Nippostrongylus brasiliensis: Mast cell populations in rats

Wells, Phyllis D.

doi:10.1016/0014-4894(71)90066-x

Cited by 15 publications

(5 citation statements)

References 5 publications

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“…These results suggest that the character and regulatory factors of airway goblet cells differ from those of the gastrointestinal tract and that other trefoil peptides may be present in the lung. In addition, as reported previously [32], at days 14 and 21 after infection, marked mastocytosis was observed in the lung (data not shown). Since it has been reported that mast cell proteases may induce airway gland secretion [33], mast cells may contribute, at least in part, to the goblet cell response.…”

Section: Discussionsupporting

confidence: 69%

Goblet Cell Hyperplasia in the Airway of <i>Nippostrongylus brasiliensis</i>-Infected Rats

Tomita

Kobayashi²,

Itoh³

et al. 2000

Respiration

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Background: In rats, the intestinal parasite Nippostrongylus brasiliensis is recognized as a strong inducer of intestinal goblet cell hyperplasia. Although this parasite migrates through the airways during the course of its infection, airway goblet cell response remains unknown. Objective: This study was designed to examine airway goblet cell response during the course of N. brasiliensis infection in rats and to characterize these goblet cells. Methods: Airway goblet cells were stained with Alcian blue and periodic acid-Schiff. To characterize the goblet cells, mebendazole treatment, lectin histochemistry, and RNA blot analysis using probes for rat MUC2 and trefoil peptides were examined. Results: Airway and small intestinal goblet cell hyperplasia were observed at days 14 and 21 after infection but not at day 7. In rats treated with mebendazole, goblet cell hyperplasia was not present in the small intestine, but was observed in the lung on day 14. These results indicate that airway goblet cell hyperplasia may be induced by local pulmonary factors. By lectin histochemistry, the stainability of airway goblet cells at day 21 was similar to that of small intestine goblet cells even though rat MUC2 and trefoil peptide mRNA were not detected in the lung. Conclusions: Airway goblet cell hyperplasia observed at days 14 and 21 after N. brasiliensis infection may be induced by local factors. Airway goblet cells have characteristics that differ from those of the small intestine.

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Section: Discussionsupporting

confidence: 69%

Goblet Cell Hyperplasia in the Airway of <i>Nippostrongylus brasiliensis</i>-Infected Rats

Tomita

Kobayashi²,

Itoh³

et al. 2000

Respiration

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“…Increased levels of RMCPII were also recorded in lung and MLN following infection with N. brasiliensis. Mast cell infiltration of MLN has been reported in Nippostrongylw-infected rats [21] and pulmonary mastocytosis has been observed to be associated with larval migration [22]. The results suggest that a proportion of the additional mast cells induced by parasite infection are MMC.…”

Section: Discussionmentioning

confidence: 93%

Gut mucosal mast cells in Nippostrongylus‐primed rats are the major source of secreted rat mast cell protease II following systemic anaphylaxis

King

Miller

Woodbury³

et al. 1986

Eur J Immunol

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The distribution of the predominant chymotrypsin-like enzyme of mucosal mast cells (rat mast cell protease II: RMCP II) was examined in naive and Nippostrongylus-primed rats both before and after the induction of systemic anaphylaxis. Anaphylactic secretion of RMCP II following i.v. challenge of primed rats with worm antigen was accompanied by significant depletion of this enzyme from the jejunal and gastric mucosae; the concentrations were not altered in the ileum and colon. Despite significant increases in the levels of RMCP II in lung and mesenteric lymph node following infection with N. brasiliensis there was no anaphylactic depletion of this enzyme from these sites. No RMCP II was detected in liver, spleen, kidney or bone marrow either before or after systemic anaphylaxis. Mucosal mast cells were depleted from the jejunal, gastric and colonic mucosae following antigen challenge of primed rats. These data provide further evidence that gastrointestinal mucosal mast cells are the major source of secreted RMCP II following systemic anaphylaxis in the rat.

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“…In conclu sion, gut exposure to N. brasiliensis is sufficient to cause local MMC hyperplasia and mucosal surfaces distant from the parasite can also be involved in the response. It is unclear at present whether MMC in nonintestinal mucosae are also affected [11,13]. The general significance of the findings is that immune re sponses at one mucosal site may affect both the posi tion and the number of MMC in distant mucosae, thus rendering the mast cells more accessible to aller gens and increasing the potential for tissue-damaging immediate-type hypersensitivity reactions.…”

Section: Discussionmentioning

confidence: 90%

“…The im portance of local factors in the mucosa is suggested by the large MMC response in the intestine at the site of maximum worm numbers [4,10]. However, systemic effects of infestation have been observed on lung mast cells [11] and on MMC in antigen-free heterotopic iso grafts of gut [10]. The latter studies used larval infesta tions and it is probable that changes in lung mast cells were due to direct local stimulation by migrating lar vae, while anomalous migration of larvae directly in to transplanted gut segments cannot be excluded [12].…”

Section: Introductionmentioning

confidence: 99%

Local and Systemic Factors Regulating Mucosal Mast Cells

Pitts¹,

Mayrhofer²

1983

Int Arch Allergy Immunol

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The contributions of local and systemic factors to the regulation of mucosal mast cells and globule leukocytes have been examined in the rat. Nippostrongylus brasiliensis has been used to provide a potent immunological stimulus for mucosal mast cell hyperplasia and the roles of intestinal and extraintestinal sensitization observed by comparison of the gut mast cell responses to larval and adult worm infestations. Systemic effects of adult worm infestations have been examined in isolated Thiry-Vella loops of intestine. It is concluded that the extraintestinal phase of larval infestation is not obligatory for a gut mast cell response and that mast cell hyperplasia and globule leukocyte formation are not dependent on direct contact with the parasite or its products. The dissemination of the mast cell response and the general significance of the results are discussed.

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Nippostrongylus brasiliensis: Mast cell populations in rats

Cited by 15 publications

References 5 publications

Goblet Cell Hyperplasia in the Airway of <i>Nippostrongylus brasiliensis</i>-Infected Rats

Goblet Cell Hyperplasia in the Airway of <i>Nippostrongylus brasiliensis</i>-Infected Rats

Gut mucosal mast cells in Nippostrongylus‐primed rats are the major source of secreted rat mast cell protease II following systemic anaphylaxis

Local and Systemic Factors Regulating Mucosal Mast Cells

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