Absence of intestinal mast cell response in congenitally athymic mice during Trichinella spiralis infection

Ruitenberg, E. J.; Elgersma, Anneke

doi:10.1038/264258a0

Cited by 265 publications

(172 citation statements)

References 8 publications

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“…As with the role of IL-5 in promoting eosinophil responses, IL-9 acts mainly as a maturation factor for mucosal mast cells, [90][91][92] and is largely T cell derived, [93][94][95] although it can be secreted by ILC2, 96 as well as by mast cells themselves 97,98 that in turn promote enhanced secretion of IL-25, IL-33, and TSLP from epithelial cells. 99 As a result, T. muris and H. polygyrus expulsion are impaired in mast cell-deficient mice 99,100 as well as upon administration of neutralizing IL-9 antibodies, 101,102 although it should be noted that studies using mast celldeficient mice (c-kit mutants) suffer from possible confounding factors given the role for c-kit on many other cell types, and thus remain to be clarified.…”

Section: Transmissionmentioning

confidence: 99%

Immunity to gastrointestinal nematode infections

2018

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Section: Transmissionmentioning

confidence: 99%

Immunity to gastrointestinal nematode infections

2018

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“…The densities of mast cells in tissues were calculated per mm 2 and are expressed throughout as mean …”

Section: Data Analysesmentioning

confidence: 99%

“…4-0 . 8% formaldehyde are required for staining of mucosal mast cell granules with methylene blue, toluidine blue, or alcian blue [1][2][3]. In contrast, the granules of connective tissue mast cells in the skin and other organs can be stained after fixation with these fixatives as well as with 10% neutral buffered formalin.…”

Section: Introductionmentioning

confidence: 99%

Tissue-dependent differences in the asynchronous appearance of mast cells in normal mice and in congenic mast cell-deficient mice after infusion of normal bone marrow cells

Friend

Austen

et al. 1996

Clinical and Experimental Immunology

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SUMMARYThe time courses of the appearance of tissue mast cells in six sites were compared in normal WBB6F 1 -= As assessed by morphometric analysis of Carnoy's solution-fixed, methylene blue-stained tissue sections, the density of mast cells in the stomach mucosa, stomach submucosa, and spleen of = mice reached maximal levels by 8 weeks of age, whereas the density of mast cells in the skin, extraparenchymal airway walls, and lung parenchyma did not reach maximal levels until 18 weeks of age. When 8-week-old W = W v mice were infused with 2 2 10 7 bone marrow cells from = mice, mast cells appeared in the stomach mucosa and submucosa after 2 . 5 weeks, in the spleen and extraparenchymal airway walls after 5 weeks, and in the lung parenchyma after 10 weeks. Twenty weeks after bone marrow infusion, the mast cell densities in the spleen, stomach mucosa, and stomach submucosa were seven-, 13-, and five-fold greater, respectively, than those in age-matched = mice, but were eight-, two-, and fivefold lower in the skin, extraparenchymal airway walls, and lung parenchyma, respectively. Thus, those tissues that in =W v mice to assess mast cell dependency. Our results indicate that the capacity to restore a mast cell-dependent response in a particular tissue of the latter mice may relate to the local mast cell density and whether the immunological challenge activates mast cells only in that tissue or systematically with attendant widespread release of proinflammatory mediators.

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“…However, substantially less is known about the fate of expanded populations of these granulocytes during the recovery phase of an inflammatory response. A commonly used disease model to understand MC and eosinophil development in the mouse is the transient, T cell-dependent eosinophilia and mastocytosis that occurs in the intestines of helminth-infected mice and rats (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). In the jejunum of these helminth-infected animals, IL-5 plays a central role in the eosinophilia (11,17), whereas c-kit ligand, IL-3, IL-4, IFN-␥, and TNF-␣ play central roles in the mastocytosis (9,12,13,16,18).…”

mentioning

confidence: 99%

Senescent Jejunal Mast Cells and Eosinophils in the Mouse Preferentially Translocate to the Spleen and Draining Lymph Node, Respectively, During the Recovery Phase of Helminth Infection

Friend¹,

Gurish

Austen

et al. 2000

The Journal of Immunology

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Because mice infected with Trichinella spiralis experience a pronounced, but transient, mastocytosis and eosinophilia in their intestine, this disease model was used to follow the fate of senescent T cell-dependent mast cells (MCs) and eosinophils. Very few MCs or eosinophils undergoing apoptosis were found in the jejunum during the resolution phase of the infection, even though apoptotic MCs were common in the large intestine. Although the mesenteric draining lymph nodes contained large numbers of apoptotic eosinophils, MCs were rarely found at this location. During the recovery phase, large numbers of MCs were present in the spleen, and many of these cells possessed segmented nuclei. These splenic MCs were not proliferating. Although MCs from the jejunum and spleen of noninfected mice failed to express mouse MC protease (mMCP) 9, essentially all of the MCs in the jejunal submucosa and spleen of T. spiralis-infected mice expressed this serine protease during the recovery phase. The MCs in the jejunum expressed mMCP-9 before any mMCP-9-containing cells could be detected in the spleen. The fact that mMCP-9-containing MCs were detected in splenic blood vessels as these cells began to disappear from the jejunum supports the view that many jejunal MCs translocate to the spleen during the recovery phase of the infection. During this translocation process, some senescent jejunal MCs undergo nuclear segmentation. These studies reveal for the first time different exit and disposal pathways for T cell-dependent eosinophils and MCs after their expansion in the jejunum during a helminth infection.

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Absence of intestinal mast cell response in congenitally athymic mice during Trichinella spiralis infection

Cited by 265 publications

References 8 publications

Immunity to gastrointestinal nematode infections

Immunity to gastrointestinal nematode infections

Tissue-dependent differences in the asynchronous appearance of mast cells in normal mice and in congenic mast cell-deficient mice after infusion of normal bone marrow cells

Senescent Jejunal Mast Cells and Eosinophils in the Mouse Preferentially Translocate to the Spleen and Draining Lymph Node, Respectively, During the Recovery Phase of Helminth Infection

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