased during the first month of PR in responders. This increase was negatively correlated with Streptoccus and Lautropia, known to be enriched in severe cases of COPD. Simultaneously, an anti-inflammatory commensal of the respiratory tract, Rothia, correlated strongly and negatively with several pro-inflammatory markers, whose levels were generally boosted by PR. Conversely, in non-responders, the observed decline in Prevotella correlated negatively with Streptococcus and Lautropia whose fluctuations co-occurred with several pro-inflammatory markers. Conclusions: PR is associated with changes in oral microbiota. Consistent patterns of bacteria/pro-inflammatory markers among responders and non-responders were unraveled, which may contribute to explain the success of PR.

Competing Interest Statement

The authors have declared no competing interest.

Clinical Protocols

https://pubmed.ncbi.nlm.nih.gov/31151409/

Funding Statement

This study is integrated in PRIME, Pulmonary Rehabilitation and microbiota in exacerbations of COPD GENIAL, Genetic and Clinical markers of COPD trajectory and MicroAgeing, The role of microbiota in ageing, funded by Programa Operacional de Competitividade e Internacionalizacao, COMPETE, through Fundo Europeu de Desenvolvimento Regional - FEDER (POCI-010145-FEDER-028806 and POCI-01-0145-FEDER-007628), Fundacao para a Ciencia e Tecnologia - FCT (PTDC/DTP-PIC/2284/2014, PTDC/SAU-SER/28806/2017 and PTDC/BIA-EVL/30212/2017) and under the project UIDB/04501/2020. S. Melo-Dias was supported by Grant SFRH/BD/140908/2018 from FCT. A. Sousa was funded from national funds through FCT, Fundacao para a Ciencia e a Tecnologia, I.P., under the Scientific Employment Stimulus - Institutional Call - reference CEECINST/00026/2018.

Author Declarations

I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained.

Yes

The details of the IRB/oversight body that provided approval or exemption for the research described are given below:

A cross-sectional study was conducted. Ethical approvals were obtained from Administracao Regional de Saude Centro (64/2016) and from Centro Hospitalar do Baixo Vouga (08-03-17). Written informed consent was obtained from all participants.

I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals.

Yes

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Data Availability

The dataset supporting the conclusions of this article is included within the article (and its additional file(s)). Furthermore, raw sequencing data was deposited in National Centre for Biotechnology Informations (NCBI) Sequence Read Archive (SRA) (BioProject PRJNA872131).

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