R Furugen1, H Hayashida, T Saito. 1. Department of Oral Health, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Abstract
OBJECTIVES: It was reported that periodontitis is associated with increased serum resistin levels. We examined whether there was a difference between the release of resistin from neutrophils incubated lipopolysaccharide (LPS) from Porphyromonas gingivalis and with LPS from Escherichia coli, and which cell-surface receptors and intracellular kinases were involved in this process. METHODS: Several concentrations of P. gingivalis-LPS and E. coli-LPS were added to neutrophils, supernatant from cultured neutrophils was collected, and resistin levels were measured by ELISA. To examine signaling pathways, neutrophils were pretreated with monoclonal antibodies against CD14, CD18, TLR2, and TLR4, and specific inhibitors of PI3K and MAPKs. RESULTS: Resistin release from neutrophils was induced both by P. gingivalis-LPS and E. coli-LPS, but resistin release by P. gingivalis-LPS was weaker than E. coli-LPS in low concentrations. Resistin release was decreased by pretreatment with monoclonal antibodies against CD14, CD18, and TLR4, but not by TLR2. Moreover, it was decreased by inhibitors of PI3K, JNK, and p38 MAPK, but not by ERK1/2. CONCLUSIONS: Resistin release from neutrophils was induced by both P. gingivalis-LPS and E. coli-LPS. This was decreased by CD14, CD18, and TLR4 and was dependent on PI3K, JNK, and p38 MAPK, but not on ERK1/2 in intracellular pathways of neutrophils.
OBJECTIVES: It was reported that periodontitis is associated with increased serum resistin levels. We examined whether there was a difference between the release of resistin from neutrophils incubated lipopolysaccharide (LPS) from Porphyromonas gingivalis and with LPS from Escherichia coli, and which cell-surface receptors and intracellular kinases were involved in this process. METHODS: Several concentrations of P. gingivalis-LPS and E. coli-LPS were added to neutrophils, supernatant from cultured neutrophils was collected, and resistin levels were measured by ELISA. To examine signaling pathways, neutrophils were pretreated with monoclonal antibodies against CD14, CD18, TLR2, and TLR4, and specific inhibitors of PI3K and MAPKs. RESULTS: Resistin release from neutrophils was induced both by P. gingivalis-LPS and E. coli-LPS, but resistin release by P. gingivalis-LPS was weaker than E. coli-LPS in low concentrations. Resistin release was decreased by pretreatment with monoclonal antibodies against CD14, CD18, and TLR4, but not by TLR2. Moreover, it was decreased by inhibitors of PI3K, JNK, and p38 MAPK, but not by ERK1/2. CONCLUSIONS: Resistin release from neutrophils was induced by both P. gingivalis-LPS and E. coli-LPS. This was decreased by CD14, CD18, and TLR4 and was dependent on PI3K, JNK, and p38 MAPK, but not on ERK1/2 in intracellular pathways of neutrophils.
Authors: Christina Warinner; João F Matias Rodrigues; Rounak Vyas; Christian Trachsel; Natallia Shved; Jonas Grossmann; Anita Radini; Y Hancock; Raul Y Tito; Sarah Fiddyment; Camilla Speller; Jessica Hendy; Sophy Charlton; Hans Ulrich Luder; Domingo C Salazar-García; Elisabeth Eppler; Roger Seiler; Lars H Hansen; José Alfredo Samaniego Castruita; Simon Barkow-Oesterreicher; Kai Yik Teoh; Christian D Kelstrup; Jesper V Olsen; Paolo Nanni; Toshihisa Kawai; Eske Willerslev; Christian von Mering; Cecil M Lewis; Matthew J Collins; M Thomas P Gilbert; Frank Rühli; Enrico Cappellini Journal: Nat Genet Date: 2014-02-23 Impact factor: 38.330
Authors: Johanna Snäll; Anna Linnér; Julia Uhlmann; Nikolai Siemens; Heike Ibold; Marton Janos; Adam Linder; Bernd Kreikemeyer; Heiko Herwald; Linda Johansson; Anna Norrby-Teglund Journal: Sci Rep Date: 2016-02-18 Impact factor: 4.379