Nematode galectin binds IgE and modulates mast cell activity

Mast cell degranulation is the major mechanism influencing establishment and survival of the abomasal nematode Teladorsagia circumcincta and probably many other gastrointestinal nematodes. Host galectins-3 and -9 have been shown to bind IgE and positively and negatively influence mast cell degranula...

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Published in:Veterinary parasitology Vol. 311; p. 109807
Main Authors: Donskow-Łysoniewska, Katarzyna, Maruszewska-Cheruiyot, Marta, Krawczak-Wójcik, Katarzyna, Gonzalez, Jorge F., Hernández, Julia N., Stear, Michael J.
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Language:English
Published: Elsevier B.V 01-11-2022
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Abstract Mast cell degranulation is the major mechanism influencing establishment and survival of the abomasal nematode Teladorsagia circumcincta and probably many other gastrointestinal nematodes. Host galectins-3 and -9 have been shown to bind IgE and positively and negatively influence mast cell degranulation. As incoming nematodes produce large amounts of galectin, we hypothesised that nematode galectin competes with host galectin and inhibits mast cell degranulation. ELISA was used to show that nematode galectin reduced total IgE activity. Galectin also reduced the binding of sheep IgE to the surface of a mast cell line and decreased the release of LCT-4 and Beta hexosaminidase but not MMP-9. These results indicate that nematode galectin influences mast cell degranulation and identify a potential immunomodulatory mechanism used by nematodes to enhance their establishment and survival. [Display omitted] •Sheep from a resistant breed had higher IgE anti-galectin activity than susceptible sheep.•Nematode galectin binds IgE and reduces apparent IgE concentrations.•Nematode galectin inhibits mast cell degranulation.•Nematodes produce galectin to enhance their establishment and survival.
AbstractList Mast cell degranulation is the major mechanism influencing establishment and survival of the abomasal nematode Teladorsagia circumcincta and probably many other gastrointestinal nematodes. Host galectins-3 and -9 have been shown to bind IgE and positively and negatively influence mast cell degranulation. As incoming nematodes produce large amounts of galectin, we hypothesised that nematode galectin competes with host galectin and inhibits mast cell degranulation. ELISA was used to show that nematode galectin reduced total IgE activity. Galectin also reduced the binding of sheep IgE to the surface of a mast cell line and decreased the release of LCT-4 and Beta hexosaminidase but not MMP-9. These results indicate that nematode galectin influences mast cell degranulation and identify a potential immunomodulatory mechanism used by nematodes to enhance their establishment and survival. [Display omitted] •Sheep from a resistant breed had higher IgE anti-galectin activity than susceptible sheep.•Nematode galectin binds IgE and reduces apparent IgE concentrations.•Nematode galectin inhibits mast cell degranulation.•Nematodes produce galectin to enhance their establishment and survival.
ArticleNumber 109807
Author Maruszewska-Cheruiyot, Marta
Hernández, Julia N.
Krawczak-Wójcik, Katarzyna
Donskow-Łysoniewska, Katarzyna
Gonzalez, Jorge F.
Stear, Michael J.
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  organization: Laboratory of Parasitology, General Karol Kaczkowski Military Institute of Hygiene and Epidemiology, Kozielska 4, 01-163 Warsaw, Poland
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  givenname: Jorge F.
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  givenname: Julia N.
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  givenname: Michael J.
  surname: Stear
  fullname: Stear, Michael J.
  organization: Department of Animal, Plant and Soil Science, Agribio, La Trobe University, Bundoora, VIC 3086, Australia
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CitedBy_id crossref_primary_10_3390_ijms24032283
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Keywords Galectin
Degranulation
Host-parasite interaction
Mast cell
IgE
Teladorsagia circumcincta
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Snippet Mast cell degranulation is the major mechanism influencing establishment and survival of the abomasal nematode Teladorsagia circumcincta and probably many...
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SubjectTerms Degranulation
Galectin
Host-parasite interaction
IgE
Mast cell
Teladorsagia circumcincta
Title Nematode galectin binds IgE and modulates mast cell activity
URI https://dx.doi.org/10.1016/j.vetpar.2022.109807
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