Peritoneal lavage fluid alters patterns of eicosanoid production in murine bone marrow-derived and peritoneal macrophages: Dependency on inflammatory state of the peritoneum

Inflammation ◽  
1993 ◽  
Vol 17 (6) ◽  
pp. 743-756 ◽  
Author(s):  
Sally E. Wenzel ◽  
John B. Trudeau ◽  
David W. H. Riches ◽  
Jay Y. Westcott ◽  
Peter M. Henson
Cells ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 82
Author(s):  
Wanhai Qin ◽  
Xanthe Brands ◽  
Hisatake Matsumoto ◽  
Joe M. Butler ◽  
Cornelis van’t Veer ◽  
...  

Tet methylcytosine dioxygenase 2 (Tet2) mediates demethylation of DNA. We here sought to determine the expression and function of Tet2 in macrophages upon exposure to lipopolysaccharide (LPS), and in the host response to LPS induced lung and peritoneal inflammation, and during Escherichia (E.) coli induced peritonitis. LPS induced Tet2 expression in mouse macrophages and human monocytes in vitro, as well as in human alveolar macrophages after bronchial instillation in vivo. Bone marrow-derived macrophages from myeloid Tet2 deficient (Tet2fl/flLysMCre) mice displayed enhanced production of IL-1β, IL-6 and CXCL1 upon stimulation with several Toll-like receptor agonists; similar results were obtained with LPS stimulated alveolar and peritoneal macrophages. Histone deacetylation was involved in the effect of Tet2 on IL-6 production, whilst methylation at the Il6 promoter was not altered by Tet2 deficiency. Tet2fl/flLysMCre mice showed higher IL-6 and TNF levels in bronchoalveolar and peritoneal lavage fluid after intranasal and intraperitoneal LPS administration, respectively, whilst other inflammatory responses were unaltered. E. coli induced stronger production of IL-1β and IL-6 by Tet2 deficient peritoneal macrophages but not in peritoneal lavage fluid of Tet2fl/flLysMCre mice after in vivo intraperitoneal infection. Tet2fl/flLysMCre mice displayed enhanced bacterial growth during E. coli peritonitis, which was associated with a reduced capacity of Tet2fl/flLysMCre peritoneal macrophages to inhibit the growth of E. coli in vitro. Collectively, these data suggest that Tet2 is involved in the regulation of macrophage functions triggered by LPS and during E. coli infection.


Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 4080-4085 ◽  
Author(s):  
Maria Pini ◽  
Melissa E. Gove ◽  
Joseph A. Sennello ◽  
Jantine W. P. M. van Baal ◽  
Lawrence Chan ◽  
...  

Adipokines, cytokines mainly produced by adipocytes, are active participants in the regulation of inflammation. Administration of zymosan (ZY) was used to investigate the regulation and role of adipokines during peritonitis in mice. Injection of ZY led to a significant increase in leptin levels in both serum and peritoneal lavage fluid, whereas a differential trend in local vs. systemic levels was observed for both resistin and adiponectin. The role of leptin in ZY-induced peritonitis was investigated using leptin-deficient ob/ob mice, with and without reconstitution with exogenous leptin. Leptin deficiency was associated with delayed resolution of peritoneal inflammation induced by ZY, because ob/ob mice had a more pronounced cellular infiltrate in the peritoneum as well as higher and prolonged local and systemic levels of IL-6, TNFα, IL-10, and chemokine (C-X-C motif) ligand 2 compared with wild-type mice. Reconstitution with exogenous leptin exacerbated the inflammatory infiltrate and systemic IL-6 levels in ob/ob mice while inhibiting production of TNFα, IL-10, and chemokine (C-X-C motif) ligand 2. In contrast with the important role of leptin in regulating each aspect of ZY-induced peritonitis, adiponectin deficiency was associated only with a decreased inflammatory infiltrate, without affecting cytokine levels. These findings point to a complex role for adipokines in ZY-induced peritonitis and further emphasize the interplay between obesity and inflammation.


