| Research Abstract |
Infection is a desperate fight between pathogens and infected hosts, and each side prepares dexterous strategies to endure the attack from the other side. Thus, infection should be stressful both for invading microorganisms and infected hosts. Accordingly, it is conceivable that expression of heat shock proteins (HSPs) is an essential process for both pathogens and host mice. In a series of study using various protozoa which use different mechanisms of evasion from host defense systems, we examined the function of HSPs contributing to the evasion or the host-defense. Following results were obtained by those investigations.
1. Contribution of HSP65 to host-defense.
1) In mice acquired resistance against some pathogens, γδ, NK or NKT cells, those of which play essential roles in initial stages of host defense against toxoplasma, trypanosoma cruzi and Leishmania major, respectively, express HSP65 in host macrophage and contribute to host-defense. 2) On the other hand, in susceptible mice or mice infected with high virulent strains of protozoa, those protozoa evade host defense systems via preventing the expression of HSP65.
2. Contribution of HSP to pathogen-evasion in the case of with Plasmodium yoelii (mouse malaria).
1) A low virulent strain of P.yoelii fails to express HSP90 and this strain can not survive within the infected host. 2) On the other hand, a high virulent strain have a potential to express the HSP, then they can survive in the infected host mice. 3) It is noteworthy that the high virulent strain prepare tricky expression mechanisms. That is, they express HSP90 only when they are attacked by host defense systems in resistant mice.
It is very important to further elucidate the rule or relationships between the expression of HSPs and parasite-evasion/host defense. This direction of research should provide a direction for development of vaccines for various infections with obligate intracellular pathogens.
|
