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Fig. 2 | Respiratory Research

Fig. 2

From: Recent advances in vitamin D implications in chronic respiratory diseases

Fig. 2

Overview of vitamin D on regulating inflammatory responses in respiratory diseases. Exposure to air pollutants, allergens or pathogens activates epithelial cells and alveolar macrophages releasing cytokines and chemokines. Inhaled smoke irritants increase the production of reactive oxygen species (ROS) and nitric oxide (NO) by epithelial cells. Alveolar macrophages and neutrophils release proteases to degrade the extracellular matrix (ECM) proteins resulting in alveolar wall destruction. Dendritic cells are the link between innate and adaptive immunity, involved in antigen recognition and phagocytosis. Vitamin D reduces the symptoms of caused by these irritants and pathogens. PRRs pathogen recognition receptors, TLRs Toll-like receptors, NLR nucleotide-binding oligomerization domain (NOD)-like receptors, ACE2 angiotensin-converting enzyme 2, TCR T-cell receptor, MHC II major histocompatibility complex class II, CD co-stimulatory domain, IL interleukin, Th- T helper cells, TNF-α tumor necrosis factor alpha, IFN interferon, IgE immunoglobin E, NK natural killer cell, EMT Epithelial-mesenchymal transition, COPD chronic obstructive pulmonary disease, ALI/ARDS acute lung injury/acute respiratory distress syndrome, − /  + vitamin D, inhibitory/beneficial effect

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