Expression of cytokines and co-stimulatory molecules in the Toxoplasma gondii-infected dendritic cells of C57BL/6 and BALB/c mice

Abstract

Toxoplasma gondii is an intracellular protozoan parasite which can infect most warm-blooded animals and humans. Among the different mouse models, C57BL/6 mice are more susceptible to T. gondii infection compared to BALB/c mice, and this increased susceptibility has been attributed to various factors, including T-cell responses. Dendritic cells (DCs) are the most prominent type of antigen-presenting cells and regulate the host immune response, including the response of T-cells. However, differences in the DC responses of these mouse strains to T. gondii infection have yet to be characterized. In this study, we cultured bone marrow-derived DCs (BMDCs) from BALB/c and C57BL/6 mice. These cells were infected with T. gondii. The activation of the BMDCs was assessed based on the expression of cell surface markers and cytokines. In the BMDCs of both mouse strains, we detected significant increases in the expression of cell surface T-cell co-stimulatory molecules (major histocompatibility complex (MHC) II, CD40, CD80, and CD86) and cytokines (tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-12p40, IL-1β, and IL-10) from 3 h post-T. gondii infection. The expression of MHC II, CD40, CD80, CD86, IFN-γ, IL-12p40, and IL-1β was significantly higher in the T. gondii-infected BMDCs obtained from the C57BL/6 mice than in those from the BALB/c mice. These findings indicate that differences in the activation status of the BMDCs in the BALB/c and C57BL/6 mice may account for their differential susceptibility to T. gondii.

Contrasting Disease Progression, Microglia Reactivity, Tolerance, and Resistance to <em>Toxoplasma gondii</em> Infection in Two Mouse Strains

“…By day 43 dpi, BALB/c mice continued to spend more time in areas with feline odors, suggesting that the behavioral alterations noted at 22 dpi may have become enduring. The immune response of infected Swiss albino mice is similar to that observed in C57Bl6 infected mice [73][74], and previous reports comparing BALB/c and C57Bl6 lineages have also reported an increase in macrophage numbers during the late stages (56 dpi) of the disease in BALB/c mice compared to C57Bl6 infected mice. Additionally, activation pathways associated with neuropathology and neuroinflammation in BALB/c mice are downregulated compared to their counterparts in C57BL/6 mice [73][74][75].…”

“…The immune response of infected Swiss albino mice is similar to that observed in C57Bl6 infected mice [73][74], and previous reports comparing BALB/c and C57Bl6 lineages have also reported an increase in macrophage numbers during the late stages (56 dpi) of the disease in BALB/c mice compared to C57Bl6 infected mice. Additionally, activation pathways associated with neuropathology and neuroinflammation in BALB/c mice are downregulated compared to their counterparts in C57BL/6 mice [73][74][75]. Such studies highlight how alterations in the host immune response influence pathogenicity to T. gondii infection.…”

Toxoplasma gondii IST suppresses inflammatory and apoptotic responses by inhibiting STAT1-mediated signaling in IFN-γ/TNF-α-stimulated hepatocytes

“…Toxoplasma gondii is an obligate intracellular protozoan that can invade and replicate in various warm-blooded animals cells [ 1 , 2 ]. After cell invasion by T. gondii , dense granules discharge secretory proteins that regulate parasitophorous vacuole formation, host cell pathogenicity, and immunity for survival [ 3 , 4 ].…”