Thymus Dependence of the Adoptive Transfer of Intestinal Mastocytopoiesis in &lt;i&gt;Trichinella spirali&lt;/i&gt;&lt;i&gt;s&lt;/i&gt;-lnfected Mice

Parmentier, H.K.; Ruitenberg, E. J.; Elgersma, Anneke

doi:10.1159/000233109

Cited by 13 publications

(12 citation statements)

References 11 publications

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“…MMC re sponses can be adoptively transferred into and be ac celerated in infected recipients by T cells [1,25,29].…”

Section: Introductionmentioning

confidence: 99%

“…In mice, MMC-like precursor cells can be found throughout the body, including the gut [5]. However, intestinal helminth infections induce a lo cal MMC response that is restricted to the gut and as sociated lymphoid tissue only [25], suggesting the in volvement of local environmental processes. It has as yet not been established how antigenic stimuli in the gut are translated into a localized mastocytosis via immune T cells residing not only in gut-associated lymph nodes but also in spleen and peripheral lym phoid tissue.…”

Section: Introductionmentioning

confidence: 99%

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Involvement of Serotonin in Intestinal Mastocytopoiesis and Inflammation during a <i>Trichinella spiralis </i>Infection in Mice

Parmentier¹,

Vries

Ruitenberg

et al. 1987

Int Arch Allergy Immunol

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The involvement of serotonin in the regulation of intestinal mastocytopoiesis and inflammation has been investigated in mice infected with Trichinella spiralis. Two serotonin antagonists, methysergide and ketanserin, were examined for their ability to interfere with jejunal pathology comprising the influx of mucosal mast cells and other inflammatory cells during an infection with T. spiralis and with worm expulsion. In vitro analysis of the frequence of mast cell precursors in bone marrow, blood, spleen and intestinal tissue suggested that the mucosal mast cell response during a T. spiralis infection is probably due to invasion and local maturation in the gut of mast cell precursors, and may be mediated by T-cell-derived mast cell growth factors. Since both serotonin antagonists inhibited the mucosal mast cell response in T. spiralis-infected mice and diminished the influx of eosinophilic granulocytes, goblet cell hyperplasia, and villous atrophy, it was concluded that during a T. spiralis infection in mice release of serotonin may provide an environment that facilitates the local influx in the gut of inflammatory cells. Since worm expulsion was not affected by the serotonin antagonists, these results suggest that worm expulsion can occur without a mast cell and or eosinophilic granulocyte influx. The role of serotonin release by as yet unidentified serotonin-containing cells in the gut in relation with T cell regulation is discussed.

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“…MMC re sponses can be adoptively transferred into and be ac celerated in infected recipients by T cells [1,25,29].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Involvement of Serotonin in Intestinal Mastocytopoiesis and Inflammation during a <i>Trichinella spiralis </i>Infection in Mice

Parmentier¹,

Vries

Ruitenberg

et al. 1987

Int Arch Allergy Immunol

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“…5,7 It is also clear that the mast cell depends on the presence of antigen-specific CD4 T-helper cells of the Th2 phenotype. 36 Furthermore, cytokines secreted by these cells locally in the intestine (such as interleukin 3 [IL-3], -4, -9, and -10) act together or in concert with non-CD4-derived factors (such as SCF and transforming growth factor ␤ [TGF-␤]) to complete mucosal mast cell differentiation. Details of the likely events leading to the generation of the CD4 T-cell response in the lymph node draining the intestine during the response to infection are relatively well defined.…”

mentioning

confidence: 99%

In vivo exit of c-kit+/CD49dhi/β7+ mucosal mast cell precursors from the bone marrow following infection with the intestinal nematode Trichinella spiralis

Pennock

Grencis

2004

Blood

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We have used the parasite helminth Trichinella spiralis to study the generation and differentiation of mast cell progenitors in the bone marrow of mice, as this infection triggers an intestinal mastocytosis which correlates with parasite expulsion. C-kit ؉ mast cell progenitors have previously been defined by methylcellulose colony-forming units and by limiting dilution assays in vitro. In vivo experiments have demonstrated the essential requirement by mast cells for specific integrin expression. We have defined 2 c-kit ؉ populations in the bone marrow, one of which coexpresses CD49d/␤7 integrin, a marker essential for small intestine immigration. We have confirmed the phenotype of these cells by using antagonistic anti-c-kit antibody in vivo. Our data show that the loss of c-kit ؉ /␤7 ؉ cells from the bone marrow correlates with their appearance in the blood and precedes detection of mature mast cells in the gut by 3 days. This exit correlates with an increase in soluble stem cell factor (SCF) in the serum, suggesting that the c-kit/SCF interaction may be chemotactic or haptotactic in nature. This study shows that during infection the bone marrow environment generates mast cells destined for the intestinal mucosa before their exit into the periphery, indicating a clear interplay between infection site and hematopoietic tissue. IntroductionThe existence of mast cell progenitors (MCp's) in various tissues has been clearly demonstrated by in vitro culture and limiting dilution assays, 1-3 although isolation and phenotypic analysis of these cells ex vivo has been more elusive. It was not until 1996 that a committed precursor for the mast cell lineage was first identified in mouse fetal blood, using c-kit (stem cell factor receptor) as a surface marker. 4 c-kit is unique in that it is expressed on primitive and pluripotent stem cells, then subsequently retained by committed MCp's, making the latter presently more identifiable by their response to growth factors in vitro than by their expression of particular cell surface markers. Moreover, few studies in vivo have investigated early mast cell differentiation under conditions of infectious challenge and have largely concentrated on their steadystate production. This lack of investigation is particularly surprising, because a major role for mast cells is in mediating responses to antigenic and infectious challenge.Trichinella spiralis is a gut-dwelling nematode which causes intestinal hyperplasia and mastocytosis. Because this correlates well with worm expulsion, 5-7 we are interested in understanding the generation of mast cells to dissect the mechanisms governing the resolution of infection. Previous work with bone marrow chimeras 8 has shown that mast cell deficiency in W/W v mice is primarily a hematopoietic and not a lymphopoietic defect. 6 Limiting dilution assays have defined resting mast cell progenitor populations in many different tissues, including small and large intestine, lung, spleen, and bone marrow. 3 It is possible to adoptively transfer a high prod...

