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首页> 美国卫生研究院文献>Infection and Immunity >Human and rat macrophages mediate fungistatic activity against Rhizopus species differently: in vitro and ex vivo studies.
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Human and rat macrophages mediate fungistatic activity against Rhizopus species differently: in vitro and ex vivo studies.

机译：人类和大鼠的巨噬细胞介导的针对根霉菌种的抑菌活性不同：体外和离体研究。

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Both rat alveolar macrophages and a human macrophages cell line with characteristics of human tissue (e.g., alveolar) macrophages (THP-1) were found to inhibit the germination of Rhizopus spores. However, the conditions under which fungistatic activity occurs are different for these two cell types. The inhibition of Rhizopus spore germination by rat alveolar macrophages requires the activation of macrophages and the presence of serum and L-arginine. During rat alveolar macrophage-mediated fungistatic activity, L-arginine is oxidized to nitric. Human macrophage-mediated fungistatic activity is similar to that mediated by rat macrophages in terms of the serum requirement, but it does not require L-arginine. Human macrophages did not produce any nitrite detectable by the colorimetric assay. Their ability to inhibit germination was enhanced by the combination of endotoxin and gamma interferon. The inhibition of Rhizopus spore germination by rat alveolar macrophages is thus mediated by the generation of nitric oxide, whereas the mechanism of similar inhibition by human macrophages remains poorly understood. Serum samples from diabetic rats as well as from patients with diabetes or uremia decreased the inhibitory effect of macrophages on spore germination. Dialysis of the serum samples against a buffered salt solution antagonized this phenomenon, indicating that a low-molecular-weight factor in the sera of patients with diabetes or uremia may modulate local antifungal defense mechanisms. The absence of L-arginine-dependent nitrogen oxidation in human macrophages, compared with its presence in rat alveolar macrophages, under conditions during which fungistatic activity occurs suggests that this phenomenon is species specific.
机译：发现大鼠肺泡巨噬细胞和具有人类组织（例如，肺泡）巨噬细胞（THP-1）特征的人类巨噬细胞细胞系均抑制根霉孢子的萌发。但是，对于这两种细胞类型，发生抑菌活性的条件是不同的。大鼠肺泡巨噬细胞对根霉孢子萌发的抑制作用需要活化巨噬细胞，并存在血清和L-精氨酸。在大鼠肺泡巨噬细胞介导的抑菌活性期间，L-精氨酸被氧化为硝酸。就血清需求而言，人巨噬细胞介导的抑菌活性类似于大鼠巨噬细胞介导的抑菌活性，但它不需要L-精氨酸。人巨噬细胞未产生比色测定法可检测到的任何亚硝酸盐。内毒素和γ干扰素的结合增强了它们抑制发芽的能力。因此，大鼠肺泡巨噬细胞对根霉孢子萌发的抑制作用是由一氧化氮的产生介导的，而对人类巨噬细胞类似抑制作用的机制尚不清楚。来自糖尿病大鼠以及患有糖尿病或尿毒症的患者的血清样品降低了巨噬细胞对孢子萌发的抑制作用。用缓冲盐溶液对血清样品进行透析可拮抗这种现象，表明糖尿病或尿毒症患者血清中的低分子量因子可能会调节局部的抗真菌防御机制。与在大鼠肺泡巨噬细胞中存在抑菌活性的条件下相比，人类巨噬细胞中不存在L-精氨酸依赖性氮氧化，表明该现象是物种特异性的。

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