Immunomodulatory Effects of Cold Stress on Mice Infected Intraperitoneally with a 50% Lethal Dose of <i>Toxoplasma gondii</i>

Abstract

Cofactors such as stress have been suspected to play a role in the susceptibility to opportunistic infections. Toxoplasma gondii is one of the major opportunistic infectious agents in immunocompromised individuals, and infection can be modulated by external factors such as stress. Objective: The purpose of this study was to examine the in vivo and in vitro role of cold stress (CS) in the pathogenesis of T. gondii infection and its impact on regulatory cytokines in this model. Methods: Mice subjected to CS and control animals were infected intraperitoneally with an LD₅₀ of PD2 T. gondii tachyzoites, and the outcome of the infection was determined. In addition, peritoneal macrophages obtained from CS and non-stressed mice were infected in vitro with T. gondii. The number of infected macrophages, the number of intracellular parasites and the production of interferon (IFN)-γ, interleukin (IL)-12, and tumor necrosis factor (TNF)-α were determined. Results: CS applied before intraperitoneal inoculation increased susceptibility against T. gondii infection. Peritoneal cells from CS mice contained significantly higher numbers of intracellular parasites and infected macrophages compared to those from non-stressed animals. IFN-γ production was initially high in the CS group but decreased significantly after 36 h. Opposite results were found in the non-stressed group. Macrophages from CS mice persistently produced high levels of TNF-α and IL-12 and peaked after 36 h. Levels of these cytokines were lower or absent in the non-stressed group. Conclusion: These results suggest that CS increased the host susceptibility to intraperitoneal T. gondii infection by modulating the function of macrophages and the production of cytokines (IFN-γ) involved in the early control of infection.

The role of heat shock proteins in inflammatory injury induced by cold stress in chicken hearts

“…Acute immobilization and cold water-immersion stress increased TNF-α level at different time points (0, 30, 60, and 120 min) after stress in rats (Liu et al 2012b). Macrophages from cold-stressed mice persistently produced high levels of TNF-alpha (Aviles and Monroy 2001). So, in our study, the increased inflammation factors suggested that the myocardial inflammatory response was induced by cold stress, which may lead to myocardial injury.…”

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

“…Moreover, increased survival was found in mice infected orally with T. gondii and subjected to cold water stress as compared with controls [743]. In contrast, such stress had deleterious outcomes when mice were infected intraperitoneally [721]. These findings may support our suggestion that cold stressinduced host innate immune modulations during latent chronic T. gondii infection also may be partly responsible for the prevention of hypoglycemia-induced neuronal death by hypothermia.…”

“…Several authors showed that cold stress profoundly modulated immune response and the outcome of infections because many mediators released during physical stress, such as glucocorticoids and catecholamines, influenced the growth and multiplication of pathogens, including T. gondii [711,[721][722][723][724]. Cold stress can suppress [725,726] or enhance [727,728] immunity by inducing and/or enhancing the synthesis of specific proteins with relevant roles in transcription, translation, and recombination [729,730].…”

Active hexose correlated compound enhances the immune function of mice in the hindlimb-unloading model of spaceflight conditions

“…These assays were performed as described previously, with some modifications (7). Briefly, mice that received injection of 2 ml ip of thioglycollate broth 5 days previous to sample collection were killed by cervical dislocation.…”