Quantitation of Immediate and Delayed Hypersensitivity Responses in &lt;i&gt;Trichinella&lt;/i&gt;-Infected Mice

Gabriel, B.W.; Justus, David E.

doi:10.1159/000232352

Cited by 15 publications

(3 citation statements)

References 14 publications

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“…The responsible compo nent in immune serum appears to be homocytotropic antibodies, because the ability to reject the parasite cannot be transferred by heat-treated immune serum in which IgE is inactivated. This supports the propo sal [21][22][23] that type 1 hypersensitivity is involved in rapid rejection. Our results indicate that intestinal fluid secretion, which accompanies rapid rejection, is also dependent on IgE, confirming physiologically that immune serum conveys intestinal hypersensitiza tion.…”

Section: Discussionsupporting

confidence: 83%

Involvement of Type I Hypersensitivity in Rapid Rejection of Trichinella spiralis from Adult Rats

Zhang¹,

Castro²

1990

Int Arch Allergy Immunol

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The role of type I hypersensitivity in the rapid rejection of Trichinella spiralis from actively, and passively immunized rats was examined. Net intestinal fluid secretion, which occurs during the rejection of the parasites, was used to verify the expression of local anaphylaxis and was examined for its possible role in the rejection process. Worm establishment in the small intestine 30 min after intraduodenal inoculation was significantly reduced in rats that were passively immunized with immune serum containing anti- Trichinella IgE as compared with recipients of normal serum. Worm-induced fluid secretion in immune rats was completely inhibited by the combined action of indomethacin and diphenhydramine. However, worm rejection was not affected. L-651,392, a 5-lipoxygenase inhibitor, also failed to prevent rejection. Ketanserin (a serotonin S₂ receptor antagonist) and MDL-72222 (a serotonin S₃ receptor antagonist) together blunted the rapid rejection response and reduced fluid secretion. Furthermore, intra-arterial perfusion of serotonin into nonimmune rats caused fluid secretion and reduced worm establishment. In nonimmune rats prostaglandin E₂, cholera toxin, and hypertonic Krebs-mannitol solution were used to evoke the same level of intestinal fluid secretion as that induced by reinfection in immune rats or by serotonin in nonimmune hosts. When larvae were inoculated into the secreting gut, their infectivity was unaffected. The results suggest that anaphylaxis is involved in the rapid rejection of T. spiralis in immune rats and that serotonin is a possible chemical mediator of worm rejection. Although the mode of action of serotonin in the rejection process remains unknown, its possible involvement through fluid secretion can be ruled out.

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Section: Discussionsupporting

confidence: 83%

Involvement of Type I Hypersensitivity in Rapid Rejection of Trichinella spiralis from Adult Rats

Zhang¹,

Castro²

1990

Int Arch Allergy Immunol

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“…Primary and secondary T. spiralis-induced intestinal inflammation has been regarded to be of DTH nature [9]. Also a se quence of T cell activities during helminthic infec tions has been proposed [36].…”

Section: Discussionmentioning

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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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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“…Like humans suffering from trichinosis, T. spiralis-infected mice produce strong IgE responses (15,16). The infusion of purified T. spiralis immune IgE into rats has been shown to confer rapid parasite expulsion to naive animals and the suppression of active IgE responses using anti-IgE in rats has been reported to markedly impair parasite clearance (17)(18)(19).…”

Section: Igorous Ige Ab Production Is a Characteristic Response Durmentioning

confidence: 99%

IgE Enhances Parasite Clearance and Regulates Mast Cell Responses in Mice Infected with Trichinella spiralis

Gurish

Bryce

Hong

et al. 2004

The Journal of Immunology

171

160

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Trichinella spiralis infection elicits a vigorous IgE response and pronounced intestinal and splenic mastocytosis in mice. Since IgE both activates mast cells (MC) and promotes their survival in culture, we examined its role in MC responses and parasite elimination in T. spiralis-infected mice. During primary infection, wild-type but not IgE-deficient (IgE−/−) BALB/c mice mounted a strong IgE response peaking 14 days into infection. The splenic mastocytosis observed in BALB/c mice following infection with T. spiralis was significantly diminished in IgE−/− mice while eosinophil responses were not diminished in either the blood or jejunum. Similar levels of peripheral blood eosinophilia and jejunal mastocytosis occurred in wild-type and IgE-deficient animals. Despite the normal MC response in the small intestine, serum levels of mouse MC protease-1 also were lower in parasite-infected IgE−/− animals and these animals were slower to eliminate the adult worms from the small intestine. The number of T. spiralis larvae present in the skeletal muscle of IgE−/− mice 28 days after primary infection was about twice that in BALB/c controls, and the fraction of larvae that was necrotic was reduced in the IgE-deficient animals. An intense deposition of IgE in and around the muscle larvae was observed in wild-type but not in IgE null mice. We conclude that IgE promotes parasite expulsion from the gut following T. spiralis infection and participates in the response to larval stages of the parasite. Furthermore, our observations support a role for IgE in the regulation of MC homeostasis in vivo.

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Quantitation of Immediate and Delayed Hypersensitivity Responses in <i>Trichinella</i>-Infected Mice

Cited by 15 publications

References 14 publications

Involvement of Type I Hypersensitivity in Rapid Rejection of Trichinella spiralis from Adult Rats

Involvement of Type I Hypersensitivity in Rapid Rejection of Trichinella spiralis from Adult Rats

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

IgE Enhances Parasite Clearance and Regulates Mast Cell Responses in Mice Infected with Trichinella spiralis

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