Svezhova N V, Kirpichnikova K M, Gamaleĭ I A
Institute of Cytology RAS, St. Petersburg.
Tsitologiia. 2001;43(8):822-7.
Cryptosporidiosis in an opportunistic infection which poses a significant threat to the immunodeficient patients (including people with AIDS). The aim of the present work was to study whether oxidative burst, known as a nonspecific immune response of macrophages, may be modulated in vitro by persisting oocysts of a coccidian pathogen Cryptosporidium parvum. Live oocysts of C. parvum engulfed by murine perithoneal macrophages may persist within the phagosomes and retain their initial morphology for about 7 days following oocyst injection into macrophage monolayer. A short-term interaction of adherent macrophages with C. parvum oocyst suspension for 5-15 min caused oxidative burst in these macrophages. After a while, the intensity of this oxidative burst smoothly decreased to vanish within the following 2-6 h oocyst-macrophage cultivation. Dead oocysts caused no oxidative burst in macrophages. Co-cultivation of macrophages with oocysts for 1.0-1.5 days led to the appearance of macrophages, which had oocysts both contacting the cell surface and existing inside the phagosomes. In these macrophages the oxidative burst in response to the addition of a chemotactic peptide (fMLP) was considerably higher than in uninfected control cells. During a 1-4 day co-cultivation, the degree of oxidative burst caused by fMLP in macrophages containing only phagocytosed oocysts did not differ from that in the non-infected (oocyst-free) control. The data obtained enable us to propose that the products of oxidative burst in macrophages, formed in response to the interaction with C. parvum oocysts, do not kill the oocysts. These can survive for a long time in the phagosomes of macrophages. Such a long persistence of oocysts in phagosomes does not affect the capability of macrophages for oxidative burst in response to the action of fMLP.
隐孢子虫病是一种机会性感染，对免疫缺陷患者（包括艾滋病患者）构成重大威胁。本研究的目的是探讨作为巨噬细胞非特异性免疫反应的氧化爆发是否可在体外被球虫病原体微小隐孢子虫的持续卵囊所调节。被小鼠腹膜巨噬细胞吞噬的微小隐孢子虫活卵囊可在吞噬体内持续存在，并在将卵囊注射到巨噬细胞单层后约7天内保持其初始形态。贴壁巨噬细胞与微小隐孢子虫卵囊悬液短期相互作用5 - 15分钟会导致这些巨噬细胞发生氧化爆发。一段时间后，这种氧化爆发的强度会平稳下降，并在随后2 - 6小时的卵囊 - 巨噬细胞培养过程中消失。死卵囊不会在巨噬细胞中引发氧化爆发。巨噬细胞与卵囊共培养1.0 - 1.5天会导致出现这样的巨噬细胞，其卵囊既接触细胞表面又存在于吞噬体内。在这些巨噬细胞中，添加趋化肽（fMLP）后引发的氧化爆发明显高于未感染的对照细胞。在1 - 4天的共培养过程中，仅含有吞噬卵囊的巨噬细胞中由fMLP引发的氧化爆发程度与未感染（无卵囊）对照细胞中的程度没有差异。所获得的数据使我们能够提出，巨噬细胞中因与微小隐孢子虫卵囊相互作用而形成的氧化爆发产物不会杀死卵囊。这些卵囊可在巨噬细胞的吞噬体内长期存活。卵囊在吞噬体内如此长时间的持续存在并不影响巨噬细胞对fMLP作用产生氧化爆发的能力。
