Stadnyk A W, Baumann H, Gauldie J
Seattle Biomedical Research Institute, Washington.
Immunology. 1990 Apr;69(4):588-95.
During acute inflammation, the mammalian liver responds with increased production and secretion of a series of plasma glycoproteins, collectively termed the acute-phase proteins, resulting from the release at the site of inflammation of polypeptide cytokines, including IL-1 and IL-6, which interact with receptors on hepatocytes and alter gene expression. This attribute of the systemic acute-phase response was studied throughout the course of infection with two nematode parasites in rats. Significant increases in serum haptoglobin, alpha 1-acid glycoprotein and alpha 1-cysteine protease inhibitor were detected coincident with episodes of skin, lung and intestinal pathology during Nippostrongylus brasiliensis, but were not seen during Trichinella spiralis, infection of the rat despite similar intestinal pathology. These changes were seen at both the protein and mRNA levels in the liver. Infection with T. spiralis was not anti-inflammatory, as macrophages from various sites could be induced in vitro to release inflammatory cytokines, and in vivo induction of inflammation by turpentine injection was similar in control and infected animals. However, macrophage populations recovered from animals infected with T. spiralis were not activated. Moreover, intestinal infection alone with intestinal stages of N. brasiliensis also failed to elicit the systemic acute-phase protein response, requiring an explanation involving skin and lung for the acute-phase response during gut inflammation in a primary infection with N. brasiliensis. Taken together, these data suggest that during the intestinal phase of nematode infection, with pathological changes to the gut, the systemic acute-phase response is not elicited through compromise or lack of stimulation of inflammatory cells in the intestine. The systemic parameters of the acute-phase response may not be a component of gastrointestinal pathology.
在急性炎症期间，哺乳动物肝脏会通过增加一系列血浆糖蛋白的产生和分泌做出反应，这些血浆糖蛋白统称为急性期蛋白，这是由炎症部位释放的多肽细胞因子（包括白细胞介素-1和白细胞介素-6）引起的，这些细胞因子与肝细胞上的受体相互作用并改变基因表达。在大鼠感染两种线虫寄生虫的整个过程中，对全身急性期反应的这一特性进行了研究。在巴西日圆线虫感染期间，血清触珠蛋白、α1-酸性糖蛋白和α1-半胱氨酸蛋白酶抑制剂显著增加，同时伴有皮肤、肺部和肠道病变，但在旋毛虫感染大鼠期间，尽管肠道病变相似，却未观察到这些变化。这些变化在肝脏的蛋白质和mRNA水平上均可见。旋毛虫感染并非抗炎性的，因为来自各个部位的巨噬细胞在体外可被诱导释放炎性细胞因子，并且在体内，对照动物和感染动物通过松节油注射诱导的炎症相似。然而，从感染旋毛虫的动物中回收的巨噬细胞群体未被激活。此外，仅感染巴西日圆线虫肠道阶段也未能引发全身急性期蛋白反应，这需要对巴西日圆线虫初次感染时肠道炎症期间急性期反应涉及皮肤和肺部的情况作出解释。综上所述，这些数据表明，在线虫感染的肠道阶段，尽管肠道出现病理变化，但全身急性期反应并非通过肠道炎性细胞受到损害或缺乏刺激而引发。急性期反应的全身参数可能不是胃肠道病理的组成部分。
