title: Surfactant protein A is expressed in the central nervous system of rats with experimental autoimmune encephalomyelitis, and suppresses inflammation in human astrocytes and microglia.
abstract: The collectin surfactant protein‑A (SP‑A), a potent host defense molecule, is well recognized for its role in the maintenance of pulmonary homeostasis and the modulation of inflammatory responses. While previous studies have detected SP‑A in numerous extrapulmonary tissues, there is still a lack of information regarding its expression in central nervous system (CNS) and potential effects in neuroinflammatory diseases, such as multiple sclerosis (MS). The present study used experimental autoimmune encephalomyelitis (EAE), the most commonly used animal model of MS, to investigate the expression of SP‑A in the CNS at different stages of disease progression. In addition, in vitro experiments with lipopolysaccharide (LPS)‑stimulated human astrocytes and microglia were performed to investigate the potential role of SP‑A in the modulation of CNS inflammatory responses. The results of the present study demonstrated widespread distribution of SP‑A in the rat CNS, and also identified specific expression patterns of SP‑A at different stages of EAE. In vitro, the current study revealed that treatment of human astrocytes and microglia with LPS promoted SP‑A expression in a dose‑dependent manner. Furthermore, exogenous SP‑A protein significantly decreased Toll‑like receptor 4 and nuclear factor‑κB expression, and reduced interleukin‑1β and tumor necrosis factor‑α levels. The results of the current study indicate a potential role for SP‑A in the modulation of CNS inflammatory responses.
authors.affiliation: Department of Neurology, Shengjing Hospital, Affiliated Hospital of China Medical University. Shenyang, Liaoning 110004, P.R. China.
authors.forename: Xue
authors.initials: X
authors.lastname: Yang
authors.affiliation: Department of Neurology, Shengjing Hospital, Affiliated Hospital of China Medical University. Shenyang, Liaoning 110004, P.R. China.
authors.forename: Jun
authors.initials: J
authors.lastname: Yan
authors.affiliation: Department of Neurology, Shengjing Hospital, Affiliated Hospital of China Medical University. Shenyang, Liaoning 110004, P.R. China.
authors.forename: Juan
authors.initials: J
authors.lastname: Feng
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000276:immunology / Q000378:metabolism*; D015415:Biomarkers; D039481:CD11b Antigen / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000235:genetics* / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005455:Fluorescent Antibody Technique; D015870:Gene Expression; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators; D008070:Lipopolysaccharides / Q000276:immunology; D017628:Microglia / Q000276:immunology / Q000378:metabolism*; D037662:Pulmonary Surfactant-Associated Protein A / Q000235:genetics* / Q000378:metabolism; D051381:Rats
chemical_list: D015415:Biomarkers; D039481:CD11b Antigen; D016207:Cytokines; C000614142:Gfap protein, rat; D005904:Glial Fibrillary Acidic Protein; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D037662:Pulmonary Surfactant-Associated Protein A