Deficiency of Group VIA phospholipase A2 Primes the Cytokine Releases by Kupffer cells and Lymphocytes

2015 ◽  
Vol 53 (12) ◽  
Author(s):  
J Inhoffen ◽  
S Tuma-Kellner ◽  
W Stremmel ◽  
W Chamulitrat
1993 ◽  
Vol 293 (1) ◽  
pp. 143-150 ◽  
Author(s):  
G M Hatch ◽  
D E Vance ◽  
D C Wilton

A novel fluorescence assay for phospholipase A2 [Wilton (1990) Biochem. J. 266, 435-439] has been used to study the Group-II rat liver mitochondrial enzyme, and a number of novel properties of this enzyme were identified. (1) The enzyme activity was located in the liver macrophages (Kupffer cells) while negligible activity was associated with hepatocytes. (2) Although subcellular fractionation of whole liver confirmed the predominantly mitochondrial location of this enzyme activity, the analysis of the hepatocyte-free Kupffer-cell-enriched fraction revealed a different enzyme distribution, with the majority of activity being associated with the microsomal membrane fraction. (3) Bacterial endotoxin has been previously shown to be scavenged by Kupffer cells in rats. Treatment of rats with bacterial lipopolysaccharide (endotoxin) resulted in a dramatic time- and dose-dependent increase in liver phospholipase A2 activity. (4) It is known that injection of endotoxin into rodents results in elevated serum phospholipase A2 activity, while a similar phenomenon is seen in the condition of septic shock in man. The source of this serum enzyme was unknown. In this study perfusion of livers from rats pretreated with lipopolysaccharide with physiological saline demonstrated a 6-fold increase in phospholipase A2 activity in the perfusate compared with sham-treated controls, with only minor release of hepatic lipase. (5) Western-blot analysis confirmed an increased release of this Group-II phospholipase A2 into the perfusate of lipopolysaccharide-treated rats compared with sham-treated controls. These results suggest that liver Kupffer cells are a major source of the endotoxin-induced serum Group-II phospholipase A2 activity associated with bacterial infection and trauma.


1984 ◽  
Vol 140 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Manfred BIRMELIN ◽  
Dieter MARME ◽  
Ernst FERBER ◽  
Karl DECKER

1989 ◽  
Vol 9 ◽  
pp. S178 ◽  
Author(s):  
H. Krease ◽  
P. Dieter ◽  
A. Schulze-Specking ◽  
K. Decker

1992 ◽  
Vol 40 (11) ◽  
pp. 1659-1664 ◽  
Author(s):  
H Kiyohara ◽  
H Egami ◽  
Y Shibata ◽  
K Murata ◽  
S Ohshima ◽  
...  

The light microscopic and immunohistochemical distribution of human Group II phospholipase A2 (M-PLA2) in digestive organs of both human fetus and adult, with a new monoclonal antibody (MAb) against M-PLA2, was investigated semiquantitatively. The immunoreactivity was distributed similarly in the adult and fetal epithelium of the esophagus, duodenum, and small intestine, and in the acinar, islet, and duct cells of the pancreas. The epithelium of adult gallbladder was immunoreactive. Paneth cells, especially the secretory apparatus, were strongly immunoreactive. Hepatic Küpffer cells and macrophages of the adult spleen were also immunoreactive. These results suggest that these cells contain secretory-type Group II PLA2, which may be involved in host defensive mechanisms, such as phagocytosis in human digestive organs. In the adult colon, the immunoreactivity was observed only in the ascending colon and was not found in the transverse, descending, sigmoid, or rectal colon. The immunoreactivity was not found in fetal colon. Similarly, immunoreactivity was found in hepatocytes and Küpffer cells of adult liver but not in fetal liver. By contrast, strong immunoreactivity was observed in the epithelium of the fetal stomach but not in adult stomach except in gastric neck cells. This suggests that the expression of M-PLA2 may be related to cell differentiation in particular organs.


Author(s):  
O. T. Minick ◽  
E. Orfei ◽  
F. Volini ◽  
G. Kent

Hemolytic anemias were produced in rats by administering phenylhydrazine or anti-erythrocytic (rooster) serum, the latter having agglutinin and hemolysin titers exceeding 1:1000.Following administration of phenylhydrazine, the erythrocytes undergo oxidative damage and are removed from the circulation by the cells of the reticulo-endothelial system, predominantly by the spleen. With increasing dosage or if animals are splenectomized, the Kupffer cells become an important site of sequestration and are greatly hypertrophied. Whole red cells are the most common type engulfed; they are broken down in digestive vacuoles, as shown by the presence of acid phosphatase activity (Fig. 1). Heinz body material and membranes persist longer than native hemoglobin. With larger doses of phenylhydrazine, erythrocytes undergo intravascular fragmentation, and the particles phagocytized are now mainly red cell fragments of varying sizes (Fig. 2).


Author(s):  
Masako Yamada ◽  
Yutaka Tanuma

Although many fine structural studies on the vertebrate liver have been reported on mammals, avians, reptiles, amphibians, teleosts and cyclostomes, there are no studies on elasmobranchii liver except one by T. Ito etal. (1962) who studied it on light microscopic level. The purpose of the present study was to as certain the ultrastructural details and cytochemical characteristics of normal elasmobranchii liver and was to compare with the other higher vertebrate ones.Seventeen Scyliorhinus torazame, one kind of elasmobranchii, were obtained from the fish stock of the Ueno Zoo aquarium, Ueno, Tokyo. The sharks weighing about 300-600g were anesthetized with MS-222 (Sigma), and the livers were fixed by perfusion fixation via the portal vein according to the procedure of Y. Saito et al. (1980) for 10 min. Then the liver tissues were immersed in the same fixative for 2 hours and postfixed with 1% OsO4-solution in 0.1 Mc acodylate buffer for one hour. In order to make sure a phagocytic activity of Kupffer cells, latex particles (0.8 μm in diameter, 0.05mg/100 g b.w.) were injected through the portal vein for one min before fixation. For preservation of lipid droplets in the cytoplasm, a series of these procedure were performed under ice cold temperature until the end of dehydration.


2001 ◽  
Vol 120 (5) ◽  
pp. A361-A361
Author(s):  
K UCHIKURA ◽  
T WADA ◽  
Z SUN ◽  
S HOSHINO ◽  
G BULKLEY ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A356-A356
Author(s):  
T KONO ◽  
J IWAMOTO ◽  
K ISHIKAWA ◽  
Y EBISAWA ◽  
T AOKI ◽  
...  

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