对产气荚膜梭菌基因工程菌株的使用表明，在实验性气性坏疽中，血管白细胞郁滞的发生需要α毒素和θ毒素两者。
Use of genetically manipulated strains of Clostridium perfringens reveals that both alpha-toxin and theta-toxin are required for vascular leukostasis to occur in experimental gas gangrene.
作者信息
Ellemor D M, Baird R N, Awad M M, Boyd R L, Rood J I, Emmins J J
机构信息
Department of Pathology and Immunology, Monash Medical School, Alfred Hospital, Prahran, Victoria 3181, Australia.
出版信息
Infect Immun. 1999 Sep;67(9):4902-7. doi: 10.1128/IAI.67.9.4902-4907.1999.
Abstract
A hallmark of gas gangrene (clostridial myonecrosis) pathology is a paucity of leukocytes infiltrating the necrotic tissue. The cause of this paucity most likely relates to the observation of leukocyte aggregates at the border of the area of tissue necrosis, often within the microvasculature itself. Infecting mice with genetically manipulated strains of Clostridium perfringens type A (deficient in either alpha-toxin or theta-toxin production) resulted in significantly reduced leukocyte aggregation when alpha-toxin was absent and complete abrogation of leukocyte aggregation when theta-toxin was absent. Thus, both alpha-toxin and theta-toxin are necessary for the characteristic vascular leukostasis observed in clostridial myonecrosis.
摘要
气性坏疽（梭菌性肌坏死）病理的一个标志是浸润坏死组织的白细胞数量稀少。这种稀少的原因很可能与在组织坏死区域边界处观察到的白细胞聚集有关，这种聚集通常发生在微血管本身。用基因操作的A型产气荚膜梭菌菌株（缺乏α毒素或θ毒素产生）感染小鼠，当缺乏α毒素时，白细胞聚集显著减少，当缺乏θ毒素时，白细胞聚集完全消失。因此，α毒素和θ毒素都是梭菌性肌坏死中观察到的特征性血管白细胞淤滞所必需的。
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