Abstract

IntroductionWithin the pathogenesis of the chronic obstructive pulmonary disease (COPD) there are interactions between different inflammatory mediators that are enhanced during an exacerbation. Arginase is present in bronchial epithelial cells, endothelial, fibroblasts and alveolar macrophages, which make it a probable key enzyme in the regulation of inflammation and remodelling. We aimed to find a potential relationship between arginase activity, inflammatory mediators in COPD patients in stable phase and during exacerbations.MethodsWe performed a prospective, observational study of cases and controls, with 4 study groups (healthy controls, stable COPD, COPD during an exacerbation and COPD 3 months after exacerbation). We measured arginase, inflammation markers (IL-6, IL-8, TNF-∝, IFN-γ and C reactive protein), and mediators of immunity: neutrophils, monocytes, total TCD3 + lymphocytes (CD3ζ), CD4 + T cells, CD8 + T cells, NK cells.ResultsA total of 49 subjects were recruited, average age of 69.73 years (59.18% male). Arginase activity is elevated during an exacerbation of COPD, and this rise is related to an increase in IL-6 production. The levels of IL-6 and IL-8 remained elevated in patients with COPD at 3 months after hospital exacerbation.We did not find a clear relationship between arginase activity, immunity or with the degree of obstruction in COPD patients.ConclusionsArginase activity is elevated during an exacerbation of COPD, and it could be related to an increase in the production of IL-6. Levels of IL-6, IL-8, and arginase activity remain elevated in patients with COPD at 3 months after hospital exacerbation. Arginase activity could contribute to the development of COPD.

Highlights

  • Within the pathogenesis of the chronic obstructive pulmonary disease (COPD) there are interactions between different inflammatory mediators that are enhanced during an exacerbation

  • Arginase activity is elevated during an exacerbation of COPD, and it could be related to an increase in the production of IL-6

  • Levels of IL-6, IL-8, and arginase activity remain elevated in patients with COPD at 3 months after hospital exacerbation

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Summary

Introduction

Within the pathogenesis of the chronic obstructive pulmonary disease (COPD) there are interactions between different inflammatory mediators that are enhanced during an exacerbation. Arginase is present in bronchial epithelial cells, endothelial, fibroblasts and alveolar macrophages, which make it a probable key enzyme in the regula‐ tion of inflammation and remodelling. We aimed to find a potential relationship between arginase activity, inflamma‐ tory mediators in COPD patients in stable phase and during exacerbations. Patients with stable COPD have elevated serum levels of circulating pro-inflammatory mediators, such as C-reactive protein (CRP), fibrinogen, interleukin (IL)-6, and IL-8 [3], and there is an increase in T lymphocytes in the lung, predominantly CD8+ (cytotoxic) [4]. Th1 cells are responsible for the production of interferon-gamma (IFN-γ), a probable cause of emphysema [5]

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