Background/Aims To investigate the molecules possibly influencing the recruitment and migration of leucocytes in murine ocular toxoplasmosis, the kinetics of the messenger RNA expression levels of cytokines, chemokines, chemokine receptors and adhesion molecules in the retina were analysed.
Methods Retina and brain were obtained sequentially from Toxoplasma gondii Fukaya strain-infected wild-type (WT) C57BL/6 and interferon gamma (IFN-γ) knockout (GKO) mice of the same background. The mRNA expression levels of these molecules were analysed by real-time PCR assay.
Results In the retina of WT mice the expression levels of IFN-γ, interleukin 17A, CCL3, CCL4, CCL5, CXCL1, CXCL2, CXCL10, CCR5, CCR7, CXCR2, CXCR3 and intracellular adhesion molecule 1 increased, reaching peaks approximately 14–28 days after infection. The expression levels of CXCR4 and CXCR5 were absent and very low, respectively, during the infection. In the brain of WT mice, the kinetic patterns of these expression levels tended to be the same as in the retina except CXCR4. On the other hand, in GKO mice these molecules, except CXCL1, CXCL2 and CXCR2, remained at basal levels.
Conclusion In murine ocular toxoplasmosis, cytokines, chemokines, chemokine receptors and adhesion molecules were involved in the pathogenesis, and IFN-γ played a pivotal role.
- chemokine receptor
- experimental and laboratory
- Toxoplasma gondii
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
Funding This study was funded by grant-in-aid 20592071 from the Japanese Science Promotion Society, an acceleration programme for international talent promotion 20-research-49 from the Ministry of Education, Culture, Sports, Science and Technology of Japan, and a grant for scientific research from the Japan Medical Women's Association.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.