scholarly journals Volatile Fatty Acid, Metabolic By-Product of Periodontopathic Bacteria, Induces Apoptosis in WEHI 231 and RAJI B Lymphoma Cells and Splenic B Cells

1998 ◽  
Vol 66 (6) ◽  
pp. 2587-2594 ◽  
Author(s):  
Tomoko Kurita-Ochiai ◽  
Kuniyasu Ochiai ◽  
Kazuo Fukushima
Keyword(s):  
Fatty Acid ◽  
B Cells ◽  
Dna Fragmentation ◽  
Butyric Acid ◽  
Volatile Fatty Acid ◽  
Chromatin Condensation ◽  
Raji Cells ◽  
Periodontopathic Bacteria ◽  
Wehi 231 ◽  
Induced Apoptosis

ABSTRACT The ability of butyric acid, an extracellular metabolite from periodontopathic bacteria, to induce apoptosis in murine WEHI 231 cells, splenic B cells, and human RAJI cells was examined. The culture filtrate of Porphyromonas gingivalis,Prevotella loescheii, and Fusobacterium nucleatum, which contains high a percentage of butyric acid, induced DNA fragmentation in WEHI 231 cells. Volatile fatty acid, especially butyric acid, significantly suppressed B-cell viability in a concentration-dependent fashion. The DNA fragmentation assay indicated that butyric acid rapidly induced apoptosis in WEHI 231 cells (with 1.25 mM butyric acid and 6 h after treatment), splenic B cells (with 1.25 mM butyric acid), and RAJI cells (with 2.5 mM butyric acid). Incubation of WEHI 231 cells with butyric acid for 16 h resulted in the typical ladder pattern of DNA fragmentation and the apoptoic change such as chromatin condensation and hypodiploid nuclei. Cell cycle analysis implied that butyric acid arrested the cells at the G1 phase. The inhibitory assay suggested that butyric acid-induced apoptosis of WEHI 231 and splenic B cells was inhibited by W-7, a calmodulin inhibitor. These results suggest that calmodulin-dependent regulation is involved in the signal transduction pathway of butyric acid.

LSP1 regulates anti-IgM induced apoptosis in WEHI-231 cells and normal immature B-cells

1999 ◽  
Vol 36 (6) ◽  
pp. 349-359 ◽  
Author(s):  
J Jongstra-Bilen ◽  
A Wielowieyski ◽  
V Misener ◽  
J Jongstra
Keyword(s):  
B Cells ◽  
Wehi 231 ◽  
Immature B Cells ◽  
Induced Apoptosis

Identification of the volatile fatty acid in the peripheral blood and rumen of cattle and the blood of other species

1951 ◽  
Vol 2 (1) ◽  
pp. 92 ◽  
Author(s):  
GL McClymont
Keyword(s):  
Acetic Acid ◽  
Fatty Acid ◽  
Propionic Acid ◽  
Butyric Acid ◽  
Peripheral Blood ◽  
Molecular Basis ◽  
Volatile Fatty Acid ◽  
Volatile Fatty Acids ◽  
Bovine Blood ◽  
Mean Values

Volatile fatty acid isolated from nine samples of peripheral blood from four cows contained, on a molecular basis, from 90.0 to 97.0 per cent. of acetic acid (mean 93.3 per cent.). The remainder comprised, as mean values, propionic acid, 2.39 per cent.; butyric acid, 2.61 per cent.; and a group of at least three acids between butyric and octanoic, 1.84 per cent. The significance of the high proportion of acetic acid in the volatile fatty acid of bovine peripheral blood is discussed. Only traces of esterified acids lower than octanoic could be found in bovine blood lipides. Volatile fatty acids were found also in the blood of the rabbit, guinea pig, horse, and pig and in human plasma. Here again a high proportion of acetic acid was recorded. Volatile fatty acid isolated from nine samples of ruminal contents from two cows contained on a molecular basis from 52.3 to 69.0 per cent. of acetic acid (mean 60.0 per cent.). The remainder comprised, as mean values, propionic acid, 21.8 per cent.; butyric acid, 14.4 per cent.; and acids higher than butyric (apparently largely valeric and hesanoic), 3.8 per cent. This limited number of analyses indicated no gross effect of type of feed on the proportion of the acids in the rumen.

Carbohydrate digestibility and nitrogen metabolism in sheep fed untreated or sulphur dioxide-treated wheat straw and poultry litter

1990 ◽  
Vol 114 (1) ◽  
pp. 115-121 ◽  
Author(s):  
J. Miron ◽  
R. Solomon ◽  
E. Yosef ◽  
D. Ben-Ghedalia
Keyword(s):  
Fatty Acid ◽  
Wheat Straw ◽  
Nitrogen Metabolism ◽  
Butyric Acid ◽  
Sulphur Dioxide ◽  
Volatile Fatty Acid ◽  
Poultry Litter ◽  
Ammonia Concentration ◽  
Apparent Digestibility ◽  
Carbohydrate Digestibility

