Immunomodulatory effects of cold stress on mice infected intraperitoneally with a 50% lethal dose of Toxoplasma gondii

Hernan Aviles, Fernando P Monroy

Research output: Contribution to journalArticle

18 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)6-12
Number of pages7
JournalNeuroImmunoModulation
Volume9
Issue number1
DOIs
StatePublished - 2001

Fingerprint

Lethal Dose 50
Toxoplasma
Toxoplasmosis
Macrophages
Interferons
Interleukin-12
Cytokines
Parasites
Tumor Necrosis Factor-alpha
Opportunistic Infections
Peritoneal Macrophages
Infection Control
Infection

Keywords

  • Cold stress
  • IFN-γ
  • IL-12
  • Immunomodulation
  • Infection
  • Macrophages
  • TNF-α
  • Toxoplasma gondii

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Immunology

Cite this

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title = "Immunomodulatory effects of cold stress on mice infected intraperitoneally with a 50{\%} lethal dose of Toxoplasma gondii",
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.",
keywords = "Cold stress, IFN-γ, IL-12, Immunomodulation, Infection, Macrophages, TNF-α, Toxoplasma gondii",
author = "Hernan Aviles and Monroy, {Fernando P}",
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AU - Aviles, Hernan

AU - Monroy, Fernando P

PY - 2001

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N2 - 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.

AB - 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.

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