Parasites and Host Interactions (48)Food Allergy and Anaphylaxis Research (45)Mast cells and histamine (27)Allergic Rhinitis and Sensitization (23)Asthma and respiratory diseases (22)
Murangi T, Mans B, Pienaar R, Botha M, Facey-Thomas H, et al.
The journal of allergy and clinical immunology. Global •
The presence of galactose-α-1,3-galactose (alpha-gal) in tick salivary antigens has been implicated to initiate host IgE responses resulting in sensitization to alpha-gal. We sought to investigate the presence of alpha-gal in different anatomic locations in native South African tick species at different feeding and developmental stages and the ability of sera from our allergic cohort to bind to these tick proteins. Alpha-gal-containing proteins in laboratory-reared ticks at different feeding and developmental stages were detected through Western blotting and immunohistochemical staining. IgE and IgG4 toward the tick proteins were analyzed via ELISA. There is differential expression of alpha-gal in endemic South African ticks and . Immunoblotting demonstrated an increase in the prominence of alpha-gal-containing protein bands in salivary glands to be proportional to feeding time. Alpha-gal in both fed and unfed ticks was localized in the salivary acini and testes. IgE and IgG4 to antigens were significantly raised in alpha-gal-allergic individuals. There was a correlation between anti- IgE and anti-alpha-gal IgE in the alpha-gal-allergic group. Inhibition of human serum anti-alpha-gal IgE to and proteins was significantly reduced by the addition of bovine thyroglobulin. We anticipate repeated exposure to differentially expressed and alpha-gal-containing salivary proteins during feeding to cause alpha-gal sensitization.
Murangi T, Prakash P, Moreira BP, Basera W, Botha M, et al.
The Journal of allergy and clinical immunology •
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. 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. 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. 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. 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.