SUMMARYDigestibility of neutral detergent fibre (NDF) and monosaccharide components of diets containing 60% untreated straw (UTS) or straw treated with sulphur dioxide (TS) and poultrylitter (1:1) plus 40% concentrate at 700 g/day intake was examined in sheep equipped with rumen and duodenal cannulas. An all-concentrate diet (CD) served as a reference ration. The SO2 treatment of straw increased the apparent digestibility of the NDF, glucose, xylose, arabinose and galactose components of the diet from 58·9, 86·7, 55·7, 82·5 and 91·8%, respectively, in the UTS diet to 73·8, 92·6, 77·8, 88·9 and 94·6%, respectively, in the TS diet. Whereas digestion of NDF and glucose in sheep on the TS diet was slightly lower than in those on the CD diet, digestion of xylose, arabinose and galactose was higher. Thus, the digestibility of total monosaccharides in th TS diet was 90·2 % and that of the CD diet only 61% units higher. The SO2 treatment also increased the total rumen volatile fatty acid (VFA) concentration and the proportion of butyric acid in the total VFA compared with the UTS diet.Rumen ammonia concentration was 7 mg/100 ml lower and nonammonia nitrogen (NAN) flowto the duodenum was 1·3 g/day higher in sheep fed the TS diet compared with the CD diet. The quantity of duodenal N absorbed in the intestine was 10·7 g/day in the TS diet, close to the value of 11·6 g/day found with the CD diet.The similarity between the TS and CD diets in total monosaccharides digestion and duodenal Nabsorption, confirms the findings of earlier studies that a TS diet is a highly productive ration.Complementary interaction between the SO2-treated straw and poultry litter components of the TS diet is discussed.

scholarly journals Inhibition of c-myc expression induces apoptosis of WEHI 231 murine B cells.

1996 ◽  
Vol 16 (9) ◽  
pp. 5015-5025 ◽  
Author(s):  
M Wu ◽  
M Arsura ◽  
R E Bellas ◽  
M J FitzGerald ◽  
H Lee ◽  
...  
Keyword(s):  
B Cells ◽  
Specific Inhibitor ◽  
Related Factor ◽  
B Cell Tolerance ◽  
B Lymphoma Cells ◽  
Wehi 231 ◽  
Enhanced Expression ◽  
Myc Gene ◽  
Nf Kappab ◽  
Induced Apoptosis

Treatment of WEHI 231 immature B-lymphoma cells with an antibody against their surface immunoglobulin (anti-Ig) induces apoptosis and has been studied extensively as a model of B-cell tolerance. Anti-Ig treatment of exponentially growing WEHI 231 cells results in an early transient increase in c-myc expression that is followed by a decline to below basal levels; this decrease in c-myc expression immediately precedes the induction of cell death. Here we have modulated NF-kappaB/Rel factor activity, which regulates the rate of c-myc gene transcription, to determine whether the increase or decrease in c-Myc-levels mediates apoptosis in WEHI 231 cells. Addition of the serine/threonine protease inhibitor N-tosyl-L-phenylalanine chloromethyl ketone (TPCK), which blocks the normally rapid turnover of the specific inhibitor of NF-kappaB/Rel IkappaBalpha in these cells, caused a drop in Rel-related factor binding. TPCK treatment resulted in decreased c-myc expression, preventing the usual increase seen following anti-Ig treatment. Whereas inhibition of the induction of c-myc expression mediated by anti-Ig failed to block apoptosis, reduction of c-myc expression in exponentially growing WEHI 231 cells induced apoptosis even in the absence of anti-Ig treatment. In WEHI 231 clones ectopically expressing c-Myc, apoptosis induced by treatment with TPCK or anti-Ig was significantly diminished and cells continued to proliferate. Furthermore, apoptosis of WEHI 231 cells ensued following enhanced expression of Mad1, which has been found to reduce functional c-Myc levels. These results indicate that the decline in c-myc expression resulting from the drop in NF-kappaB/Rel binding leads to activation of apoptosis of WEHI 231 B cells.

scholarly journals Fas Induces Cytoplasmic Apoptotic Responses and Activation of the MKK7-JNK/SAPK and MKK6-p38 Pathways Independent of CPP32-like Proteases

1997 ◽  
Vol 139 (4) ◽  
pp. 1005-1015 ◽  
Author(s):  
Fumiko Toyoshima ◽  
Tetsuo Moriguchi ◽  
Eisuke Nishida
Keyword(s):  
Cell Death ◽  
Dna Fragmentation ◽  
Morphological Changes ◽  
Chromatin Condensation ◽  
Cysteine Proteases ◽  
Cellular Responses ◽  
Jurkat Cells ◽  
Mitogen Activated Protein Kinase ◽  
Fas Signaling ◽  
Induced Apoptosis

