FUNCTION OF HSPs IN TOXOPLASMA GONDII INFECTION

1. FUNCTION OF HSPs IN TOXOPLASMA GONDII INFECTION Sedighi.m & Faridi.a student of vetirenary schoolEmail:ashkan.faridi@yahoo.com University of bu-Ali sina ABSTRACT • TOXOPLASMA GONDII: • Theobligate intracellular protozoan Toxoplasmagondii is a widespread opportunistic parasite of humans and other animals. It normally, establishes itself within brain and skeletal muscle tissues, persisting for the life of the host. his parasite enters RESULTS Expression of HSP on Peritoneal Macrophages of Mice Infected with T. gondii: To determine whether 65-kDa HSP could be induced in vivo in mice infected with T. gondii, micewere infected with two strains differing greatly in virulence a low-virulence Beverley strain or a high-virulence RH strain. When the mice had been inoculated with a sub lethal dose (1 x 102) of Beverley strain of T. gondiibradyzoites, they suffered from acute symptoms of infection reflected by ruffled hair, hunched posture, and fever on days 10-14 after inoculation. Thereafter the mice regained a healthy appearance and could be shown to have established both immunity and a latent T. gondii infection. By contrast, mice infected with 1 x 102 tachyzoites of RH strain died within 10 days of an acute infection. As shown in Fig. 1 (lan3), the expression of HSP as reflected in a electroblot analysis was demonstrable in PEC from mice infected 10 days earlier with the low-virulence Beverley strain of T. gondii. In contrast, HSP were not expressed in the macrophages from mice infected with RH strain (lane 4) or in macrophages of uninfected mice (lane 2). FIG. 1. Expression of 65-kDa (kD) HSP in PEC of mice infected with T. gondii. Lanes: 1, HSP65 as standard (10 u.g of protein); 2, PEC lysates from normal mouse (10 jig of protein); 3, PEC lysates10 days after infection of mice with 1 x 104 bradyzoites of Beverleystrain T. gondii; 4, PEC of mice 5 days after infection with 1 x 104tachyzoites of RH strain (10 ,ug of protein); 5, lysate of tachyzoites of RH strain (5 ,ig of protein); and 6, lysate of bradyzoites of Beverley strain of T. gondii (5 ,ug of protein) equivalent to -1 x 106 organisms. • its host via GI-tract,& in pregnant woman can cross the placenta , possibly leading to hydrocephalus or microcephaly or intrauterine death. study have shown behavioral changes in humans including slow reaction time & a six fold increased risk of traffic accidents among infected men. • Heat shock protein: the exposure of cells to a variety of stressful conditions such as infection, immunization, elevated temperature, or stressful chemical intoxication lead to the transcription of a highly conserved set of genes and, subsequently, to the syntheses of a family of polypeptides called heat shock proteins(HSPs). HSP appear to be produced by many cells to preserve cellular functions under a variety of conditions of stress, including infection DISCUSSION:In this article we show that when amice infect with low-virulent toxoplasma in its PEC lysate express HSPs & in infected or uninfected with variety of strain of this parasite done exist this HSP. in fact,show that a pathogen like low-virulent toxoplasma if macrophages produce immune system can resistant to toxoplasma & if this polypeptide don’t synthesis, immuono system can not perform its work correctly & toxoplasma can be severe. HSP have a direct role in resistance in immuono system against all pathogen. (its function liked to a target) • CUNCLUTION • As first step after infection with a low-virulence of Toxoplasma, circulating γδ T cells recognize either Toxoplasma-derived HSP65 or host-derived HSP65, and then they accumulate and activated. • At the second step, macrophages activated by γδ T cells probably via certain cytokine pathways exhibit enhanced respiratory burst releasing noxious molecules, e.g. oxy-gen metabolites, a major protective mechanism against intracellular pathogens like T. gondii. • As the third step, activated macrophages synthesize endogenous HSP65 for protection against these toxic molecules, for repairment of damaged functions of themselves or for effective antigen-presentation. • Finally, either γδ T cells and αβ T cells reactive to HSP65 or αβ T cells specific for Toxoplasma antigen further accumulate and are activated. Such T cells directly destroy the host macrophages or activate macrophages to kill the intracellular Toxoplasma parasites (Fig. 2). MATERIALS AND METHODS Animals:Female mice were used for experiments at10-8 weeks of age. Parasite:A low-virulence Beverley strained a high-virulence RH strain of T.gondii. Infection and Immunization:Micewere infected with 1 x104 bradyzoites of Beverley strain or 1 x 104 tachyzoites of RH strain. Immunoblotting: protein extract of PEC homogenates derived from mice immunized with T.gondii cell mixed with lysate buffer. The protein sample were suspended and denatured in sample buffer and boiled a 100 degree for 3 min. the protein separated by SDS/PAGE at 20 mA for 1hr.purified 65-KDa mycobacterial protein. REFERENCES 1.Text book of clinical protozologym.jGharavi 2. Lindquist, S. (2005) Annu. Rev. Biochem. 55, 1151-1191. 3. Schlesinger, M. J. (2005) J. Cell Biol. 103, 321-325. 4. Pelham, H. (2008) Nature (London) 332, 776-777. 5. Young, D. B., Lathigra, R., Hendrix, R., Sweetser, D. &Young, R. A. (1988) 6.Jpn J.protozool.vol.35,no.1.(2002) 7.Proc. Nati. Acad. Sci. USA 8. Kaufmann, S. H. 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