Human amnion mesenchymal cells inhibit lipopolysaccharide-induced TNF-α and IL-1β production in THP-1 cells

Abstract

BackgroundHuman amnion mesenchymal cells (hAMCs), isolated from the amniotic membrane of human placenta, are a unique population of mesenchymal stem cells. Recent studies demonstrated that hAMCs could inhibit the activities and functions of several immune cells. However, their effect on inflammatory macrophages is largely unknown. This study investigated the effect of hAMCs on expression of inflammatory cytokines and mitogen-activated protein kinases (MAPKs)/NF-κB pathway in human THP-1 macrophages induced by lipopolysaccharide (LPS).ResultsThe levels of TNF-α and IL-1β secreted by LPS- stimulated THP-1 cells were increased significantly compared with those in the control group. After co-culture with different numbers of hAMCs, the levels of TNF-α and IL-1β in LPS-stimulated THP-1 cells were significantly reduced compared with the LPS group. The mRNA expression of TNF-α and IL-1β were also markedly inhibited. Moreover, treating LPS-stimulated THP-1 cells with hAMCs supernatants could also suppress TNF-α and IL-1β production in THP-1 cells. Important signaling pathways involved in the production of TNF-α and IL-1β were affected by hAMCs co-culture: hAMCs remarkably suppressed NF-κB activation and down-regulated the phosphorylation of ERK and JNK in LPS- stimulated THP-1 cells.ConclusionsHuman amnion mesenchymal cells inhibited the production of TNF-α and IL-1β secreted by LPS-stimulated THP-1 cells, partly through the suppression of NF-κB activation and ERK and JNK phosphorylation.

Differential Effector Response of Amnion‐ and Adipose‐Derived Mesenchymal Stem Cells to Inflammation; Implications for Intradiscal Therapy

“…Mechanistically, it has been shown that IL‐10 inhibits nuclear factor‐κβ (NF‐κβ) signaling by preserving IκBα thus preventing nuclear translocation of NF‐κβ in addition to preventing DNA binding . Others have shown that AM‐MSCs inhibit IL‐1β and TNF‐α production by suppressing NF‐κβ activation and extracellular signal‐regulated kinase and c‐JUN N‐terminal kinase phosphorylation . Thus, it is possible that differences in intracellular NF‐κβ signaling, which could be due to differences in sensitivity to inflammatory cytokines between AD‐ and AM‐MSCs, could account for our findings herein, however further studies are required.…”

“…31 Others have shown that AM-MSCs inhibit IL-1β and TNF-α production by suppressing NF-κβ activation and extracellular signal-regulated kinase and c-JUN N-terminal kinase phosphorylation. 32 Thus, it is possible that differences in intracellular NF-κβ signaling, which could be due to differences in sensitivity to inflammatory cytokines between JOURNAL OF ORTHOPAEDIC RESEARCH ® NOVEMBER 2019 Another key difference observed comparing MSC types was that the presence of inflammation detrimentally impacted chondrogenesis of AD-MSCs to a greater extent compared with AM-MSCs. It is well established that the presence of TNF-α and/or IL-1β impairs chondrogenesis of MSCs.…”

Construction of a lentiviral vector containing shRNA targeting ADAM17 and its role in attenuating endotoxemia in mice

“…Inflammatory cells, including activated neutrophils and granulocytes, may exert an important role in the pathophysiological processes of SIRS ( 7 , 8 ). In addition, tumor necrosis factor-α (TNF-α) is an important inflammatory mediator released from cells stimulated by LPS ( 9 ). TNF-α is additionally hypothesized to be an important contributor to SIRS, as it appears early, peaks rapidly and exhibits numerous host functions ( 10 ).…”

Experimental study of tendon sheath repair via decellularized amnion to prevent tendon adhesion

“…The experimental results suggested that decellularized amniotic membrane has anti-inflammatory and anti-adhesive effects. The amniotic membrane by expression of interleukin-1 receptor antagonist (IL-1 Ra) reduced inflammation caused by IL-1, upregulated the release of IL-4, IL-10, matrix metalloproteinase inhibitors, and other active substances to enhance the capability to resist tissue inflammation, and promoted tissue cell repair and anti-scar effect in the injured region[ 25 – 30 ].…”