Autoimmunity and COPD: Clinical Implications

Gaetano Caramori, Paolo Ruggeri, Antonino Di Stefano, Sharon Mumby, Giuseppe Girbino, Ian M Adcock, Paul Kirkham

Research output: Contribution to journalReview article

Abstract

COPD is a leading cause of morbidity and mortality worldwide. Long-term cigarette smoking is the cause of > 90% of COPD cases in Westernized countries. However, only a fraction of chronic heavy smokers develop symptomatic COPD by age 80. COPD is characterized by an abnormal immune response in the lower airways, and its progression is associated with infiltration of the lung by innate and adaptive inflammatory immune cells that form lymphoid follicles. There is growing evidence that both cellular- and antibody-mediated autoimmunity has a fundamental role in the pathogenesis of stable COPD. In particular, carbonyl-modified proteins may help to drive autoimmunity in COPD and cause the characteristic small airways abnormalities and even contribute to the pathogenesis of pulmonary emphysema. Although direct, indirect, and circumstantial evidence of a role for autoimmunity in stable patients with COPD has been identified, no cause-and-effect relationship between autoimmunity and the mechanisms of COPD has been firmly established in man. As such, the potential contribution of an autoimmune response to the pathogenesis of COPD exacerbation is still being investigated and represents an area of active research. Many drugs targeting autoimmune responses are already available, and the results of controlled clinical trials are awaited with great interest. The potential for measuring specific serum autoantibodies as biomarkers to predict clinical phenotypes or progression of stable COPD is promising.

Original languageEnglish
Pages (from-to)1424-1431
Number of pages8
JournalChest
Volume153
Issue number6
DOIs
Publication statusPublished - Jun 2018

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Autoimmunity
Chronic Obstructive Pulmonary Disease
Pulmonary Emphysema
Controlled Clinical Trials
Drug Delivery Systems
Autoantibodies
Biomarkers
Smoking
Lymphocytes
Morbidity
Phenotype
Lung
Mortality
Antibodies
Serum

Cite this

Caramori, G., Ruggeri, P., Di Stefano, A., Mumby, S., Girbino, G., Adcock, I. M., & Kirkham, P. (2018). Autoimmunity and COPD: Clinical Implications. Chest, 153(6), 1424-1431. https://doi.org/10.1016/j.chest.2017.10.033

Autoimmunity and COPD : Clinical Implications. / Caramori, Gaetano; Ruggeri, Paolo; Di Stefano, Antonino; Mumby, Sharon; Girbino, Giuseppe; Adcock, Ian M; Kirkham, Paul.

In: Chest, Vol. 153, No. 6, 06.2018, p. 1424-1431.

Research output: Contribution to journalReview article

Caramori, G, Ruggeri, P, Di Stefano, A, Mumby, S, Girbino, G, Adcock, IM & Kirkham, P 2018, 'Autoimmunity and COPD: Clinical Implications', Chest, vol. 153, no. 6, pp. 1424-1431. https://doi.org/10.1016/j.chest.2017.10.033
Caramori G, Ruggeri P, Di Stefano A, Mumby S, Girbino G, Adcock IM et al. Autoimmunity and COPD: Clinical Implications. Chest. 2018 Jun;153(6):1424-1431. https://doi.org/10.1016/j.chest.2017.10.033
Caramori, Gaetano ; Ruggeri, Paolo ; Di Stefano, Antonino ; Mumby, Sharon ; Girbino, Giuseppe ; Adcock, Ian M ; Kirkham, Paul. / Autoimmunity and COPD : Clinical Implications. In: Chest. 2018 ; Vol. 153, No. 6. pp. 1424-1431.
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AU - Ruggeri, Paolo

AU - Di Stefano, Antonino

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AU - Girbino, Giuseppe

AU - Adcock, Ian M

AU - Kirkham, Paul

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N2 - COPD is a leading cause of morbidity and mortality worldwide. Long-term cigarette smoking is the cause of > 90% of COPD cases in Westernized countries. However, only a fraction of chronic heavy smokers develop symptomatic COPD by age 80. COPD is characterized by an abnormal immune response in the lower airways, and its progression is associated with infiltration of the lung by innate and adaptive inflammatory immune cells that form lymphoid follicles. There is growing evidence that both cellular- and antibody-mediated autoimmunity has a fundamental role in the pathogenesis of stable COPD. In particular, carbonyl-modified proteins may help to drive autoimmunity in COPD and cause the characteristic small airways abnormalities and even contribute to the pathogenesis of pulmonary emphysema. Although direct, indirect, and circumstantial evidence of a role for autoimmunity in stable patients with COPD has been identified, no cause-and-effect relationship between autoimmunity and the mechanisms of COPD has been firmly established in man. As such, the potential contribution of an autoimmune response to the pathogenesis of COPD exacerbation is still being investigated and represents an area of active research. Many drugs targeting autoimmune responses are already available, and the results of controlled clinical trials are awaited with great interest. The potential for measuring specific serum autoantibodies as biomarkers to predict clinical phenotypes or progression of stable COPD is promising.

AB - COPD is a leading cause of morbidity and mortality worldwide. Long-term cigarette smoking is the cause of > 90% of COPD cases in Westernized countries. However, only a fraction of chronic heavy smokers develop symptomatic COPD by age 80. COPD is characterized by an abnormal immune response in the lower airways, and its progression is associated with infiltration of the lung by innate and adaptive inflammatory immune cells that form lymphoid follicles. There is growing evidence that both cellular- and antibody-mediated autoimmunity has a fundamental role in the pathogenesis of stable COPD. In particular, carbonyl-modified proteins may help to drive autoimmunity in COPD and cause the characteristic small airways abnormalities and even contribute to the pathogenesis of pulmonary emphysema. Although direct, indirect, and circumstantial evidence of a role for autoimmunity in stable patients with COPD has been identified, no cause-and-effect relationship between autoimmunity and the mechanisms of COPD has been firmly established in man. As such, the potential contribution of an autoimmune response to the pathogenesis of COPD exacerbation is still being investigated and represents an area of active research. Many drugs targeting autoimmune responses are already available, and the results of controlled clinical trials are awaited with great interest. The potential for measuring specific serum autoantibodies as biomarkers to predict clinical phenotypes or progression of stable COPD is promising.

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