IL-1β converting enzyme (ICE) family cysteine proteases are subdivided into three groups; ICE-, CPP32-, and Ich-1–like proteases. In Fas-induced apoptosis, activation of ICE-like proteases is followed by activation of CPP32-like proteases which is thought to be essential for execution of the cell death. It was recently reported that two subfamily members of the mitogen-activated protein kinase superfamily, JNK/SAPK and p38, are activated during Fas-induced apoptosis. Here, we have shown that MKK7, but not SEK1/ MKK4, is activated by Fas as an activator for JNK/ SAPK and that MKK6 is a major activator for p38 in Fas signaling. Then, to dissect various cellular responses induced by Fas, we used several peptide inhibitors for ICE family proteases in Fas-treated Jurkat cells and KB cells. While Z-VAD-FK which inhibited almost all the Fas-induced cellular responses blocked the activation of JNK/SAPK and p38, Ac-DEVD-CHO and Z-DEVD-FK, specific inhibitors for CPP32-like proteases, which inhibited the Fas-induced chromatin condensation and DNA fragmentation did not block the activation of JNK/SAPK and p38. Interestingly, these DEVD-type inhibitors did not block the Fas-induced morphological changes (cell shrinkage and surface blebbing), induction of Apo2.7 antigen, or the cell death (as assessed by the dye exclusion ability). These results suggest that the Fas-induced activation of the JNK/SAPK and p38 signaling pathways does not require CPP32-like proteases and that CPP32-like proteases, although essential for apoptotic nuclear events (such as chromatin condensation and DNA fragmentation), are not required for other apoptotic events in the cytoplasm or the cell death itself. Thus, the Fas signaling pathway diverges into multiple, separate processes, each of which may be responsible for part of the apoptotic cellular responses.

Butyric Acid Induces Apoptosis in Inflamed Fibroblasts

2008 ◽  
Vol 87 (1) ◽  
pp. 51-55 ◽  
Author(s):  
T. Kurita-Ochiai ◽  
S. Seto ◽  
N. Suzuki ◽  
M. Yamamoto ◽  
K. Otsuka ◽  
...  
Keyword(s):  
Butyric Acid ◽  
Caspase 3 ◽  
Chromatin Condensation ◽  
Dependent Manner ◽  
Gingival Fibroblasts ◽  
T And B Cells ◽  
Healthy Humans ◽  
Extracellular Metabolite ◽  
Induced Apoptosis ◽  
Dose Dependent

Butyric acid, an extracellular metabolite from periodontopathic bacteria, induces apoptosis in murine and human T- and B-cells, whereas intact gingival fibroblasts isolated from healthy humans are resistant to butyric-acid-induced apoptosis. We examined the susceptibility of inflamed gingival fibroblasts isolated from adult persons with periodontitis to butyric-acid-induced apoptosis. Butyric acid significantly suppressed the viability of inflamed gingival fibroblasts and induced apoptosis in a dose-dependent manner. The incubation of inflamed gingival fibroblasts with butyric acid induced DNA fragmentation and apoptotic changes such as chromatin condensation, hypodiploid nuclei, and mitochondrial injury. Furthermore, butyric-acid-induced apoptosis in inflamed gingival fibroblasts was reduced by caspase-3/7, -6, -8, and -9 inhibitors. Thus, inflamed gingival fibroblasts from adult persons with periodontitis appear to be highly susceptible to mitochondria- and caspase-dependent apoptosis induced by butyric acid, compared with healthy gingival fibroblasts.

scholarly journals RasGRP1 Sensitizes an Immature B Cell Line to Antigen Receptor-induced Apoptosis

2004 ◽  
Vol 279 (19) ◽  
pp. 19523-19530 ◽  
Author(s):  
Benoit Guilbault ◽  
Robert J. Kay
Keyword(s):  
T Cells ◽  
B Cells ◽  
B Cell ◽  
Cell Line ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Wehi 231 ◽  
Induced Apoptosis

RasGRP1 is a guanine nucleotide exchange factor that activates Ras GTPases and is activated downstream of antigen receptors on both T and B lymphocytes. Ras-GRP1 provides signals to immature T cells that confer survival and proliferation, but RasGRP1 also promotes T cell receptor-mediated deletion of mature T cells. We used the WEHI-231 cell line as an experimental system to determine whether RasGRP1 can serve as a quantitative modifier of B cell receptor-induced deletion of immature B cells. A 2-fold elevation in RasGRP1 expression markedly increased apoptosis of WEHI-231 cells following B cell receptor ligation, whereas a dominant negative mutant of RasGRP1 suppressed B cell receptor-induced apoptosis. Activation of ERK1 or ERK2 kinases was not required for RasGRP1-mediated apoptosis. Instead, elevated RasGRP1 expression caused down-regulation of NF-κB and Bcl-xL, which provide survival signals counter-acting apoptosis induction by B cell receptor. Inhibition of NF-κB was sufficient to enhance B cell receptor-induced apoptosis of WEHI-231 cells, and ligation of co-stimulatory receptors that activate NF-κB suppressed the ability of RasGRP1 to promote B cell receptor-induced apoptosis. These experiments define a novel apoptosis-promoting pathway leading from B cell receptor to the inhibition of NF-κB and demonstrate that differential expression of RasGRP1 has the potential to modulate the sensitivities of B cells to negative selection following antigen encounter.

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