» Articles » PMID: 37719029

Effects of And/or Spiramycin As an Adjunct in Toxoplasmosis Infection Challenged with Diabetes

Abstract

The current study assessed the anti-parasitic impact of probiotics on 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 probiotictreated (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.

References
1.
Wherry E . T cell exhaustion. Nat Immunol. 2011; 12(6):492-9. DOI: 10.1038/ni.2035. View

2.
El Saftawy E, Shash R, Aboulhoda B, Arsanyos S, Albadawi E, Abou-Fandoud S . Insights into immunopathology and triggering of apoptosis in chronic cerebral toxoplasmosis using murine models. Trop Biomed. 2021; 38(2):53-62. DOI: 10.47665/tb.38.2.037. View

3.
Munoz M, Heimesaat M, Danker K, Struck D, Lohmann U, Plickert R . Interleukin (IL)-23 mediates Toxoplasma gondii-induced immunopathology in the gut via matrixmetalloproteinase-2 and IL-22 but independent of IL-17. J Exp Med. 2009; 206(13):3047-59. PMC: 2806449. DOI: 10.1084/jem.20090900. View

4.
Washino T, Moroda M, Iwakura Y, Aosai F . Toxoplasma gondii infection inhibits Th17-mediated spontaneous development of arthritis in interleukin-1 receptor antagonist-deficient mice. Infect Immun. 2012; 80(4):1437-44. PMC: 3318428. DOI: 10.1128/IAI.05680-11. View

5.
Beeman N, Webb P, Baumgartner H . Occludin is required for apoptosis when claudin-claudin interactions are disrupted. Cell Death Dis. 2012; 3:e273. PMC: 3288343. DOI: 10.1038/cddis.2012.14. View