Cytokine production capabilities of human primary monocyte-derived macrophages from patients with diabetes mellitus type 2 with and without diabetic peripheral neuropathy

摘要: Introduction Monocytes from patients with diabetes mellitus type 2 (DM2) are dysfunctional, persistently primed, and prone to a proinflammatory phenotype. This may alter the phenotype of their differentiation macrophages result in diabetic peripheral neuropathy (DPN), nerve damage, sensitization, chronic pain. We have previously demonstrated that CD163 is molecule promotes an anti-inflammatory cellular human primary macrophages, but this has not been proven DM2 or DPN. Thus, we hypothesize DPN display altered functional related cytokine production induction expression will promote more homeostatic by reducing responsiveness. Patients methods tested these hypotheses vitro using blood monocyte-derived healthy subjects without Cells were incubated presence absence 5 µg/mL lipopolysaccharide (LPS). The concentrations interleukin-10, interleukin-6, tumor necrosis factor-alpha (TNF-α), TGF-β, monocyte chemoattractant protein-1 (MCP-1) measured ELISA assays. Macrophages transfected empty vector plasmid containing gene mannosylated polyethylenimine nanoparticles. Results Our results show nonstimulated constitutive primed state deficient cytokines upon challenge when compared macrophages. produced control group, effect was partial Conclusion suggest adopt complex only partially reversed induction. Future experiments focused on elucidating differential responsiveness between