Food and Waterborne Parasitology (Sep 2023)

Effects of Lactobacilli acidophilus and/or spiramycin as an adjunct in toxoplasmosis infection challenged with diabetes

  • Enas A. El Saftawy,
  • Safaa A. Turkistani,
  • Hadel M. Alghabban,
  • Emad A. Albadawi,
  • Basma EA Ibrahim,
  • Suzan Morsy,
  • Mohamed F. Farag,
  • Nashwah S. Al Hariry,
  • Rania Y. Shash,
  • Aly Elkazaz,
  • Noha M. Amin

Journal volume & issue
Vol. 32
p. e00201

Abstract

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The current study assessed the anti-parasitic impact of probiotics on Toxoplasma gondii infection either solely or challenged with diabetes in Swiss albino mice. The study design encompassed group-A (diabetic), group-B (non-diabetic), and healthy controls (C). Each group was divided into infected-untreated (subgroup-1); infected and spiramycin-treated (subgroup-2); infected and probiotic-treated (subgroup-3); infected and spiramycin+ probiotic-treated (subgroup-4). Diabetic-untreated animals exhibited acute toxoplasmosis and higher cerebral parasite load. Overall, various treatments reduced intestinal pathology, improved body weight, and decreased mortalities; nevertheless, probiotic + spiramycin exhibited significant differences. On day 7 post-infection both PD-1 and IL-17A demonstrated higher scores in the intestine of diabetic-untreated mice compared with non-diabetics and healthy control; whereas, claudin-1 revealed worsening expression. Likewise, on day 104 post-infection cerebral PD-1 and IL-17A showed increased expressions in diabetic animals. Overall, treatment modalities revealed lower scores of PD-1 and IL-17A in non-diabetic subgroups compared with diabetics. Intestinal and cerebral expressions of IL-17A and PD-1 demonstrated positive correlations with cerebral parasite load. In conclusion, toxoplasmosis when challenged with diabetes showed massive pathological features and higher parasite load in the cerebral tissues. Probiotics are a promising adjunct to spiramycin by ameliorating IL-17A and PD-1 in the intestinal and cerebral tissues, improving the intestinal expression of claudin-1, and efficiently reducing the cerebral parasite load.

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