Abstract
Different families of endogenous lectins use complementary defense strategies against pathogens. They may recognize non-self glycans typically found on pathogens and/or host glycans. The collectin and galectin families are prominent examples of these two lectin categories. Collectins are C-type lectins that contain a carbohydrate recognition domain and a collagen-like domain. Members of this group include surfactant protein A (SP-A) and D (SP-D), secreted by the alveolar epithelium to the alveolar fluid. Lung collectins bind to several microorganisms, which results in pathogen aggregation and/or killing, and enhances phagocytosis of pathogens by alveolar macrophages. Moreover, SP-A and SP-D influence macrophage responses, contributing to resolution of inflammation, and SP-A is essential for tissue-repair functions of macrophages. Galectins also function by interacting directly with pathogens or by modulating the immune system in response to the infection. Direct binding may result in enhanced or impaired infection of target cells, or can have microbicidal effects. Immunomodulatory effects of galectins include recruitment of immune cells to the site of infection, promotion of neutrophil function, and stimulation of the bactericidal activity of infected macrophages. Moreover, intracellular galectins can serve as danger receptors, promoting autophagy of the invading pathogen. This review will focus on the role of collectins and galectins in pathogen clearance and immune response activation in infectious diseases of the respiratory system.
Highlights
Host defense in the lung is exceptionally, if not uniquely, challenging
In this review we focus on the role of lung soluble collagenous C-type lectins (SP-A and SP-D) and galectins
Lung collectins enhance the clearance of pathogens by four different mechanisms: (i) By aggregating pathogens to which they bind, which hinders their entry into epithelial cells and facilitates their removal, either by mucociliary clearance or by phagocytosis by aMΦs and recruited neutrophils [7, 8, 30, 31, 34]. (ii) By binding to neutrophil extracellular traps (NET)-DNA and to bacteria simultaneously, thereby promoting bacterial trapping by the NETs [35]. (iii) By enhancing phagocytosis of IgG-opsonized particles [36] and complement-coated particles [36, 37]. (iv) By up-regulating expression of cell-surface receptors involved in microbial recognition, such as mannose receptor [38] and scavenger receptor SR-AI/II [39]
Summary
Host defense in the lung is exceptionally, if not uniquely, challenging. The alveolar boundary is clearly the most vulnerable body interface. The review describes biochemical and structural aspects of lung collectins and their role in antimicrobial immunity and alveolar immune homeostasis, and the involvement of galectins in the response to respiratory infectious diseases, including expression, binding to pathogens, modulatory effects on immune cells, and intracellular functions. Lung collectins enhance the clearance of pathogens by four different mechanisms: (i) By aggregating pathogens to which they bind, which hinders their entry into epithelial cells and facilitates their removal, either by mucociliary clearance or by phagocytosis by aMΦs and recruited neutrophils [7, 8, 30, 31, 34].
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