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Level of serum IL-33 and emphysema paraseptal in clove cigarette smoker with spontaneous pneumothorax: A case report

A young male clove cigarette smoker experienced spontaneous pneumothorax and later paraseptal emphysema was detected on high-resolution computed tomography (HRCT) scan without respiratory symptoms. Smoking is a known risk factor for emphysema. Paraseptal emphysema is a type of emphysema that rarely...

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Detalles Bibliográficos
Autores principales: Koesoemoprodjo, Winariani, Maranatha, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7300223/
https://www.ncbi.nlm.nih.gov/pubmed/32577372
http://dx.doi.org/10.1016/j.rmcr.2020.101133
Descripción
Sumario:A young male clove cigarette smoker experienced spontaneous pneumothorax and later paraseptal emphysema was detected on high-resolution computed tomography (HRCT) scan without respiratory symptoms. Smoking is a known risk factor for emphysema. Paraseptal emphysema is a type of emphysema that rarely causes respiratory symptoms, nevertheless, usually accompanied by spontaneous pneumothorax. Interleukin 33 (IL-33) is an alarmin cytokine that belongs to the IL-1 family. The effects of IL-33 depend on its structure. In its mature form, it is a cytokine alarmin that binds to ST2 (suppression of tumorigenicity) receptors on the surface of macrophages and innate immune cells to drive Th1/Th2 immune responses, causing oxidative stress, and increased IL-33 production causes polarization of alveolar macrophages to an M2 phenotype. In this study, long-term exposure to clove cigarette smoke caused an increased serum level of IL-33 (43.72 pg/mL) and paucigranulocytic airway inflammation. In paucigranulocytic inflammation, IL-33 is involved in lung parenchymal damage presumably through oxidative stress, activation of alveolar macrophage and increased MMP12 secretion, resulting in alveolar destruction and airspace enlargement.