Chronic obstructive pulmonary disease (COPD), also called chronic bronchitis and emphysema, which is characterized by irreversible airflow obstruction and alveolar destruction. COPD affects more than 400 million people and continues to be the third cause of death worldwide. Risk factors are cigarette smoking and environmental pollutants such as chemicals and dust. Genetic factors are also involved. Some phenotypes of COPD patients have frequent COPD episodes, resulting in a rapid deterioration in lung function and poor outcomes [1]. Inflammation, particularly of the small airways, is characterized by accumulation of inflammatory cells, such as neutrophils, macrophages, and dendritic cells. These cells, along with airway epithelial cells, release reactive oxygen species (ROS), cytokines, chemokines, elastase, and matrix metalloproteinases (MMPs) that are responsible for the pathogenesis of COPD. In α1,6 fucosyltransferase (Fut8) deficient mice, growth retardation and emphysema occur [2]. It was for the first time reported that keratan sulfate (KS) disaccharide, Gal(6-SO-3)-GlcNAc(6-SO-3) (referred to as L4), suppressed IL-12 production in macrophages stimulated with lipopolysaccharides and interferon-γ [3]. The anti-inflammatory effect of L4 was reported in mice models of emphysema [4] through the langerin-macrophage capping protein (CapG) axis [5] represents a potential therapeutic target for the treatment of COPD.