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Why tick bites induce red meat allergy in humans?

. © INRA, A. Cabezas-Cruz
Updated on 09/25/2018
Published on 09/25/2018
Keywords:

Unlike most food allergies, in which symptoms occur within minutes of consuming the allergen, allergic reactions related to the Alpha-gal syndrome are delayed. The symptoms can appear four to six hours after a meal containing red meat. The first report of the association between tick bites and red meat allergy was in 2007 when the Australian allergist Professor Sheryl van Nunen described 24 cases of meat allergy associated with tick bites. Later in 2009, Professor Thomas Platts-Mills identified the molecule causing these severe allergic reactions. Patients allergic to red meat, Platts-Mills discovered, had allergic antibodies to a complex sugar called galactose-alpha-1,3-galactose, or alpha-gal for short.

Currently, it is generally accepted that ticks that cause Alpha-gal syndrome carry alpha-gal molecules from the blood of the animals they commonly bite, such as cows, sheep and rabbits. It is then believed that when an alpha-gal-charged tick bites a human, the tick injects alpha-gal into the person inducing allergic antibodies. This implies that tick larvae that never fed before cannot induce the Alpha-gal syndrome. This accepted wisdom was challenged by Dr. Alejandro Cabezas-Cruz and his colleagues of the UMR BIPAR (Anses, EnvA, INRA), located in the Laboratory for Animal Health of Anses (Maisons-Alfort) and Spain  who asked whether ticks were able to produce their own alpha-gal. In a manuscript published in the journal Scientific Reports (https://rdcu.be/7mlF), Cabezas-Cruz reported the discovery of three tick genes encoding for galactosyltransferase enzymes that can produce alpha-gal. When human and bacterial cells that do not produce alpha-gal where transformed with these genes, these alpha-gal-negative cells became alpha-gal positive. In addition, when these genes were knockdown using RNA interference, the levels of tick alpha-gal decreased. The researchers further showed that the tick-borne bacteria, Anaplasma phagocytophilum, induce the expression of one of these genes, which resulted in the increase of tick alpha-gal.

This study has two main implications. Firstly, it shows that ticks do not need to feed on any animal to carry alpha-gal. Therefore, the bite of any tick stage, including larvae, can induce Alpha-gal syndrome. Secondly, tick infected by the bacteria Anaplasma phagocytophilum may have higher levels of alpha-gal increasing the probability of inducing Alpha-gal syndrome. This influences our current way of thinking about tick-pathogen interactions since according to these results, the consequences of microbial infection of ticks are not only related to transmission of pathogens to animals and/or humans, but also to the increased ability that infected ticks may have to induce alpha-gal syndrome in humans.

Reference

Alejandro Cabezas-Cruz, Pedro J. Espinosa, Pilar Alberdi, Ladislav Šimo, James J., Valdés, Lourdes Mateos-Hernández, Marinela Contreras, Margarita Villar Rayo, José de la Fuente. 2018. Tick galactosyltransferases are involved in α-Gal synthesis and play a role during Anaplasma phagocytophilum infection and Ixodes scapularis tick vector development.  Scientific Reports (2018). 8:14224
DOI:10.1038/s41598-018-32664-z

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