The effects of Fasciola hepatica recombinant proteins (peroxiredoxin and cathepsin L1) on Crohn's disease experimental model.
Fasciola hepatica
cathepsin L1
colitis
excretory-secretory
inflammation
peroxiredoxin
Journal
Parasite immunology
ISSN: 1365-3024
Titre abrégé: Parasite Immunol
Pays: England
ID NLM: 7910948
Informations de publication
Date de publication:
Jan 2024
Jan 2024
Historique:
revised:
19
11
2023
received:
09
04
2022
accepted:
04
12
2023
medline:
26
1
2024
pubmed:
26
1
2024
entrez:
26
1
2024
Statut:
ppublish
Résumé
The immunomodulatory potential of the excretory-secretory (E/S) proteins of the helminths has been shown in previous investigations. This study evaluated the effects of the recombinants and excretory-secretory proteins of the Fasciola hepatica on induced colitis in Balb/c mice. The F. hepatica Recombinant proteins, Cathepsin L1 and Peroxiredoxin, and E/S proteins were intraperitoneally injected into the three mice groups as the case groups, while the control groups received PBS. Colitis was induced in mice by intraluminal administration of the 2, 4, 6-Trinitrobenzenesulfonic acid solution (TNBS). After 8 h, the case groups received the second dosage of the treatments, and it was repeated 24 h later. The immunological, pathological, and macroscopic changes were evaluated 3 days after colitis induction. The macroscopic evaluation revealed significantly lower inflammatory scores in the mice treated with recombinant Peroxiredoxin (rPRX) and recombinant Cathepsin L1 (rCL1). Despite the macroscopic observation, the pathological finding was insignificant between the groups. IFN-γ secretion was significantly lower in splenocytes of the groups that received rPRX, rCL1, and E/S than the controls. IL-10 showed significantly higher levels in groups treated with rPRX and rCL1 than controls, whereas the level of IL-4 was not statistically significant. Excretory-secretory proteins of the F. hepatica showed immunomodulatory potency and the main effects observed in this study were through the reduction of inflammatory cytokine and inflammation manifestation as well as induction of anti-inflammatory cytokines.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13019Subventions
Organisme : Tehran University of Medical Sciences
ID : 950-02-27-31275
Informations de copyright
© 2024 John Wiley & Sons Ltd.
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