辅助基因调控因子在耐甲氧西林假中葡萄球菌毒力表达和生物膜形成中的作用

C. Jung, Ya-Chih Huang, J. Chia, Chih-Chieh Hsu, C. Chou
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摘要

假中质葡萄球菌引起的软组织感染是一种典型的生物膜相关传染病。近年来,人类耐甲氧西林假中间葡萄球菌(MRSP)感染的发生率有所增加。本研究分别通过体外实验和小鼠脓皮病模型研究了MRSP和MRSP[配方:见文]诱导皮肤感染的不同辅助基因调控因子(agr)型的毒力。从台湾北部采集了47株犬临床MRSP分离株,并将其分为4种agr型,即I型(52%)、II型(2%)、III型(35%)和IV型(10%)。大多数MRSP分离株属于强(49%)或中等(42.5%)生物膜生产者。III型77、III型79和IV型n10菌株对皮肤的损伤程度均大于I型58和II型n3菌株,但差异不显著。agr III型77、III型79和IV型n10菌株对细胞粘附、细胞侵袭和细胞毒性的影响强于其他MRSP菌株。然而,这些MRSP分离株的生物膜形成能力与引起小鼠皮肤脓肿的毒力差异无关。从临床样本中分离出的agr III型77、III型79和IV型n10 MRSP菌株显示引起脓皮病的细菌毒力增加,值得进一步的基因组研究。
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PERFORMANCE OF ACCESSORY GENE REGULATOR IN VIRULENCE EXPRESSION AND BIOFILM FORMATION OF METHICILLIN-RESISTANT STAPHYLOCOCCUS PSEUDINTERMEDIUS
Staphylococcus pseudintermedius-induced soft tissue infection is a typical biofilm-related infectious disease. Recently, the occurrence of methicillin-resistant S. pseudintermedius (MRSP) infections in humans has increased. In this study, the virulence of different accessory gene regulator (agr) types of MRSP and MRSP[Formula: see text]induced skin infection were investigated through in vitro studies and the murine pyoderma model, respectively. Forty-seven canine clinical MRSP isolates were collected from northern Taiwan and classified into four agr types, namely, type I (52%), type II (2%), type III (35%), and type IV (10%). The majority of the MRSP isolates belonged to either strong (49%) or moderate (42.5%) biofilm producers. The skin damages induced by type III 77, type III 79, and type IV n10 isolates were larger than those induced by type I 58 and type II n3 isolates, but not by a significant degree. The effects of cell adhesion, cell invasion and cell cytotoxicity tests for agr type III 77, type III 79, and type IV n10 isolates were stronger than those caused by other types of MRSP isolates. However, the biofilm formation ability of these MRSP isolates did not show association with their virulence differences for causing murine skin abscesses. The agr type III 77, type III 79, and type IV n10 isolates of MRSP from the clinical samples revealed increased bacterial virulence for causing pyoderma, which is worthy of further genomic studies.
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