| Heat shock reaction, i.e. stress reaction, is a mechanism of making the cells adapt to or survive peripheral disadvantage circumstances. Followed it, many heat shock proteins(stressing proteins) produce. Elizabeth A. Craig et al. considered the heat shock protein7O(HsplO) should be a "thermometer" of cells challenged by sub-fatal sfimuli, such asheat. So we could verify that the cells or yeasts produced heat shock reaction(HSR) by detecting the Hsp7O. This article documented the MIC of amphotericin B(AmB) of previous and posterior the heat stressing(42℃×30min) Cryptococci according to documentary M-27 regulated by NCCLS. The result said the pre- MIC was lower than post- one(P=0.002). It indicated that MIC detected in lab(30℃) sh9uld be lower than in vivo(37℃). Subsequently, we got the Hsp70 of Crypto cocci neoformans stressed by heat(sub-fatal, 42℃ and constitutive 37℃ stressing) through Western blotting in term of the high homologue of Hsp70, which verified that the yeasts produced the HSR. The results indicated that in clinic the difference of sensitivity to AmB in vivo and in vitro was not only related to immune system, but also to the changes of metabolism in yeasts, such as heat shock reaction. So we should consider these factors'effect on modifying the usage of drugs in clinic. AmB has effects of osmiotic and oxidative stress on cells. They both could induce the HSR/Hsp7O, and it protects the yeasts. So low dosage usage of the drug could also induce the HSR, and it lowers the sensitivity to the yeasts. In general, patient's temperature arranges from 37℃ to 40℃ According to Gabriele and our experrment, we knew that the HSR-couidalso be induced in vivo. At the same time, we got the Hsp70 in our experiment according to the 6 high homologue of antibody(mouse's Ab to Hsp70 of human, pig, dog, etc.). So we conferred that the human anti-Hsp70 antibody of Cryptococcus neoformans could cross-react with human Hsp70. It may be a new virulence factor in Cryptococcus neoformans. |
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