Pretreatment of macrophages with low-dose endotoxin (LPSp) profoundly alters cytokine release in response to subsequent LPSa activation. These qualitative and quantitative alterations in cytokine release have been termed macrophage reprogramming. Macrophage activation by LPS is thought to occur via a mechanism involving an early protein tyrosine kinase (PTK) phosphorylation step. PTK inhibition with genistein or herbimycin A blocks LPSa-stimulated secretion of tumor necrosis factor (TNF) and interleukin-1 (IL-1). In this study we investigated whether a PTK pathway participates in LPSp pretreatment reprogramming. We show that LPSp pretreatment inhibited TNF and augmented IL-1 release in response to subsequent LPSa stimulation. Blockade of PTK activation pathways during the interval when macrophages were exposed to LPSp prevented mitogen-activated protein kinase phosphorylation, as well as LPSp-stimulated release of TNF and IL-1, but did not block LPSp reprogramming effects. We conclude that LPSp pretreatment reprogramming of macrophage cytokine production does not require PTK activation.
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http://dx.doi.org/10.1002/jlb.61.1.88 | DOI Listing |
Anticancer Res
July 2017
Department of Integrated and Holistic Immunology, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Background/aim: Recent studies reported that lipopolysaccharide (LPS) exhibits beneficial effects on prevention of immune-related diseases by activating macrophages. We previously demonstrated that pre-treatment with LPS derived from Pantoea agglomerans (LPSp) activated amyloid β (Aβ) phagocytosis in mouse primary microglia. In the present study, we further examined the promotory effect on phagocytosis of phagocytic particles in the C8-B4 microglia cell line.
View Article and Find Full Text PDFAnticancer Res
July 2016
Department of Integrated and Holistic Immunology, Faculty of Medicine, Kagawa University, Miki-cho, Kagawa, Japan Control of Innate Immunity, Technology Research Association, Kagawa, Japan Research Institute for Healthy Living, Niigata University of Pharmacy and Applied Life Sciences, Niigata, Japan.
Background/aim: Monophosphoryl lipid A, lipopolysaccharide (LPS)-derived Toll-like receptor (TLR) 4 agonist, has been shown to be effective in the prevention of Alzheimer's disease (AD) by enhancing phagocytosis of amyloid β (Aβ) by brain microglia. Our recent study demonstrated that oral administration of LPS derived from Pantoea agglomerans (LPSp) activates peritoneal macrophages and enhances the phagocytic activity via TLR4 signaling pathway; however, the effect of LPSp on Aβ phagocytosis in microglia is still unknown.
Materials And Methods: Primary microglial cells were isolated from adult mouse brain by enzymatic digestion, following myelin removal and magnetic separation of cluster of differentiation (CD) 11b.
Am J Surg
July 2008
Department of Surgical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Background: The finding of a solid or cystic mass in the pancreas is becoming more common secondary to the increasing use of cross-sectional imaging and the improved sensitivity of such studies for the detection of pancreatic abnormalities. Because of the aggressive natural history of pancreatic cancer, this has caused concern that all pancreatic abnormalities may be cancer as well as confusion over proper diagnostic and treatment algorithms. This review provides an overview of the natural history, diagnostic considerations, and treatment recommendations for the less common tumors of the pancreas which can be misinterpreted as pancreatic cancer including: solid pseudopapillary tumors (SPT), acinar cell carcinoma (ACC), lymphoplasmacytic sclerosing pancreatitis (LPSP), primary pancreatic lymphoma (PPL), and metastatic renal cell carcinoma to the pancreas.
View Article and Find Full Text PDFShock
August 2000
Department of Surgery, Hennepin County Medical Center, University of Minnesota, Minneapolis 55415, USA.
Lipopolysaccharide (LPSp) pretreatment inhibits TNF secretion in endotoxin-tolerant macrophages via alterations in signal transduction pathways of LPS activation (LPSa). Protein kinase C inhibitors prevent TNF release in response to LPSa and direct protein kinase C activation with phorbol myristate acetate (PMA) restores TNF secretion after LPSp. In the current experiments the effect of protein kinase C modulation on LPSa-stimulated ERK 1/2 activation was investigated.
View Article and Find Full Text PDFJ Trauma
October 1998
Department of Surgery, Hennepin County Medical Center, University of Minnesota, Minneapolis 55415, USA.
Background: Lipopolysaccharide activation (LPSa) of macrophages is thought to occur via a CD14-dependent mechanism with a requirement for the serum factor, lipopolysaccharide binding protein. LPS-stimulated, CD14-dependent signal transduction is associated with phosphorylation of mitogen-activated protein kinase (MAPK), nuclear factor-kappaB (NF-kappaB) translocation, and secretion of tumor necrosis factor (TNF) and interleukin-1 (IL-1). Macrophage endotoxin tolerance after low-dose LPS pretreatment (LPSp) is characterized by inhibition of LPSa-stimulated TNF and augmentation of IL-1 secretion.
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