University of Saskatchewan, Saskatoon, Canada.
Can J Microbiol. 2010 Jun;56(6):522-6. doi: 10.1139/w10-034.
Salmonella enterica serovar Enteritidis (Salmonella Enteritidis) is one of the major causes of bacterial food-borne illness in humans. During the course of infection, Salmonella Enteritidis uses 2 type III secretion systems (T3SS), one of which is encoded on Salmonella pathogenicity island 1 (SPI-1). SPI-1 plays a major role in the invasion process. In the present study, we evaluated the effect of sera against the SPI-1 T3SS components on invasion in vitro using polarized human intestinal epithelial cells (Caco-2). Antisera to SipD protected Caco-2 cells against entry of wild-type Salmonella Enteritidis. On the other hand, sera against InvG, PrgI, SipA, SipC, SopB, SopE, and SopE2 did not affect Salmonella Enteritidis entry. To illustrate the specificity of anti-SipD mediated inhibition, SipD-specific antibodies were depleted from the serum. Antiserum depleted of SipD-specific antibodies lost its capacity to inhibit Salmonella Enteritidis entry. Thus, we demonstrate for the first time that antibodies against the SPI-1 needle tip protein (SipD) inhibit Salmonella Enteritidis invasion and that the SipD protein may be an important target in blocking SPI-1 mediated virulence of Salmonella Enteritidis.
肠炎沙门氏菌血清型肠炎（肠炎沙门氏菌）是人类细菌性食源性疾病的主要原因之一。在感染过程中，肠炎沙门氏菌使用 2 种 III 型分泌系统（T3SS），其中一种编码在沙门氏菌致病岛 1（SPI-1）上。SPI-1 在入侵过程中起主要作用。在本研究中，我们使用极化人肠道上皮细胞（Caco-2）评估了针对 SPI-1 T3SS 成分的血清对体外入侵的影响。针对 SipD 的抗血清可保护 Caco-2 细胞免受野生型肠炎沙门氏菌的侵袭。另一方面，针对 InvG、PrgI、SipA、SipC、SopB、SopE 和 SopE2 的血清不影响肠炎沙门氏菌的进入。为了说明抗 SipD 介导的抑制的特异性，从血清中耗尽了针对 SipD 的特异性抗体。耗尽 SipD 特异性抗体的抗血清丧失了抑制肠炎沙门氏菌进入的能力。因此，我们首次证明了针对 SPI-1 针状蛋白（SipD）的抗体抑制肠炎沙门氏菌侵袭，并且 SipD 蛋白可能是阻断 SPI-1 介导的肠炎沙门氏菌毒力的重要靶标。
