Effect of titanium surface topography on macrophage activation and secretion of proinflammatory cytokines and chemokines

2004 ◽  
Vol 70A (2) ◽  
pp. 194-205 ◽  
Author(s):  
Ali K. Refai ◽  
Marcus Textor ◽  
Donald M. Brunette ◽  
J. Douglas Waterfield
2011 ◽  
Vol 12 (5) ◽  
pp. 1900-1911 ◽  
Author(s):  
Enrica Saino ◽  
Maria Letizia Focarete ◽  
Chiara Gualandi ◽  
Enzo Emanuele ◽  
Antonia I. Cornaglia ◽  
...  

2021 ◽  
Vol 22 (13) ◽  
pp. 6921
Author(s):  
Norihisa Nishimura ◽  
Kosuke Kaji ◽  
Koh Kitagawa ◽  
Yasuhiko Sawada ◽  
Masanori Furukawa ◽  
...  

Recent studies have suggested that an alteration in the gut microbiota and their products, particularly endotoxins derived from Gram-negative bacteria, may play a major role in the pathogenesis of liver diseases. Gut dysbiosis caused by a high-fat diet and alcohol consumption induces increased intestinal permeability, which means higher translocation of bacteria and their products and components, including endotoxins, the so-called “leaky gut”. Clinical studies have found that plasma endotoxin levels are elevated in patients with chronic liver diseases, including alcoholic liver disease and nonalcoholic liver disease. A decrease in commensal nonpathogenic bacteria including Ruminococaceae and Lactobacillus and an overgrowth of pathogenic bacteria such as Bacteroidaceae and Enterobacteriaceae are observed in cirrhotic patients. The decreased diversity of the gut microbiota in cirrhotic patients before liver transplantation is also related to a higher incidence of post-transplant infections and cognitive impairment. The exposure to endotoxins activates macrophages via Toll-like receptor 4 (TLR4), leading to a greater production of proinflammatory cytokines and chemokines including tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8, which play key roles in the progression of liver diseases. TLR4 is a major receptor activated by the binding of endotoxins in macrophages, and its downstream signal induces proinflammatory cytokines. The expression of TLR4 is also observed in nonimmune cells in the liver, such as hepatic stellate cells, which play a crucial role in the progression of liver fibrosis that develops into hepatocarcinogenesis, suggesting the importance of the interaction between endotoxemia and TLR4 signaling as a target for preventing liver disease progression. In this review, we summarize the findings for the role of gut-derived endotoxemia underlying the progression of liver pathogenesis.


2019 ◽  
Vol 476 (1) ◽  
pp. 85-99 ◽  
Author(s):  
Ivana Y. Quiroga ◽  
Magali Pellon-Maison ◽  
Amanda L. Suchanek ◽  
Rosalind A. Coleman ◽  
Maria R. Gonzalez-Baro

AbstractMacrophage classical M1 activation via TLR4 triggers a variety of responses to achieve the elimination of foreign pathogens. During this process, there is also an increase in lipid droplets which contain large quantities of triacylglycerol (TAG) and phospholipid (PL). The functional consequences of this increment in lipid mass are poorly understood. Here, we studied the contribution of glycerolipid synthesis to lipid accumulation, focusing specifically on the first and rate-limiting enzyme of the pathway: glycerol-3-phosphate acyltransferase (GPAT). Using bone marrow-derived macrophages (BMDMs) treated with Kdo2-lipid A, we showed that glycerolipid synthesis is induced during macrophage activation. GPAT4 protein level and GPAT3/GPAT4 enzymatic activity increase during this process, and these two isoforms were required for the accumulation of cell TAG and PL. The phagocytic capacity of Gpat3−/− and Gpat4−/− BMDM was impaired. Additionally, inhibiting fatty acid β-oxidation reduced phagocytosis only partially, suggesting that lipid accumulation is not necessary for the energy requirements for phagocytosis. Finally, Gpat4−/− BMDM expressed and released more pro-inflammatory cytokines and chemokines after macrophage activation, suggesting a role for GPAT4 in suppressing inflammatory responses. Together, these results provide evidence that glycerolipid synthesis directed by GPAT4 is important for the attenuation of the inflammatory response in activated macrophages.


2017 ◽  
Vol 130 (17) ◽  
pp. 2033-2040 ◽  
Author(s):  
Ting Yang ◽  
Yan Li ◽  
Zhe Lyu ◽  
Kewu Huang ◽  
Chris J Corrigan ◽  
...  

2002 ◽  
Vol 62 ◽  
pp. S12-S22 ◽  
Author(s):  
Marta Ruiz-Ortega ◽  
Mónica Ruperez ◽  
Oscar Lorenzo ◽  
Vanesa Esteban ◽  
Julia Blanco ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Theodore S. Kapellos ◽  
Asif J. Iqbal

Macrophages function as sentinel cells, which constantly monitor the host environment for infection or injury. Macrophages have been shown to exhibit a spectrum of activated phenotypes, which can often be categorised under the M1/M2 paradigm. M1 macrophages secrete proinflammatory cytokines and chemokines, such as TNF-α, IL-6, IL-12, CCL4, and CXCL10, and induce phagocytosis and oxidative dependent killing mechanisms. In contrast, M2 macrophages support wound healing and resolution of inflammation. In the past decade, interest has grown in understanding the mechanisms involved in regulating macrophage activation. In particular, epigenetic control of M1 or M2 activation states has been shown to rely on posttranslational modifications of histone proteins adjacent to inflammatory-related genes. Changes in methylation and acetylation of histones by methyltransferases, demethylases, acetyltransferases, and deacetylases can all impact how macrophage phenotypes are generated. In this review, we summarise the latest advances in the field of epigenetic regulation of macrophage polarisation to M1 or M2 states, with particular focus on the cytokine and chemokine profiles associated with these phenotypes.


2003 ◽  
Vol 426-432 ◽  
pp. 3023-3030 ◽  
Author(s):  
Barbara Nebe ◽  
Frank Lüthen ◽  
Axel Baumann ◽  
Ulrich Beck ◽  
Annette Diener ◽  
...  

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