Proteinase phenotypes and fixation properties of rat mast cells in parasitic lesions caused by <i>Mesocestoides corti</i>: selective and site‐specific recruitment of mast cell subsets

Chernin, Jack; Miller, H. R. P.; Newlands, G. F. J.; McLaren, Diane J.

doi:10.1111/j.1365-3024.1988.tb00233.x

Cited by 10 publications

(15 citation statements)

References 11 publications

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“…Chernin et al (1988) found that livers of M. cortiinfected rats contained mast cells with histochemical properties of both mucosal (MMC) and connective mast cells (CTMC), which differ in granule content (Puxeddu et al 2003). In the present study, the decline of MC numbers within the experimental period was accompanied by a significant elevation of the collagen content in all treated groups, the most in LG-treated mice.…”

Section: Discussionsupporting

confidence: 44%

Praziquantel and liposomized glucan-treatment modulated liver fibrogenesis and mastocytosis in mice infected withMesocestoides vogae(M. corti, Cestoda) tetrathyridia

Hrčková

Velebný

Daxnerová³

et al. 2005

Parasitology

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Beta-glucans are immunomodulators able to activate innate immunity and to potentiate acquired immune reactions. We investigated the impact of co-administration of liposomized beta-glucan on the larvicidal effect of the anthelmintic praziquantel (PZQ) in the livers and peritoneal cavities in mice infected with Mesocestoides vogae (M. corti). Also, within 2 weeks following therapy (up to day 29 p.i.) we examined collagen synthesis in the livers of mice by means of biochemical determination of hydroxyproline concentration, total mast cell counts and cell proliferative capacity using immunohistochemical and radiometrical methods. After co-administration of liposomized glucan (LG) and PZQ efficacy (%) was significantly higher than after treatment with either compound alone, particularly in the peritoneal cavity compared to the liver. In comparison with the control, more intense collagenesis was found in the B-liver parts (high intensity of infection) and lowering of collagen content in the A-parts (very weak infection). This effect was strongest after LG treatment and co-administration of PZQ abolished the pro-fibrotic effect of LG. In all groups, mast cell counts were higher in the B-liver parts than in the A-parts and the dynamics of mastocytosis was profoundly modulated following therapy. Whereas the effect of PZQ was only moderate, early and very strong onset was seen after LG treatment. Administration of PZQ suppressed LG induced-elevation of mast cells counts in both liver parts. Using DNA S-phase markers (BrdU and 3H-thymidine) the proliferative capacity was shown to be associated with several kinds of liver cells. Therapy significantly stimulated [3H]-thymidine incorporation (cell proliferation) only in the A-parts over that in control, the most after LG administration. In summary (i) the anthelmintic effect of PZQ could be enhanced after simultaneous administration of the immunomodulator beta-glucan entrapped in a liposomal carrier, (ii) intense mastocytosis seen after treatment with LG seems to have a direct role in the glucan's pro-fibrotic activity and can be abolished after co-administration of PZQ in a time-dependent manner, (iii) the pattern of cell proliferation indicates that in the case of PZQ treatment, the reparative processes of liver parenchyma are enhanced in an inverse correlation with the intensity of infection.

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Section: Discussionsupporting

confidence: 44%

Praziquantel and liposomized glucan-treatment modulated liver fibrogenesis and mastocytosis in mice infected withMesocestoides vogae(M. corti, Cestoda) tetrathyridia

Hrčková

Velebný

Daxnerová³

et al. 2005

Parasitology

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“…Mast cell degranulation is coincident with rapid expulsion in rats, as revealed by detection of rat mast cell protease II (RMCPII) in the serum (2); however, there is no direct evidence that mast cells contribute to expulsion. Mast cells have been reported to be the sole cellular source of RMCPII in intestinal tissue of naive rats (17,18). RMCPII-positive cells are present in the lung, liver, and primary lymphoid tissue (19); however, intestinal mast cells are very likely to be the major source of blood RMCPII, when antigenic challenge is limited to the intestine.…”

mentioning

confidence: 99%

Expulsion of Secondary Trichinella spiralis Infection in Rats Occurs Independently of Mucosal Mast Cell Release of Mast Cell Protease II

