The expressions of Gal-9 and its receptors are genetically regulated in Toxoplasma gondii-infected mice
The latest Parasitology Paper of the Month is “Galectins expressed differently in genetically susceptible C57BL/6 and resistant BALB/c mice during acute ocular Toxoplasma gondii infection” by S.-J. Chen, Y.-X. Zhang, S.-G. Huang and F.-L. Lu.
Ocular toxoplasmosis (OT), caused by Toxoplasma gondii, is the most common etiology of posterior uveitis in the world, however, many clinical features of OT remain unclear. Mice have been mostly used as the experimental model of choice for the investigation of various aspects of OT.
Lu and her co-authors’ previous work has demonstrated that genetic factor of the host is critical in determining susceptibility to experimental OT in mouse models (Lu et al. 2005). Researchers have reported that galectins are expressed by various immune cells as well as other cell types, and Tim-3/Gal-9 interaction plays a crucial role in immune regulation. Lu and her co-authors wonder whether genetic resistance to the development of ocular pathology in BALB/c mice infected with T. gondii was independent of galectins. To study the role of galectins in the resistance of BALB/c mice against intraocular infection with T. gondii, infected BALB/c mice were treated with α-lactose. Blockade of galectins by the method of α-lactose treatment was reported by Sehrawat et al (2010).
Lu and her co-authors did not find significant differences of parasite loads in the eyes or cervical lymph nodes in T. gondii-infected BALB/c with and without α-lactose treatment. In addition, the ocular immunopathology in BALB/c mice was also independent of galectins. They concluded that blockage of galectin by α-lactose is not sufficient to change the ocular immunopathology of genetic resistant BALB/c mice; the markedly different expressions of IFN-α/β between intraocular T. gondii-infected B6 and BALB/c mice may be one of the mechanisms that they are genetically susceptible or resistant to this parasite.
However, Lu and her co-authors did not do the experiment to demonstrate whether Gal-9 plays a role in the induction of OT immunopathology in B6 mice after T. gondii infection. Further experiments using Gal-9-deficient B6 mice might help answer this question. They also plan to do in vitro study by blocking the Tim-3/Gal-9 interaction to verify its role in the pathophysiology of OT. A better understanding the molecular mechanism of OT may provide crucial information to alleviate the suffering from this blindness disease.
Read the full article “Galectins expressed differently in genetically susceptible C57BL/6 and resistant BALB/c mice during acute ocular Toxoplasma gondii infection” in full for free until 30th June 2017.