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Comparative Hepatology
Published in: Comparative Hepatology 1/2004

Open Access 01-01-2004 | Proceedings

Beta2-glycoprotein I inhibition of mouse Kupffer cells respiratory burst depends on liver architecture

Authors: Ligia F Gomes, Paula R Knox, Karin A Simon-Giavarotti, Virginia BC Junqueira, Jorge Sans, Luis A Videla

Published in: Comparative Hepatology | Special Issue 1/2004

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Excerpt

Kupffer cells play important roles in the modulation of immune response, phagocytosis, and senescent cell removal [1, 2]. Hydrolytic enzymes and reactive species produce the killing effects of Kupffer cells and some degree of adjacent tissue damage [1, 3]. Liver macrophages are constantly exposed to antigens from portal circulation, to which development of full inflammatory response is useless and potentially harmful [4]. Neither tissue damage nor inflammation follows senescent cell removal by Kupffer cells, due to the physiological control of inflammation events during antigen processing [2, 5]. Apolipoproteins can modulate macrophage function [6]. Among them, beta2-glycoprotein I (beta2GPI) decreases Kupffer cells respiratory burst while increases efficiency of C. albicans killing [7]. Beta2GPI also binds phosphatidylserine (PS) residues on the surface of senescent cells, targeting them to clearance [8]. In order to get an insight on the role of beta2GPI in the silent antigen removal by Kupffer cells, perfused mouse liver was used as a model of Kupffer cell-dependent phagocytosis and related respiratory burst activity, and results were correlated with those obtained in isolated mouse non-parenchymal cells. …
Literature
1.
Decker K: The response of liver macrophages to inflammatory stimulation. Keio J Med. 1998, 47: 1-9.CrossRefPubMed
2.
Pradhan D, Krahling S, Williamson P, Schlegel RA: Multiple systems for recognition of apoptotic lymphocytes by macrophages. Mol Biol Cell. 1997, 8: 767-778.PubMedCentralCrossRefPubMed
3.
Wang J-F, Komarov P, de Groot H: Luminol chemiluminescence in rat macrophages and granulocytes: the role of NO, O2- /H2O2, and HOCl. Arch Biochem Biophys. 1993, 304: 189-196. 10.1006/abbi.1993.1338.CrossRefPubMed
4.
Witmer-Pack M, Crowley MT, Inaba K, Steinman RM: Macrophages, but not dendritic cells, accumulate colloidal carbon following administration in situ. J Cell Sci. 1993, 105: 965-PubMed
5.
Fadok VA, Bratton DL, Frasch SC, Warner ML, Henson PM: The role of phosphatidylserine in recognition of apoptotic cells by phagocytes. Cell Death Diff. 1998, 5: 551-562. 10.1038/sj.cdd.4400404.CrossRef
6.
Usynin IF, Tsyrendorzhiev DD, Khar'khovsskii AV, Poliakov LM, Panin LE: Effect of apolipoprotein A-I on lipopolissacharide-induced production of reactive oxygen metabolites by Kupffer cells of the rat. Biokhimiya, Moscow. 1996, 61: 260-265.
7.
Gomes LF, Gonáalves LM, Fonseca FLA, Celli CM, Videla LA, Chaimovich H, Junqueira VBC: Beta2-Glycoprotein I (apolipoprotein H) modulates uptake and endocytosis associated chemiluminescence in rat Kupffer cells. Free Radic Res. 2002, 36: 741-747. 10.1080/10715760290032548.CrossRefPubMed
8.
Chonn A, Semple SC, Cullis PR: Beta2-glycoprotein I is a major protein associated with very rapidly cleared liposomes in vivo, suggesting a significant role in the immune clearance of "non-self" particles. J Biol Chem. 1995, 270: 25845-25849. 10.1074/jbc.270.43.25845.CrossRefPubMed
9.
Videla LA, Tapia G, Fernández V: Influence of aging on Kupffer cell respiratory activity in relation to particle phagocytosis and oxidative stress parameters in mouse liver. Redox Report. 2001, 6: 155-159. 10.1179/135100001101536265.CrossRefPubMed
10.
Cowper KB, Currin RT, Dawson TL, Lindert KA, Lemasters JJ, Thurman RG: A new method to monitor Kupffer cell function continuously in the perfused rat liver. Biochem J. 1990, 266: 141-147.PubMedCentralCrossRefPubMed
11.
Easmon CS, Cole PJ, Willians AJ, Hastings M: The measurement of opsonic and phagocytic function by luminol chemiluminescence. Immunology. 1980, 41: 67-74.PubMedCentralPubMed
12.
Qu W, Zhong Z, Goto M, Thurman RG: Kupffer cell prostaglandin E2 stimulates parenchymal cell O2 consumption: alcohol and cell-cell communication. Am J Physiol. 1996, 270: G574-G580.PubMed
13.
Ma K, Simantov R, Zhang J, Silverstein R, Hajjar KA, McCrae KR: High affinity binding of beta2-glycoprotein I to human endothelial cells is mediated by annexin II. J Biol Chem. 2000, 275: 15541-15548. 10.1074/jbc.275.20.15541.CrossRefPubMed
14.
Murray D, Arbuzova A, Hangyás-Mihályná G, Gambhir A, Ben-Tal N, Honig B, McLaughlin S: Electrostatic Properties of Membranes Containing Acidic Lipids and Adsorbed Basic Peptides: Theory and Experiment. Biophys J. 1999, 77: 3176-3188.PubMedCentralCrossRefPubMed
15.
Dieter P, Schwende H: Protein kinase C-alpha and -beta play antagonistic roles in the differentiation process of THP-1 cells. Cell Signal. 2000, 12: 297-302. 10.1016/S0898-6568(00)00069-3.CrossRefPubMed
16.
Potoka DA, Takao S, Owaki T, Bulkley GB, Klein AS: Endothelial cells potentiate oxidant-mediated Kupffer cell phagocytic killing. Free Rad Biol Med. 1998, 24: 1217-1227. 10.1016/S0891-5849(97)00453-X.CrossRefPubMed
Metadata
Title
Beta2-glycoprotein I inhibition of mouse Kupffer cells respiratory burst depends on liver architecture
Authors
Ligia F Gomes
Paula R Knox
Karin A Simon-Giavarotti
Virginia BC Junqueira
Jorge Sans
Luis A Videla
Publication date
01-01-2004
Publisher
BioMed Central
Published in
Comparative Hepatology / Issue Special Issue 1/2004
Electronic ISSN: 1476-5926
DOI
https://doi.org/10.1186/1476-5926-2-S1-S43

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