scholarly journals Role and Regulation of Adipokines during Zymosan-Induced Peritoneal Inflammation in Mice

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 ◽  
...  
Keyword(s):  
Inflammatory Infiltrate ◽  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Wild Type ◽  
Cellular Infiltrate ◽  
Peritoneal Lavage Fluid ◽  
Peritoneal Inflammation ◽  
Leptin Deficiency ◽  
Cytokine Levels

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.

scholarly journals Neutrophil Emigration in the Skin, Lungs, and Peritoneum: Different Requirements for CD11/CD18 Revealed by CD18-deficient Mice

1997 ◽  
Vol 186 (8) ◽  
pp. 1357-1364 ◽  
Author(s):  
Joseph P. Mizgerd ◽  
Hiroshi Kubo ◽  
Gregory J. Kutkoski ◽  
Sabrina D. Bhagwan ◽  
Karin Scharffetter-Kochanek ◽  
...  
Keyword(s):  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Mutant Mice ◽  
Wild Type ◽  
Peritoneal Lavage Fluid ◽  
Alternative Pathways ◽  
Irritant Dermatitis ◽  
Blocking Antibodies ◽  
Deficient Mice

To determine the role of CD11/CD18 complexes in neutrophil emigration, inflammation was induced in the skin, lungs, or peritoneum of mutant mice deficient in CD18 (CD18−/− mutants). Peripheral blood of CD18−/− mutants contained 11-fold more neutrophils than did blood of wild-type (WT) mice. During irritant dermatitis induced by topical application of croton oil, the number of emigrated neutrophils in histological sections of dermis was 98% less in CD18−/− mutants than in WT mice. During Streptococcus pneumoniae pneumonia, neutrophil emigration in CD18−/− mutants was not reduced. These data are consistent with expectations based on studies using blocking antibodies to inhibit CD11/CD18 complexes, and on observations of humans lacking CD11/CD18 complexes. The number of emigrated neutrophils in lung sections during Escherichia coli pneumonia, or in peritoneal lavage fluid after 4 h of S. pneumoniae peritonitis, was not reduced in CD18−/− mutants, but rather was greater than the WT values (240 ± 30 and 220 ± 30% WT, respectively). Also, there was no inhibition of neutrophil emigration during sterile peritonitis induced by intraperitoneal injection of thioglycollate (90 ± 20% WT). These data contrast with expectations. Whereas CD11/CD18 complexes are essential to the dermal emigration of neutrophils during acute dermatitis, CD18−/− mutant mice demonstrate surprising alternative pathways for neutrophil emigration during pneumonia or peritonitis.

scholarly journals Role of Myeloid Tet Methylcytosine Dioxygenase 2 in Pulmonary and Peritoneal Inflammation Induced by Lipopolysaccharide and Peritonitis Induced by Escherichia coli

Cells ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 82
Author(s):  
Wanhai Qin ◽  
Xanthe Brands ◽  
Hisatake Matsumoto ◽  
Joe M. Butler ◽  
Cornelis van’t Veer ◽  
...  
Keyword(s):  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Peritoneal Macrophages ◽  
Histone Deacetylation ◽  
Peritoneal Lavage Fluid ◽  
E Coli ◽  
Peritoneal Inflammation ◽  
Enhanced Production

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.

scholarly journals Role of TNFR1 in the innate airway hyperresponsiveness of obese mice

2012 ◽  
Vol 113 (9) ◽  
pp. 1476-1485 ◽  
Author(s):  
Ming Zhu ◽  
Alison S. Williams ◽  
Lucas Chen ◽  
Allison P. Wurmbrand ◽  
Erin S. Williams ◽  
...  
Keyword(s):  
Airway Hyperresponsiveness ◽  
Bronchoalveolar Lavage Fluid ◽  
Pulmonary Inflammation ◽  
Tumor Necrosis Factor Receptor ◽  
Lavage Fluid ◽  
Forced Oscillation Technique ◽  
Obese Mice ◽  
Wild Type ◽  
Necrosis Factor

