Introduction

Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and concurrent progressive airflow limitation [1–3]. Patients may experience episodes of exacerbated respiratory symptoms, and the frequency of exacerbations requiring hospitalization increases, resulting in significant social and economic burden and one of the major causes of morbidity and mortality worldwide [4, 5]. The pathogenesis of COPD and exacerbations may be associated with inflammatory cells, including macrophages, neutrophils, and T lymphocytes [6, 7]. These cells are crucial in parenchymal destruction and development of airflow limitation in patients with COPD [8, 9].

Chemokines and their receptors regulate leukocyte adhesion and homing, and these receptors play a critical role in trafficking of leukocytes to sites of injury and inflammation [10]. In fact, the cell surface of T cells, natural killer cells, monocytes, macrophages, lymphocytes, and neutrophils express the C-C chemokine receptor (CCR)1 [11]. Previous studies have shown that elevated blood inflammation cells, chemokine levels, and CCR1 expression are associated with increased risk of exacerbations in patients with COPD [12–16]. However, the critical role of CCR1 in the progression of cigarette smoke-induced chronic inflammation remains unclear. We therefore hypothesize that CCR1 enhances airway inflammation via regulation of Janus kinase/signal transducers and activators of transcription (JAK/STAT)/nuclear factor-κB (NF-κB) signaling.

In this study, we aimed to assess CCR1 expression in peripheral blood and bronchial tissues of patients with COPD and participants who served as controls. Furthermore, we investigated chemokine levels in plasma and correlation with lung function and CCR1 expression. We also aimed to examine the inflammatory responses of MH-S cells that overexpressed or were deficient in CCR1 expression that were treated with cigarette smoke extract (CSE). https://www.aging-us.com/article/103180/text