Effects of cold stress on spleen cell proliferation and cytokine production during chronic Toxoplasma gondii infection.
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)-gamma were detected independent of the type of stimulation after CSchr and remained high throughout the experiment. CS had similar results in noninfected animals.


CONCLUSIONS
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-gamma after CSchr could be a result of spleen cells being primed by released parasites by this stressor. IFN-gamma is critical in the control of parasite reactivation.
Aviles
Hernan
H
Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, USA.
Johnson
Mary T
MT
Monroy
Fernando P
FP
D017088:AIDS-Related Opportunistic Infections / Q000276:immunology / Q000469:parasitology / Q000503:physiopathology; D000818:Animals; D000953:Antigens, Protozoan / Q000276:immunology; D002455:Cell Division / Q000276:immunology; D002908:Chronic Disease; D003080:Cold Temperature / Q000009:adverse effects*; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D007371:Interferon-gamma / Q000096:biosynthesis / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000378:metabolism; D013154:Spleen / Q000166:cytology / Q000276:immunology*; D013312:Stress, Physiological / Q000276:immunology* / Q000503:physiopathology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014122:Toxoplasma / Q000276:immunology / Q000472:pathogenicity; D014123:Toxoplasmosis / Q000276:immunology* / Q000503:physiopathology
D000953:Antigens, Protozoan; D016207:Cytokines; D012333:RNA, Messenger; D007371:Interferon-gamma