AI Article Synopsis

  • - The study investigates how Schistosoma mansoni infection affects immune responses in three different mouse strains (BALB/c, C57BL/6, and Swiss) to understand the disease's pathogenesis.
  • - Various factors, including parasite burden and immune receptor expression, were measured at different time points post-infection, revealing distinct responses among the mouse strains.
  • - Findings indicate that the Swiss mice showed better survival rates and lower infection levels, while all strains exhibited unique patterns in immune receptor activation, suggesting an important relationship between early immune response and infection control.

Article Abstract

Background: The impact of Schistosoma mansoni infection over the immune response and the mechanisms involved in pathogenesis are not yet completely understood.

Objectives: This study aimed to evaluate the expression of innate immune receptors in three distinct mouse lineages (BALB/c, C57BL/6 and Swiss) during experimental S. mansoni infection with LE strain.

Methods: The parasite burden, intestinal tissue oogram and presence of hepatic granulomas were evaluated at 7- and 12-weeks post infection (wpi). The mRNA expression for innate Toll-like receptors, Nod-like receptors, their adaptor molecules, and cytokines were determined at 2, 7 and 12 wpi in the hepatic tissue by real-time quantitative polymerase chain reaction (qPCR).

Findings: Swiss mice showed 100% of survival, had lower parasite burden and intestinal eggs, while infected BALB/c and C57BL/6 presented 80% and 90% of survival, respectively, higher parasite burden and intestinal eggs. The three mouse lineages displayed distinct patterns in the expression of innate immune receptors, their adaptor molecules and cytokines, at 2 and 7 wpi.

Main Conclusions: Our results suggest that the pathogenesis of S. mansoni infection is related to a dynamic early activation of innate immunity receptors and cytokines important for the control of developing worms.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11182339PMC
http://dx.doi.org/10.1590/0074-02760240013DOI Listing

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