2014 ◽  
Vol 140 (4) ◽  
pp. 607-612 ◽  
Author(s):  
Manabu Yamamoto ◽  
Keiji Yoshinaga ◽  
Ayumi Matsuyama ◽  
Shinichi Tsutsui ◽  
Teruyoshi Ishida

1993 ◽  
Vol 34 (6) ◽  
pp. 829-833 ◽  
Author(s):  
Jonathan H. Jaffin ◽  
M. Gage Ochsner ◽  
Frederic J. Cole ◽  
Grace S. Rozycki ◽  
Mary Kass ◽  
...  

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 408-420 ◽  
Author(s):  
G Pigoli ◽  
A Waheed ◽  
RK Shadduck

Abstract Radioiodinated L-cell-derived colony-stimulating factor (CSF) was used to characterize the binding reaction to murine bone marrow cells. The major increment in cell-associated radioactivity occurred over 24 hr incubation at 37 degrees C, but virtually no binding was observed at 4 degrees C. The reaction was saturable with approximately 1 ng/ml of purified CSF. Unlabeled CSF prevented the binding, whereas a number of other hormones and proteins did not compete for CSF uptake. Further specificity studies showed virtually no binding to human bone marrow, which is unresponsive to this form of murine CSF. Minimal CSF uptake was noted with murine peritoneal macrophages, but virtually no binding was detected with thymic, lymph node, liver, or kidney cells. The marrow cell interaction with tracer appeared to require a new protein synthesis, as the binding was prevented by cycloheximide or puromycin. Preincubation of marrow cells in medium devoid of CSF increased the degree of binding after 1 hr exposure to the tracer. This suggests that CSF binding sites may be occupied or perhaps decreased in response to ambient levels of CSF in vivo. Approximately 70% of the bound radioactivity was detected in the cytoplasm at 24 hr. This material was partially degraded as judged by a decrease in molecular weight from approximately 62,000 to 2 peaks of approximately 32,000 and approximately 49,000, but 72% of the binding activity was retained. After plateau binding was achieved, greater than 80% of the radioactivity released into the medium was degraded into biologically inactive peptides with molecular weights less than 10,000. These findings suggest that the interaction of CSF with marrow cells is characterized by binding with subsequent internalization and metabolic degradation into portions of the molecule that are devoid of biologic activity.


2005 ◽  
Vol 23 (16_suppl) ◽  
pp. 4056-4056 ◽  
Author(s):  
M. Takahashi ◽  
F. Kito ◽  
C. Kunisaki ◽  
M. Nomura ◽  
H. Akiyama ◽  
...  

1991 ◽  
Vol 54 (12) ◽  
pp. 917-921 ◽  
Author(s):  
ALAIN MENUDIER ◽  
CLAUDINE BOSIRAUD ◽  
JEAN-ALBERT NICOLAS

Wild strains of Listeria monocytogenes, Listeria ivanovii, Listeria seeligeri, Listeria innocua, and Listeria welshimeri were isolated from infected animals and foodstuffs. Their virulence was tested in Swiss mice after intraperitoneal injection of a fixed number of organisms. The presence of hemolysin was determined using the CAMP test. Bacteria were enumerated in peritoneal lavage fluid, liver, and spleen. Spleen weights were measured, and the presence of L. monocytogenes in the brain was also investigated. L. innocua, L. seeligeri, and L. welshimeri were not found to be pathogenic for mice. L. ivanovii was detected in liver, spleen, and peritoneal lavage fluid but at lower levels than L. monocytogenes (p<0.001). The pathogenic capabilities of four different serovars of L. monocytogenes (4b, 1/2a, 1/2b, 1/2c) were compared. Serovars l/2b and l/2c, which are frequently isolated from foodstuffs, were found to colonize the liver and spleen to a lesser extent than serovar 4b (p<0.01 and <0.001 respectively). The behavior of serovar l/2a, the most commonly isolated from foodstuffs, was strain dependent. Two out of the four strains tested were strongly hemolytic and were as virulent as strains of serovar 4b, while the other two were weakly hemolytic, and avirulent like L. innocua. These results could account for the relatively small number of human Listeria infections due to L. monocytogenes serogroup 1/2, despite the very frequent occurrence of this serovar in foodstuffs.


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