The purpose of this study was to examine the role of tumor necrosis factor receptor 1 (TNFR1) in the airway hyperresponsiveness characteristic of obese mice. Airway responsiveness to intravenous methacholine was measured using the forced oscillation technique in obese Cpe fat mice that were either sufficient or genetically deficient in TNFR1 ( Cpe fat and Cpe fat/TNFR1−/− mice) and in lean mice that were either sufficient or genetically deficient in TNFR1 [wild-type (WT) and TNFR1−/− mice]. Compared with lean WT mice, Cpe fat mice exhibited airway hyperresponsiveness. Airway hyperresponsives was also greater in Cpe fat/TNFR1−/− than in Cpe fat mice. Compared with WT mice, Cpe fat mice had increases in bronchoalveolar lavage fluid concentrations of several inflammatory moieties including eotaxin, IL-9, IP-10, KC, MIG, and VEGF. These factors were also significantly elevated in Cpe fat/TNFR1−/− vs. TNFR1−/− mice. Additional moieties including IL-13 were also elevated in Cpe fat/TNFR1−/− vs. TNFR1−/− mice but not in Cpe fat vs. WT mice. IL-17A mRNA expression was greater in Cpe fat/TNFR1−/− vs. Cpe fat mice and in TNFR1−/− vs. WT mice. Analysis of serum indicated that obesity resulted in systemic as well as pulmonary inflammation, but TNFR1 deficiency had little effect on this systemic inflammation. Our results indicate that TNFR1 is protective against the airway hyperresponsiveness associated with obesity and suggest that effects on pulmonary inflammation may be contributing to this protection.

CEA/CA72-4 levels in peritoneal lavage fluid are predictive factors in patients with gastric carcinoma

2014 ◽  
Vol 140 (4) ◽  
pp. 607-612 ◽  
Author(s):  
Manabu Yamamoto ◽  
Keiji Yoshinaga ◽  
Ayumi Matsuyama ◽  
Shinichi Tsutsui ◽  
Teruyoshi Ishida
Keyword(s):  
Gastric Carcinoma ◽  
Predictive Factors ◽  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Peritoneal Lavage Fluid

ALKALINE PHOSPHATASE LEVELS IN DIAGNOSTIC PERITONEAL LAVAGE FLUID AS A PREDICTOR OF HOLLOW VISCERAL INJURY

1993 ◽  
Vol 34 (6) ◽  
pp. 829-833 ◽  
Author(s):  
Jonathan H. Jaffin ◽  
M. Gage Ochsner ◽  
Frederic J. Cole ◽  
Grace S. Rozycki ◽  
Mary Kass ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Diagnostic Peritoneal Lavage ◽  
Visceral Injury ◽  
Peritoneal Lavage Fluid ◽  
Hollow Visceral Injury

Prediction of peritoneal recurrence by analysis of hTERT mRNA in peritoneal lavage fluid on gastric carcinoma

2005 ◽  
Vol 23 (16_suppl) ◽  
pp. 4056-4056 ◽  
Author(s):  
M. Takahashi ◽  
F. Kito ◽  
C. Kunisaki ◽  
M. Nomura ◽  
H. Akiyama ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Peritoneal Recurrence ◽  
Htert Mrna ◽  
Peritoneal Lavage Fluid

Virulence of Listeria monocytogenes Serovars and Listeria spp. in Experimental Infection of Mice

1991 ◽  
Vol 54 (12) ◽  
pp. 917-921 ◽  
Author(s):  
ALAIN MENUDIER ◽  
CLAUDINE BOSIRAUD ◽  
JEAN-ALBERT NICOLAS
Keyword(s):  
Listeria Monocytogenes ◽  
Peritoneal Lavage ◽  
Lavage Fluid ◽  
Fixed Number ◽  
Peritoneal Lavage Fluid ◽  
Listeria Ivanovii ◽  
Wild Strains ◽  
Camp Test ◽  
Listeria Seeligeri ◽  
Listeria Welshimeri

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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