Helicobacter pylori-Toxoplasma gondii interplay with a possible role of IL-10

• Published in: Acta tropica 2024-05, Vol.253, p.107161-107161, Article 107161
• Main Authors: Elblihy, Ayat A, El-Ghannam, Shreief, Mohamed, Sherin Z., Hamouda, Marwa M., El-Ashry, Amira H., Habib, Samar
• Format: Article
• Language: English
• Subjects: Helicobacter pylori; Il-10; Immunomodulation; Toxoplasma gondii
• ISSN: 0001-706X; 1873-6254
• DOI: 10.1016/j.actatropica.2024.107161

•IL-10 increases in the sera of Toxoplasma/ H. pylori double positive patients.•IL-10 serum levels correlate with toxoplasma IgG titers.•Toxoplasma enhance IL-10 levels in H. pylori infected patients.•High levels of IL-10 weaken the immune response against H. pylori.•Lessened immune response against H. pylori causes persistent infection. Parasites are known for their modulatory effects on the immune response. The impact of toxoplasmosis on the immune response towards H. pylori is being studied in terms of IL-10 levels. This study included 110 patients suffering from persistent dyspepsia and 50 apparently healthy controls. Stool samples were collected and tested for H. pylori using colloidal gold one step test. Sera were examined for anti-Toxoplasma IgM and IgG using ELISA. IL-10 was also tested in the sera using ELISA. We found that Toxoplasma IgM and IgG tested positive in 1.8 % and 40 % of H. pylori positive patients, respectively. H. pylori-infected patients displayed higher IL-10 levels than the healthy controls (84 versus 0.59 pg/ml, respectively, P < 0.001). Classification of H. pylori positive patients according to Toxoplasma IgG titers yielded three groups: negative (58, 52.7 %), equivocal (8, 7.3 %), and positive (44, 40 %) groups, with the highest IL-10 levels detected in the double positive than the negative and the equivocal group (215 pg/ml versus 43 and 112.5 pg/ml, respectively, P < 0.001). There was strong positive correlation between Toxoplasma IgG titers and IL-10 levels (rs = 0.82, P < 0.001). Toxoplasma enhances IL-10 production in response to H. pylori infection. This could ameliorate the inflammatory response in the gastric mucosa, and subsequently more colonization with the H. pylori is achieved, resulting in persistent infection. [Display omitted]