AI Article Synopsis
- The study investigates the role of brain-derived neurotrophic factor precursor (proBDNF) in the dysfunction of monocytes related to inflammatory diseases, highlighting its effects on human immune responses.
- ProBDNF and the neurotrophic receptor p75 were found to increase in healthy monocytes after exposure to lipopolysaccharide, leading to elevated levels of proinflammatory cytokines like IL-1β, IL-6, and TNF-α.
- In patients with Stanford type-A acute aortic dissection (AAD), proBDNF was specifically upregulated in M2-like monocytes, suggesting its involvement in inflammation, which could be mitigated by a proBDNF antibody.*
Article Abstract
Brain-derived neurotrophic factor precursor (proBDNF) has been reported to strengthen the dysfunction of monocytes/macrophages in animal studies. However, it is still unknown the roles of proBDNF in the dysfunction of monocytes in the inflammatory diseases in humans. In the present study, we showed that proBDNF and pan neurotrophic receptor p75 were significantly upregulated in monocytes from healthy donors (HD) after lipopolysaccharide treatment. Exogenous proBDNF treatment upregulated CD40 and proinflammatory cytokines expression in monocytes including interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. In Stanford type-A acute aortic dissection (AAD) patients, proBDNF was upregulated in CD14 CD163 CX3CR1 M2- but not CD14 CD68 CCR2 M1-like monocytes. In addition, sera from AAD patients activated gene expression of proinflammatory cytokines in cultured PBMCs from HD, which was attenuated by proBDNF monoclonal antibody (Ab-proB) treatment. These findings suggested that upregulation of proBDNF in M2-like monocytes may contribute to the proinflammatory response in the AAD.
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| http://dx.doi.org/10.1096/fj.201901905RR | DOI Listing |
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