Critical role of mast cells in morphine-mediated impairment of zymosan-induced peritonitis in mice

Kołaczkowska, Elżbieta; Seljelid, Rolf; Płytycz, Barbara

doi:10.1007/pl00000264

Cited by 28 publications

(27 citation statements)

References 18 publications

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“…In agreement with these studies, we observed that the PDF-induced cell influx was significantly reduced in Ws/Ws rats or in wild-type rats that were treated with cromoglycate. Along with a poor cell influx, Ws/Ws rats and rats that were treated with cromoglycate developed a weak milky spot response, which might explain the poor influx response that was found in mast cell-deficient rats in this study and during peritonitis (27,28). We therefore suggest a novel role for mast cells in the induction of a proper omental milky spot response, providing new opportunities to regulate peritoneal cell recruitment.…”

Section: Discussionmentioning

confidence: 63%

“…In addition, milky spots are the sites for local proliferation, maturation, and differentiation of macrophages (10). It has been reported that the inherited mast cell deficiency in experimental peritonitis models significantly impaired the cell influx (27,28); however, no explanation was provided. Jippo et al (29) elegantly showed that tissue mast cells, not those in the peritoneal fluid, are essential for a proper innate immunity against bacterial invasion.…”

Section: Discussionmentioning

confidence: 99%

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Novel Role for Mast Cells in Omental Tissue Remodeling and Cell Recruitment in Experimental Peritoneal Dialysis

Zareie

Fabbrini²,

Hekking³

et al. 2006

Journal of the American Society of Nephrology

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Because of its dynamic structure, the omentum plays a key role in the immunity of the peritoneal cavity by orchestrating peritoneal cell recruitment. Because mast cells accumulate in the omentum upon experimental peritoneal dialysis (PD) and may produce angiogenic/profibrotic factors, it was hypothesized that mast cells mediate omental tissue remodeling during PD. Daily treatment with conventional PD fluid (PDF) for 5 wk resulted in a strong omental remodeling response, characterized by an approximately 10-fold increase in mast cell density (P < 0.01), an approximately 20-fold increase in vessel density (P < 0.02), an approximately 20-fold increase in the number of milky spots (P < 0.01), and a four-fold increase in submesothelial matrix thickness (P < 0.0003) in wild-type rats. In contrast, all PDF-induced omental changes were significantly reduced in mast cell-deficient Ws/Ws rats or in wild-type rats that were treated orally with a mast cell stabilizer cromoglycate. A time-course experiment showed mast cell accumulation immediately before the formation of blood vessels and milky spots. Functionally, PDF evoked a peritoneal cell influx, which was significantly reduced in Ws/Ws rats (P < 0.04) and in wild-type rats that were treated with cromoglycate (P < 0.03). Cromoglycate treatment also completely prevented PDF-induced omental adhesions to the catheter tip (P ‫؍‬ 0.0002). Mesothelial damage, angiogenesis, and fibrosis of mesentery and parietal peritoneum as well as glucose absorption rate and ultrafiltration capacity proved to be mast cell independent. Data strongly support the hypothesis that mast cells mediate PDF-induced omental tissue remodeling and, subsequently, peritoneal cell influx and adhesion formation, providing therapeutic possibilities of modulating omental function.

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Novel Role for Mast Cells in Omental Tissue Remodeling and Cell Recruitment in Experimental Peritoneal Dialysis

Zareie

Fabbrini²,

Hekking³

et al. 2006

Journal of the American Society of Nephrology

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“…Compound 48/80 (1.2 mg/kg) was given daily for 4 days before the first challenge period as well as daily throughout the first challenge period for a total of 10 days (21,22). Sodium cromoglycate (cromolyn; SigmaAldrich; 400 mg/kg) was i.p.…”

Section: Induction Of Experimental Asthmamentioning

confidence: 99%

Induction and Inhibition of the Th2 Phenotype Spread: Implications for Childhood Asthma

Hayashi

Gong

Rossetto

et al. 2005

The Journal of Immunology

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The interactions between genetic and environmental factors play a major role in the development of childhood asthma. We hypothesized that a pre-existing Th2/asthmatic response can promote Th2 responses to newly encountered Ags (i.e., phenotype spread). To test this hypothesis, we developed a mouse model in which the requirements for the induction and inhibition of phenotype spread to a clinically relevant neo-allergen (i.e., ragweed) were investigated. Our results indicate that 1) phenotype spread to the neo-allergen can be induced only within the first 8 h after a bronchial challenge with the first Ag (OVA); 2) Th2 differentiation of naive CD4+ T cells occurs in bronchial lymph nodes; 3) trafficking of naive CD4+ T cells to local lymph nodes and IL-4 produced by OVA-activated Th2 cells play essential roles in the differentiation of naive CD4+ T cells to Th2 cells; and 4) suppression of the production of chemokines involved in the homing of naive CD4+ T and Th2 cells to bronchial lymph nodes by a TLR9 agonist inhibited phenotype spread and abrogated the consequent development of experimental asthma. These findings provide a mechanistic insight into Th2 phenotype spread and offer an animal model for testing relevant immunomodulatory interventions.

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“…The zymosan-induced increase in peritoneal vasopermeability is accompanied by rapid efflux of histamine from peritoneal mast cells as shown by lack of its presence in mast cell-deficient or depleted mice [11,12]. The two processes are correlated in time and both reach their maximal values 30 min after induction of inflammation [11].…”

Section: Mediators Involved In the Early Increase Of Vascular Permeabmentioning

confidence: 99%

“…Moreover, some studies were conducted on Balb/c mice with the malfunctioning mast cells (blockage of degranulation by MC membrane-stabilizator) or histamine receptors (H 1 -and H 2 -receptor antagonists preventing histamine action) [11]. Alternatively, depletion of mast cells with compound 48/80 was used [1,12]. Either treatment led to significant, albeit slight, inhibition of early vascular permeability.…”

Section: Mediators Involved In the Early Increase Of Vascular Permeabmentioning

confidence: 99%

Shedding light on vascular permeability during peritonitis: role of mast cell histamine versus macrophage cysteinyl leukotrienes

Kołaczkowska

2002

Inflamm. res.

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The inflammatory response consists of sequential steps that are essentially the same whatever the cause and wherever the site. The main purpose of inflammation is to bring fluid, proteins, and cells from the blood into the damaged tissues. Therefore there are mechanisms that allow cells and proteins to gain access to extravascular sites, where and when they are needed if damage and infection has occurred. A critical process for formation of inflammatory exudate is an increase in permeability of local blood vessels. Vasopermeability changes can be usually attributed to mast cells and their mediators but recent studies reveal that also macrophages can be involved in this process. This short commentary discusses new data on cellular origin of major vasoactive mediators, and their receptors during peritoneal inflammation in mice.

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Critical role of mast cells in morphine-mediated impairment of zymosan-induced peritonitis in mice

Abstract: Mast cell-derived factors are involved in morphine-mediated impairment of zymosan-induced peritonitis in mice.

Cited by 28 publications

References 18 publications

Novel Role for Mast Cells in Omental Tissue Remodeling and Cell Recruitment in Experimental Peritoneal Dialysis

Novel Role for Mast Cells in Omental Tissue Remodeling and Cell Recruitment in Experimental Peritoneal Dialysis

Induction and Inhibition of the Th2 Phenotype Spread: Implications for Childhood Asthma

Shedding light on vascular permeability during peritonitis: role of mast cell histamine versus macrophage cysteinyl leukotrienes

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