Arginase activity is associated with fibrosis in experimental infection with Taenia crassiceps, but does not play a major role in resistance to infection

- Arginase activity increases early after infection with Taenia crassiceps cysticerci.
- Supplementation of l-arginine does not affect cysticerci number and stage.
- Inhibition of arginase activity does not affect cysticerci number and stage.
- T. crassiceps cysticerci induce collagen deposition in the peritoneal membrane.
- Inhibition of arginase activity decreases the collagen deposition.

Murine infection with Taenia crassiceps cysticerci is used as an experimental model for human and animal cysticercosis. In this infection parasites can be found associated with an inflammatory infiltrate enriched with macrophages. Experimental evidence exists supporting a role for either NO-producing classically activated (CAMΦ) or arginase- and CD301-expressing alternatively activated macrophages (AAMΦ) in T. crassiceps resistance. In both cell types, arginine is utilized as an important mediator in macrophage effector functions. To investigate whether there is an association between arginine availability, susceptibility to T. crassiceps and other parameters such as fibrosis, BALB/c mice were infected intraperitoneally with cysticerci and treated daily with the arginase inhibitor nor-NOHA or supplemented with l-arginine and followed for eight weeks. The numbers and developmental stages of parasites were evaluated as well as the presence of CD301+ AAMΦ, arginase activity and collagen deposition in the peritoneal membrane. Treatment with the arginase inhibitor or supplementation with l-arginine did not change the parasitic load or profile of the infection. However, the arginase inhibitor significantly decreased the deposition of collagen. These results suggest that arginase activity does not interfere with parasite control during experimental infection with T. crassiceps, but it is important for fibrosis in cysticercosis.