title: Human amnion mesenchymal cells inhibit lipopolysaccharide-induced TNF-α and IL-1β production in THP-1 cells.
abstract: BACKGROUND
  Human 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).
  
  
  RESULTS
  The 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.
  
  
  CONCLUSIONS
  Human 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.
authors.affiliation: Institute of Clinical Medical Science, China-Japan Friendship Hospital, 100029, Beijing, China. junyshu@126.com.
authors.forename: Jun
authors.initials: J
authors.lastname: Shu
authors.affiliation: Institute of Basic Research in Clinical Medicine, China Academy of Chinese Medical Sciences, 100700, Beijing, China. hxj19@126.com.
authors.forename: Xiaojuan
authors.initials: X
authors.lastname: He
authors.affiliation: Institute of Clinical Medical Science, China-Japan Friendship Hospital, 100029, Beijing, China. milan_z0210@sina.com.
authors.forename: Lan
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Institute of Clinical Medical Science, China-Japan Friendship Hospital, 100029, Beijing, China. jiefu_001@sina.com.
authors.forename: Hong
authors.initials: H
authors.lastname: Li
authors.affiliation: Institute of Clinical Medical Science, China-Japan Friendship Hospital, 100029, Beijing, China. zryywangping@126.com.
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
authors.affiliation: Institute of Clinical Medical Science, China-Japan Friendship Hospital, 100029, Beijing, China. huangxiaojie2008@sina.com.
authors.forename: Xiaojie
authors.initials: X
authors.lastname: Huang
mesh_terms: D000650:Amnion / Q000166:cytology*; D006801:Humans; D053583:Interleukin-1beta / Q000096:biosynthesis* / Q000187:drug effects; D008070:Lipopolysaccharides / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008264:Macrophages / Q000378:metabolism*; D059630:Mesenchymal Stem Cells / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000187:drug effects
chemical_list: D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha