Bacterial colonization and the expression of inducible nitric oxide synthase in murine wounds
Bacterial colonization and the expression of inducible nitric oxide synthase in murine wounds
复制标题
DOI：
10.1016/s0002-9440(10)64492-6
复制
发表时间：
2002-12-01
影响因子：
6
通讯作者：
Albina, J
中科院分区：
文献类型：
--
作者：
Mahoney, E;Reichner, J;Albina, J
观察了诱导型一氧化氮合酶（iNOS）在两种小鼠创伤模型中的表达。对动物进行全层线性皮肤切口并皮下植入无菌聚乙烯醇海绵，或进行1.5 x 1.5 cm背部皮肤切除。逆转录聚合酶链反应检测iNOS mRNA在所有的细胞样本检索海绵。从海绵收获的炎性细胞裂解物的免疫印迹法未能检测到iNOS蛋白，并且切口伤口的免疫组织化学为轻度阳性。切除伤口的炎性细胞呈iNOS强阳性染色。发现皮肤伤口定植有金黄色葡萄球菌。在体内用热灭活细菌接种的海绵细胞中检测到iNOS，以及用抗生素处理的动物切除伤口中iNOS的免疫组织化学信号减少，支持细菌在伤口中诱导iNOS的作用。iNOS在切除伤口中的表达需要干扰素-γ和功能性淋巴细胞，因为干扰素-γ敲除和SCID-米色小鼠在切除伤口中表现出减弱的iNOS染色。小鼠伤口炎性细胞中iNOS的表达是对细菌定植的反应，而不是由无菌组织损伤引起的正常修复过程的一部分。
\The expression of inducible nitric oxide synthase (iNOS) in two different murine wound models was investigated. Animals were subjected to either full-thickness linear skin incision with subcutaneous implantation of sterile polyvinyl alcohol sponges, or to 1.5 x 1.5-cm dorsal skin excision. Reverse transcriptase-polymerase chain reaction detected iNOS mRNA in all cell samples retrieved from the sponges. Immunoblotting of lysates of inflammatory cells harvested from the sponges failed to detect iNOS protein, and immunohistochemistry of the incisional wound was mildly positive. inflammatory cells of excisional wounds stained strongly positive for iNOS. Cutaneous wounds were found to be colonized with Staphylococcus aureus. The detection of iNOS in cells from sponges inoculated in vivo with heat-killed bacteria and the reduction of immunohistochemical signal for iNOS in excisional wounds of animals treated with antibiotics support a role of bacteria in the induction of iNOS in wounds. The expression of iNOS in excisional wounds requires interferon-gamma and functional lymphocytes because interferon-gamma knockout and SCID-Beige mice exhibited attenuated iNOS staining in excisional wounds. The expression of iNOS in the inflammatory cells of murine wounds is a response to bacterial colonization and not part of the normal repair process elicited by sterile tissue injury.