Klimpel G R, Langley K E, Wypych J, Abrams J S, Chopra A K, Niesel D W
Department of Microbiology and Immunology, University of Texas Medical Branch Galveston, 77555-1019, USA.
J Exp Med. 1996 Jul 1;184(1):271-6. doi: 10.1084/jem.184.1.271.
Cholera toxin (CT) has been shown to induce stem cell factor (SCF) production in mouse ligated intestinal loops. Further, SCF interaction(s) with its receptor (c-kit) was shown to be important for the intestinal tract secretory response after CT exposure. In this study, we have investigated whether SCF production is induced in the intestinal tract after exposure to Salmonella typhimurium and whether this production could be an important intestinal tract response to Salmonella infection. Using a mouse ligated intestinal loop model, increased levels of SCF mRNA were detected at 2-4 h post-Salmonella challenge. Intestinal fluid obtained from Salmonella-challenged loops contained high levels of SCF by ELISA. Human and murine intestinal epithelial cell lines were also shown to have increased levels of SCF mRNA after exposure to Salmonella. Inhibition of Salmonella invasion of epithelial cells was shown to be one potentially important role for SCF:c-kit interactions in host defense to Salmonella infection. Pretreatment of human or murine intestinal cell lines with SCF resulted in a cellular state that was resistant to Salmonella invasion. Finally, mice having mutations in the white spotting (W) locus, which encodes the SCF-receptor (c-kit), were significantly more susceptible to oral Salmonella challenge than their control littermates. Taken together, the above results suggest that an important intestinal tract response to Salmonella infection is an enhanced production of SCF and its subsequent interactions with c-kit.
霍乱毒素（CT）已被证明能在小鼠结扎肠袢中诱导干细胞因子（SCF）的产生。此外，SCF与其受体（c-kit）的相互作用对于CT暴露后的肠道分泌反应很重要。在本研究中，我们调查了暴露于鼠伤寒沙门氏菌后肠道中是否会诱导SCF的产生，以及这种产生是否可能是肠道对沙门氏菌感染的重要反应。使用小鼠结扎肠袢模型，在沙门氏菌攻击后2 - 4小时检测到SCF mRNA水平升高。通过酶联免疫吸附测定法（ELISA）发现，从受到沙门氏菌攻击的肠袢中获得的肠液含有高水平的SCF。人源和鼠源肠道上皮细胞系在暴露于沙门氏菌后也显示出SCF mRNA水平升高。SCF与c-kit的相互作用在宿主抵御沙门氏菌感染中发挥的一个潜在重要作用是抑制沙门氏菌对上皮细胞的侵袭。用SCF预处理人源或鼠源肠道细胞系会导致细胞处于对沙门氏菌侵袭具有抗性的状态。最后，在编码SCF受体（c-kit）的白斑（W）位点发生突变的小鼠比其对照同窝小鼠对口服沙门氏菌攻击明显更易感。综上所述，上述结果表明肠道对沙门氏菌感染的一个重要反应是SCF的产生增加及其随后与c-kit的相互作用。
