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很早就发现内毒素血症疾患与疟疾发作有某些相似点;近来的材料认为,内毒素中毒主要是巨噬细胞对细菌脂多糖(LPS)应答而释放的因子引起的。感染文氏疟原虫佩氏亚种(P.vinckei petteri)的小鼠,当原虫密度高时则先发生内毒素血症的指征和病理特点;而且,注射小剂量LPS可增强内毒素中毒的发作。感染文氏疟原虫的小鼠,对LPS的敏感性大大提高;甚至将小量LPS(<20μg)注射给低原虫血症的小鼠,都很快发生内毒素血症症状。此外,注射LPS小鼠的血清具有诸如肿瘤坏死因子、糖皮质激素对抗因子、淋巴细胞活化因子及干扰素之类内毒素毒性介质的活性。曾推测这些介质包括有对疟原虫有害的因子;一些疟疾发作时所见到的虫体形态异常,可能与这种(些)有害因子有关。本文报告从内毒素中毒的小鼠取疟原虫,在体外显示次黄嘌呤掺合的减少,这说明它比正
It has long been discovered that there are some similarities between endotoxemic disorders and malaria episodes; recent data suggest that endotoxin toxicity is primarily caused by factors released by macrophages in response to bacterial lipopolysaccharide (LPS). Mice infected with P. vinckei petteri develop markers of endotoxemia and pathological features when protozoa density is high, and injection of low doses of LPS potentiates endotoxin toxicity attack. Mice infected with Plasmodium malaria were significantly more susceptible to LPS; even endotoxic symptoms were rapidly developed in mice injected with low doses of LPS (<20 μg). In addition, sera injected into LPS mice have activities of endotoxin toxic mediators such as tumor necrosis factor, glucocorticoid counterfactor, lymphocyte activating factor and interferon. It has been speculated that these media include factors that are detrimental to the Plasmodium; some forms of parasites seen during malaria episodes may be related to these (or some) harmful agents. This article reports that taking endotoxin-poisoned mice from malaria parasites shows a decrease in hypoxanthine incorporation in vitro, indicating that it is more positive than positive