• Jun Chen, Luqi Dai, Tao Wang, Junyun He, Yashu Wang, and Fuqiang Wen.
• Division of Pulmonary Diseases, State Key Laboratory of Biotherapy, West China Hospital, West China School of Medicine, Sichuan University , Chengdu , China.
• Ann. Med. 2019 Aug 1; 51 (5-6): 314-329.

AbstractIntroduction: C-X-C motif chemokine 5 is primarily chemotactic for neutrophils and previously shown to increase in the bronchoalveolar lavage fluid of patients with chronic obstructive pulmonary disease. However, whether C-X-C motif chemokine 5 levels correlate with lung function decline in patients or mouse model of chronic obstructive pulmonary disease was not clear. Methods: The mouse model was induced by cigarette smoke exposure. Plasma/serum and bronchoalveolar lavage fluid were obtained from patients and mouse model of chronic obstructive pulmonary disease; C-X-C motif chemokine 5 levels were assessed and correlated with lung functions and granulocyte-colony stimulating factor levels, respectively. Results: The C-X-C motif chemokine 5 levels increased and correlated to granulocyte-colony stimulating factor levels in both plasma/serum and bronchoalveolar lavage fluid obtained from patients and mouse model of chronic obstructive pulmonary disease. Circulating levels of C-X-C motif chemokine 5 correlated to lung functions decline in patients and mouse model. Conclusions: Granulocyte-colony stimulating factor might coordinate with C-X-C motif chemokine 5 in the pathogenesis of neutrophilic inflammation in chronic obstructive pulmonary disease. Circulating C-X-C motif chemokine 5 might serve as a potential blood-based biomarker to add additional modest predictive value on the preliminary screening and diagnosis of chronic obstructive pulmonary disease. Key messages Circulating C-X-C motif chemokine 5 might serve as a potential blood-based biomarker to add additional modest predictive value on the preliminary screening and diagnosis of COPD. Granulocyte-colony stimulating factor might coordinate with C-X-C motif chemokine 5 in the pathogenesis of neutrophilic inflammation in chronic obstructive pulmonary disease.

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