AI Article Synopsis

  • Toxocariasis is caused by the larvae of Toxocara canis and is a common zoonotic disease affecting humans.
  • This study investigated the role of immune cells and Bcl-2 protein in liver inflammation during T. canis infection in mice, focusing on differences between primary infection and sensitized infection.
  • Findings revealed that the presence of CD4+ and CD8+ T lymphocytes varied over time and influenced the inflammatory response in the liver, while pre-immunization with Toxocara antigens led to earlier and stronger immune cell recruitment and increased Bcl-2 expression.

Article Abstract

Toxocariasis is a soil-transmitted helminthic disease due to infection of humans by larvae of Toxocara canis (T. canis). It is one of the most commonly reported zoonotic infections in the world. The aim of this study was to characterize the key immune cells and activity of Bcl-2 in hepatic inflammation during the course of experimental infection by T. canis. Mice experimentally infected with T. canis were divided into two groups: mice with primary infection by Toxocara, and those infected after sensitization by Toxocara excretory-secretory antigen. CD4+, CD8+, and Bcl-2-expressing T lymphocytes were identified in the liver by immunohistochemistry at different durations post-infection. Recruitment of both CD4+ and CD8+ T lymphocytes within the inflammatory reaction in the liver was observed, with difference in count and localization. These cells were detected within and around Toxocara-induced granulomas as well as in isolated inflammatory foci in the portal tracts or within the hepatic parenchyma. The antiapoptotic protein Bcl-2 showed no significant change at different periods post-infection. On the other hand, immunization of mice with Toxocara excretory-secretory antigen prior to experimental infection caused earlier and more pronounced recruitment of CD4+ and CD8+ T cells to the liver and enhanced expression of Bcl-2. Moreover, CD8+ cells became more diffuse within the inflammatory infiltrate. These results suggest a dynamic change in key immune cells according to the duration of infection as well as the immune status of the host.

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http://dx.doi.org/10.1016/j.exppara.2013.02.001DOI Listing

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