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“…These and additional studies lend support to the earlier hypothesis that globule leukocytes represent a unique population of mesenchymal origin. 18,20,21,23 The function of the globule leukocyte is poorly understood. The association between globule leukocytes and parasitic infections has been well documented and recently reviewed.…”

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A Neoplasm of Globule Leukocytes in a Cat

et al. 1986

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Abstract.A neoplasm involving the ileo-cecal-colic junction, thymus, and tracheobronchial lymph nodes of a 7-year-old domestic cat was composed of dense sheets of round to oval mononuclear cells with oval to indented nuclei, moderate amounts of cytoplasm, and variable numbers of round eosinophilic granules. These granules are brown to black in phosphotungstic acid hematoxylin-stained sections and stain variably with the periodic acid-Schiff stain. They are 0.8 to 1.5 pm in diameter, limited by a single unit membrane, and have variable electron density. Light microscopic cellular morphology and staining characteristics as well as ultrastructural features of these cells are consistent with feline globule leukocytes. Morphologic features of the neoplastic cells in the present case are similar to those of the only other reported neoplasm of globule leukocytes which also involved the intestine of a cat.Globule leukocytes are found in the mucosa of the intestinal, respiratory, and urogenital systems of many species. 2,13,23,24 Although first described in 19 1 9,2y their origin and function remain controversial. Derivation of globule leukocytes from lymphocytes, 14,25 plasma eo~inophils,~ and a unique mesenchymal cell population23 has been suggested. Recent investigation has focused on the mast cell as a possible source of globule leukocytes. In the digestive tract, derivation of the globule leukocyte from the submucosal mast cell has been proposed.17 Using athymic mice, research has shown that these intestinal mast cells are thymus-dependent. 1y,26 Since proliferation of globule leukocytes has been demonstrated to be thymus-independent,18s20 intestinal mast cell origin seems unlikely. These and additional studies lend support to the earlier hypothesis that globule leukocytes represent a unique population of mesenchymal origin. 18,20,21,23 The function of the globule leukocyte is poorly understood. The association between globule leukocytes and parasitic infections has been well documented and recently reviewed.* Intracellular IgE has been demonstrated in intestinal globule leukocytes of rats with enteric parasites. l 6 Increased numbers of globule leukocytes have been shown to be associated with gastrointestinal parasitism in ~h e e p ,~ cats,12 dogs,13 rats,21 and mice.2o Also, some investigators have observed a rise in the number of intestinal globule leukocytes to be temporally associated with the phenomenon of nematode expulsion in both primary and challenge infection^.^^,^^ Neoplasia of globule leukocytes is evidently extremely rare. A neoplasm involving the terminal small intestines of a domestic cat has previously been reported;6 however, globule leukocyte neoplastic proliferations have not been described for other species. The purpose of the present report is to document a second case of globule leukocyte neoplasia and to provide detailed cytologic, histologic, and ultrastructural characterization of the neoplasm. Case HistoryA 7-year-old neutered female domestic cat was presented to the Purdue University Smal...

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Thymus Dependence of the Adoptive Transfer of Intestinal Mastocytopoiesis in <i>Trichinella spirali</i><i>s</i>-lnfected Mice

Cited by 13 publications

References 11 publications

Involvement of Serotonin in Intestinal Mastocytopoiesis and Inflammation during a <i>Trichinella spiralis </i>Infection in Mice

Involvement of Serotonin in Intestinal Mastocytopoiesis and Inflammation during a <i>Trichinella spiralis </i>Infection in Mice

In vivo exit of c-kit+/CD49dhi/β7+ mucosal mast cell precursors from the bone marrow following infection with the intestinal nematode Trichinella spiralis

A Neoplasm of Globule Leukocytes in a Cat

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