JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY | 卷:149 |
Ascaris lumbricoides and ticks associated with sensitization to galactose α1,3-galactose and elicitation of the alpha-gal syndrome | |
Article | |
Murangi, Tatenda1  Prakash, Prema2  Moreira, Bernardo Pereira2  Basera, Wisdom3,4  Botha, Maresa5  Cunningham, Stephen6  Facey-Thomas, Heidi5  Halajian, Ali7  Joshi, Lokesh6  Ramjith, Jordache8  Falcone, Franco H.2  Horsnell, William1,9  Levin, Michael E.5  | |
[1] Univ Cape Town, Wellcome Ctr Infect Dis Res Africa, Inst Infect Dis & Mol Med, Dept Pathol,Div Immunol, Cape Town, South Africa | |
[2] Justus Liebig Univ Giessen, Biomed Res Ctr Seltersberg, Inst Parasitol, Giessen, Germany | |
[3] Univ Cape Town, Sch Publ Hlth & Family Med, Cape Town, South Africa | |
[4] South African Med Res Council, Burden Dis Res Unit, Cape Town, South Africa | |
[5] Univ Cape Town, Dept Paediat, Div Paediat Allergy, Cape Town, South Africa | |
[6] Natl Univ Ireland Galway, Biomed Sci, Glycosci Grp, Galway, Ireland | |
[7] Univ Limpopo, Res Adm & Dev, Sovenga, South Africa | |
[8] Radboud Univ Nijmegen, Radboud Inst Hlth Sci, Dept Hlth Evidence, Biostat Res Grp,Med Ctr, Nijmegen, Netherlands | |
[9] Univ Birmingham, Coll Med & Dent Sci, Inst Microbiol & Infect, Birmingham, W Midlands, England | |
关键词: Alpha-gal; food allergy; galactose-alpha-1,3-galactose; helminths; meat allergy; red meat allergy; ticks; Ascaris lumbricoides; anaphylaxis; Rhipicephalus evertsi; Amblyomma hebraeum; | |
DOI : 10.1016/j.jaci.2021.07.018 | |
来源: Elsevier | |
【 摘 要 】
Background: IgE to galactose alpha-1,3 galactose (alpha-gal) causes alpha-gal syndrome (delayed anaphylaxis after ingestion of mammalian meat). Development of sensitization has been attributed to tick bites; however, the possible role of other parasites has not been well studied. Objective: Our aims were to assess the presence, relative abundances, and site of localization of alpha-gal-containing proteins in common ectoparasites and endoparasites endemic in an area of high prevalence of alpha-gal syndrome, as well as to investigate the ability of ascaris antigens to elicit a reaction in a humanized rat basophil in vitro sensitization model. Methods: Levels of total IgE, Ascaris-specific IgE, and alpha-gal IgE were measured in sera from patients with challenge-proven alpha-gal syndrome and from controls without allergy. The presence, concentration, and localization of alpha-gal in parasites were assessed by ELISA, Western blotting, and immunohistochemistry. The ability of Ascaris lumbricoides antigen to elicit IgE-dependent reactivity was demonstrated by using the RS-ATL8 basophil reporter system. Results: Alpha-gal IgE level correlated with A lumbricoides-specific IgE level. Alpha-gal protein at 70 to 130 kDa was detected in A lumbricoides at concentrations higher than those found in Rhipicephalus evertsi and Amblyomma hebraeum ticks. Immunohistochemistry was used to localize alpha-gal in tick salivary acini and the helminth gut. Non-alpha-gal-containing A lumbricoides antigens activated RS-ATL8 basophils primed with serum from subjects with alpha-gal syndrome. Conclusion: We demonstrated the presence, relative abundances, and site of localization of alpha-gal-containing proteins in parasites. The activation of RS-ATL8 IgE reporter cells primed with serum from subjects with alpha-gal syndrome on exposure to non-alpha-gal-containing A lumbricoides proteins indicates a possible role of exposure to A lumbricoides in alpha-gal sensitization and clinical reactivity.
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