Chronic obstructive pulmonary disease (
COPD), characterized by chronic
inflammation, is a recognized global health crisis.
Sialic acid-binding
immunoglobulin-like
lectin 1 (siglec1 or CD169), mainly expressed in macrophages and dendritic cells, is markedly upregulated after encountering pathogens or under acute/chronic
inflammation conditions. However, it is rarely reported that whether siglec1 plays a role in the development of
COPD. In this study, we found that siglec1 had higher expression in the lungs from
COPD rats and in peripheral blood mononuclear cells (PBMCs) from
COPD patients. Knockdown of siglec1 in vivo and in vitro dramatically decreased pro-inflammatory
cytokines production in pulmonary macrophages and alleviated pulmonary inflammatory responses in
COPD rats as well as inactivated
nuclear factor kappa B (NF-κB) signaling. In addition, we identified a new
microRNA, miR-195-5p, which has never explored in
COPD, was lower expressed in
COPD rats and PBMC of
COPD patients, and could negatively modulate siglec1 expression in macrophages. Moreover, overexpression of miR-195-5p via miR-195-5p mimics in vitro and in vivo could significantly alleviate pro-inflammatory
cytokines production in pulmonary macrophages and pulmonary inflammatory responses in
COPD rats. Together, our findings suggested that miR-195-5p inhibited the development of
COPD via targeting siglec1, which might become a therapeutic target to improve
COPD.