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Toxoplasma gondii  is able to infect a wide range of vertebrates, including humans. Studies show that cyclooxygenase-2 (COX-2) is a modulator of immune response in multiple types of infection, such as  Trypanosoma cruzi . However, the role of COX-2 during  T. gondii  infection is still unclear. The aim of this study was to investigate the role of COX-2 during infection by moderately or highly virulent strains of  T. gondii  in  Calomys callosus  rodents and human THP-1 cells.  C. callosus  were infected with 50 cysts of  T. gondii  (ME49), treated with COX-2 inhibitors (meloxicam or celecoxib) and evaluated to check body weight and morbidity. After 40 days, brain and serum were collected for detection of  T. gondii  by real-time PCR and immunohistochemistry or cytokines by CBA. Furthermore, peritoneal macrophages or THP-1 cells, infected with RH strain or uninfected, were treated with meloxicam or celecoxib to evaluate the parasite proliferation by colorimetric assay and cytokine production by ELISA. Finally, in order to verify the role of prostaglandin E 2  in COX-2 mechanism, THP-1 cells were infected, treated with meloxicam or celecoxib plus PGE 2 , and analyzed to parasite proliferation and cytokine production. The data showed that body weight and morbidity of the animals changed after infection by  T. gondii , under both treatments. Immunohistochemistry and real-time PCR showed a reduction of  T. gondii  in brains of animals treated with both COX-2 inhibitors. Additionally, it was observed that both COX-2 inhibitors controlled the  T. gondii  proliferation in peritoneal macrophages and THP-1 cells, and the treatment with PGE 2  restored the parasite growth in THP-1 cells blocked to COX-2. In the serum of  Calomys , upregulation of pro-inflammatory cytokines was detected, while the supernatants of peritoneal macrophages and THP-1 cells demonstrated significant production of TNF and nitrite, or TNF, nitrite and MIF, respectively, under both COX-2 inhibitors. Finally, PGE 2  treatment in THP-1 cells triggered downmodulation of pro-inflammatory mediators and upregulation of IL-8 and IL-10. Thus, COX-2 is an immune mediator involved in the susceptibility to  T. gondii  regardless of strain or cell types, since inhibition of this enzyme induced control of infection by upregulating important pro-inflammatory mediators against  Toxoplasma .

frontiers in microbiology

Cyclooxygenase (COX)-2 Inhibitors Reduce Toxoplasma gondii Infection and Upregulate the Pro-inflammatory Immune Response in Calomys callosus Rodents and Human Monocyte Cell Line