Astrocytes, microglia/macrophages, and neurons expressing Toll-like receptor 11 contribute to innate immunity against encephalitic Toxoplasma gondii infection

- We report Toll-like receptor 11 (TLR11) increasing in Toxoplasma gondii encephalitis.
- We report TLR11 expression is induced in astrocytes, neurons, and microglia.
- Innate immunity of Toxoplasmosis (1/3 of the population is infected) research is increasing.

Toll-like receptor 11 (TLR11) is a specific receptor for Toxoplasma gondii and uropathogenic Escherichia coli and has recently been identified in the mouse brain. In the present study, TLR11 gene expression was measured in the mouse brain by Real-time quantitative polymerase chain reaction (RT-PCR). Furthermore, the TLR11 protein expression profile was evaluated in neuroglia and neurons throughout the encephalitic period (10, 20, and 30 days after inoculation) in mice with experimentally induced T. gondii infection. In the brains of experimental (n = 21) and control (n = 7) mice, TLR11, glial fibrillary acidic protein (GFAP), cd11b, NeuN, TLR11/GFAP+, TLR11/cd11b+, and TLR11/NeuN+ cells were investigated using either indirect single- or double-labeling immunoperoxidase staining. The results indicated that TLR11 gene expression increased during chronic toxoplasmic encephalitis, and there was a variable degree of TLR11 immunopositivity among cd11b+, GFAP+, and NeuN+ cells in the brain. On the tenth day of infection, there was a significant increase in TLR11 protein and gene expression, which remained stable during the later stages of infection. In this experimental model, TLR11 expression was induced in astrocytes, neurons, and microglia/macrophages during the immune response to T. gondii infection.