Blum

Thrasher

Gagliardo

et al. 2009

The Journal of Immunology

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Our aim was to elucidate the contribution of mucosal mast cells to the effector phase of a secondary immune response to Trichinella spiralis. During secondary infection, rats expel 90–99% of T. spiralis first-stage larvae from the intestine in a matter of hours. This phenomenon appears to be unique to rats and has been called rapid expulsion. Primary intestinal infection by T. spiralis induces mastocytosis, and mast cell degranulation occurs when challenged rats exhibit rapid expulsion. These observations have engendered the view that mast cells mediate rapid expulsion. In this study, we report that. immunization of adult Albino Oxford rats by an infection limited to the muscle phase did not induce intestinal mastocytosis, yet such rats exhibited rapid expulsion when challenged orally. Although mastocytosis was absent, the protease unique to mucosal mast cells, rat mast cell protease II (RMCPII), was detected in sera at the time of expulsion. We further evaluated mast cell activity in neonatal rats that display rapid expulsion. Pups born to infected dams displayed rapid expulsion, and RMCPII was detected in their sera. By feeding pups parasite-specific mAbs or polyclonal Abs before challenge infection, it was possible to dissociate mast cell degranulation from parasite expulsion. These results indicate that rapid expulsion can occur in the absence of either intestinal mastocytosis or RMCPII release. Furthermore, release of RMCPII is not sufficient to cause expulsion. The data argue against a role for mast cells in the mechanism underlying the effector phase of protective immunity against T. spiralis in rats.

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“…Both RMCP-I1 and MMCP-1 predominate in intestinal mucosal mast cells whereas RMCP-I is located in connective tissue mast cells (Woodbury, Gruzenski & Lagunoff 1978;Gibson & Miller 1986, Newlands et at. 1987, Miller et al 1988. Our results show that there is substantial recruitment of RMCP-11-containing mast cells in the livers of infected rats and that RMCP-I1 is released systemically at the time when elimination of S. mansoni worms normally occurs.…”

mentioning

confidence: 64%

“…Substantial heterogeneity of mast cell subpopulations has been described in man (Irani & Schwartz 1990) and rodents (Enerback 1986, Befus et al 1982 and most data suggest that helminth infection in gut, liver, and other tissues in the rat is associated with recruitment of mast cells with a phenotype that is similar to or identical with that of intestinal mucosal mast cells (Enerback 1987, Miller & Jarrett 1971, Chernin et al 1988, Lindsay & Williams 1985. As yet neither the phenotype nor the in vivo function of mast cells in rodents infected with S. mansoni have been identified.…”

mentioning

confidence: 99%

Hepatic recruitment of mast cells occurs in rats but not mice infected with Schistosoma mansoni

Miller

Newlands

McKELLAR

et al. 1994

Parasite Immunology

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The pathogenesis of infection with Schistosoma mansoni in rats is distinct from that in mice. Rats are non-permissive hosts and infection is terminated in the liver before egg laying commences whereas the parasites completes its life cycle in mice. Comparison of the mast cell responses in the two species reveals that a pronounced hepatic mastocytosis occurs in the rat and this is concomitant with the demise of the parasite. The majority of recruited hepatic mast cells contain the highly soluble granule chymase, rat mast cell protease-II, which is released systemically into blood during the period of parasite elimination. In contrast, very few mast cells are found in livers of parasitized mice and none contain the soluble granule chymase mouse mast cell protease-1. However, during egg deposition in the gut, an intraepithelial mastocytosis occurs in parasitized mice. These intraepithelial cells are typical mucosal mast cells as determined by their content of mouse mast cell protease-1. Recruitment of mucosal mast cells occurs in the intestinal lamina propria of infected rats soon after the parasites migrate to the liver. These findings suggest that mast cells of the mucosal phenotype are involved in the pathogenesis of the hepatic response to infection in the rat but that, in the mouse, mucosal mastocytosis is associated with intestinal sensitization by egg antigens.

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Proteinase phenotypes and fixation properties of rat mast cells in parasitic lesions caused by Mesocestoides corti: selective and site‐specific recruitment of mast cell subsets

Cited by 10 publications

References 11 publications

Praziquantel and liposomized glucan-treatment modulated liver fibrogenesis and mastocytosis in mice infected withMesocestoides vogae(M. corti, Cestoda) tetrathyridia

Praziquantel and liposomized glucan-treatment modulated liver fibrogenesis and mastocytosis in mice infected withMesocestoides vogae(M. corti, Cestoda) tetrathyridia

Expulsion of Secondary Trichinella spiralis Infection in Rats Occurs Independently of Mucosal Mast Cell Release of Mast Cell Protease II

Hepatic recruitment of mast cells occurs in rats but not mice infected with Schistosoma mansoni

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