Immunological effects of coinfections with Toxoplasma gondii, Helicobacter pylori, and Epstein-Barr virus on anisakiasis associated phenotypes.

The hygiene hypothesis proposes that infections acquired through the fecal-oral route or contaminated food, such as Toxoplasma gondii, may protect against IgE-mediated allergic disorders. Epstein-Barr virus (EBV) has been negatively associated with atopy, while Anisakis simplex and Helicobacter pylori are associated with acute and chronic urticaria, respectively. This study aimed to explore the impact of coinfection status on anisakiasis-associated phenotypes. A total of 112 human subjects were categorized by Anisakis sensitization status and clinical phenotypes: 25 with gastroallergic anisakiasis (GAA), 64 with chronic urticaria (CU; of these, 32 sensitized to A. simplex [CU+]), and 23 controls without urticaria. Serum IgE against A. simplex and IgG against T. gondii, H. pylori, and EBV were measured to assess exposure and coinfection patterns. Serum cytokine levels of IL-2, IL-4, IL-6, IL-10, TNF-α, IFN-γ, IL-17A, and TGF-β were quantified using flow cytometry. T. gondii coinfection was significantly more prevalent in A. simplex-seropositive subjects (AK+) (95.3 %), whereas H. pylori prevalence was higher in CU patients (55.9 %). All CU+ patients showed coinfection with H. pylori and triple coinfection (A. simplex/T. gondii/H. pylori) was more frequent in CU+ than CU-. Inverse correlations occurred between anti-T. gondii IgG and IL-2, and anti-Anisakis IgE and IFN-γ; positive correlations with anti-H. pylori IgG and IL-17A, and anti-EBV IgG and IL-6. T. gondii infection is associated with anti-A. simplex IgE regardless of CU. H. pylori infection is linked to CU independently of A. simplex sensitization. Studied coinfections modulate immune responses and alter cytokine profiles underscoring complex immunoregulatory mechanisms of Anisakis allergy.