Effects of Cold Stress on Spleen Cell Proliferation and Cytokine Production during Chronic Toxoplasma gondii Infection

Hernan Aviles, Mary T. Johnson, Fernando P Monroy

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Background: Cell-mediated immunity is critical for controlling infection and preventing reactivation during the chronic phase of Toxoplasma gondii infection. In people suffering from AIDS, T. gondii is one of the major opportunistic infectious agents. Mechanisms regulating rapid development of clinical signs in previously asymptomatic patients remain unclear; however, cofactors such as stress are suspected to play a role in the susceptibility to opportunistic infections. Objective: This study examined the role of cold stress (CS) in splenocyte function during chronic T. gondii infection. Methods: Control mice and mice previously infected orally with T. gondii were subjected to CS during the chronic phase (CSchr), i.e. 90 days after infection, and in vitro cell proliferation and cytokine production were measured before (day 0) and 1, 15 and 25 days after CSchr. Splenocyte proliferation and cytokine production were measured after in vitro stimulation with concanavalin A (Con-A), anti-CD3 antibody (A-CD3) and Toxoplasma lysate antigen. Results: CSchr enhanced splenocyte proliferation in cells stimulated with Con-A and A-CD3, but it suppressed proliferation in cells stimulated with T. gondii antigens. Increased levels of interferon (IFN)-γ were detected independent of the type of stimulation after CSchr and remained high throughout the experiment. CS had similar results in noninfected animals. Conclusion: Although an overall increase in splenocyte function occurred after nonspecific stimulation, CS suppressed primed spleen cells from responding to T. gondii antigens which could lead to reactivation of latent infection. The increase in IFN-γ after CSchr could be a result of spleen cells being primed by released parasites by this stressor. IFN-γ is critical in the control of parasite reactivation.

Original languageEnglish (US)
Pages (from-to)93-102
Number of pages10
JournalNeuroImmunoModulation
Volume11
Issue number2
DOIs
StatePublished - 2004

Fingerprint

Toxoplasmosis
Toxoplasma
Spleen
Cell Proliferation
Interferons
Cytokines
Viral Tumor Antigens
Concanavalin A
Anti-Idiotypic Antibodies
Infection
Communicable Disease Control
Opportunistic Infections
Cellular Immunity
Parasites
Acquired Immunodeficiency Syndrome
Antigens
In Vitro Techniques

Keywords

  • Chronic phase
  • Cold stress
  • Cytokine
  • Immunomodulation
  • Infection
  • Mouse
  • Proliferation
  • Spleen
  • Toxoplasma gondii

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Immunology

Cite this

Effects of Cold Stress on Spleen Cell Proliferation and Cytokine Production during Chronic Toxoplasma gondii Infection. / Aviles, Hernan; Johnson, Mary T.; Monroy, Fernando P.

In: NeuroImmunoModulation, Vol. 11, No. 2, 2004, p. 93-102.

Research output: Contribution to journalArticle

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abstract = "Background: Cell-mediated immunity is critical for controlling infection and preventing reactivation during the chronic phase of Toxoplasma gondii infection. In people suffering from AIDS, T. gondii is one of the major opportunistic infectious agents. Mechanisms regulating rapid development of clinical signs in previously asymptomatic patients remain unclear; however, cofactors such as stress are suspected to play a role in the susceptibility to opportunistic infections. Objective: This study examined the role of cold stress (CS) in splenocyte function during chronic T. gondii infection. Methods: Control mice and mice previously infected orally with T. gondii were subjected to CS during the chronic phase (CSchr), i.e. 90 days after infection, and in vitro cell proliferation and cytokine production were measured before (day 0) and 1, 15 and 25 days after CSchr. Splenocyte proliferation and cytokine production were measured after in vitro stimulation with concanavalin A (Con-A), anti-CD3 antibody (A-CD3) and Toxoplasma lysate antigen. Results: CSchr enhanced splenocyte proliferation in cells stimulated with Con-A and A-CD3, but it suppressed proliferation in cells stimulated with T. gondii antigens. Increased levels of interferon (IFN)-γ were detected independent of the type of stimulation after CSchr and remained high throughout the experiment. CS had similar results in noninfected animals. Conclusion: Although an overall increase in splenocyte function occurred after nonspecific stimulation, CS suppressed primed spleen cells from responding to T. gondii antigens which could lead to reactivation of latent infection. The increase in IFN-γ after CSchr could be a result of spleen cells being primed by released parasites by this stressor. IFN-γ is critical in the control of parasite reactivation.",
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N2 - Background: Cell-mediated immunity is critical for controlling infection and preventing reactivation during the chronic phase of Toxoplasma gondii infection. In people suffering from AIDS, T. gondii is one of the major opportunistic infectious agents. Mechanisms regulating rapid development of clinical signs in previously asymptomatic patients remain unclear; however, cofactors such as stress are suspected to play a role in the susceptibility to opportunistic infections. Objective: This study examined the role of cold stress (CS) in splenocyte function during chronic T. gondii infection. Methods: Control mice and mice previously infected orally with T. gondii were subjected to CS during the chronic phase (CSchr), i.e. 90 days after infection, and in vitro cell proliferation and cytokine production were measured before (day 0) and 1, 15 and 25 days after CSchr. Splenocyte proliferation and cytokine production were measured after in vitro stimulation with concanavalin A (Con-A), anti-CD3 antibody (A-CD3) and Toxoplasma lysate antigen. Results: CSchr enhanced splenocyte proliferation in cells stimulated with Con-A and A-CD3, but it suppressed proliferation in cells stimulated with T. gondii antigens. Increased levels of interferon (IFN)-γ were detected independent of the type of stimulation after CSchr and remained high throughout the experiment. CS had similar results in noninfected animals. Conclusion: Although an overall increase in splenocyte function occurred after nonspecific stimulation, CS suppressed primed spleen cells from responding to T. gondii antigens which could lead to reactivation of latent infection. The increase in IFN-γ after CSchr could be a result of spleen cells being primed by released parasites by this stressor. IFN-γ is critical in the control of parasite reactivation.

AB - Background: Cell-mediated immunity is critical for controlling infection and preventing reactivation during the chronic phase of Toxoplasma gondii infection. In people suffering from AIDS, T. gondii is one of the major opportunistic infectious agents. Mechanisms regulating rapid development of clinical signs in previously asymptomatic patients remain unclear; however, cofactors such as stress are suspected to play a role in the susceptibility to opportunistic infections. Objective: This study examined the role of cold stress (CS) in splenocyte function during chronic T. gondii infection. Methods: Control mice and mice previously infected orally with T. gondii were subjected to CS during the chronic phase (CSchr), i.e. 90 days after infection, and in vitro cell proliferation and cytokine production were measured before (day 0) and 1, 15 and 25 days after CSchr. Splenocyte proliferation and cytokine production were measured after in vitro stimulation with concanavalin A (Con-A), anti-CD3 antibody (A-CD3) and Toxoplasma lysate antigen. Results: CSchr enhanced splenocyte proliferation in cells stimulated with Con-A and A-CD3, but it suppressed proliferation in cells stimulated with T. gondii antigens. Increased levels of interferon (IFN)-γ were detected independent of the type of stimulation after CSchr and remained high throughout the experiment. CS had similar results in noninfected animals. Conclusion: Although an overall increase in splenocyte function occurred after nonspecific stimulation, CS suppressed primed spleen cells from responding to T. gondii antigens which could lead to reactivation of latent infection. The increase in IFN-γ after CSchr could be a result of spleen cells being primed by released parasites by this stressor. IFN-γ is critical in the control of parasite reactivation.

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