Department of Inflammatory Bowel Diseases, University Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece.
Med Hypotheses. 2010 Sep;75(3):284-6. doi: 10.1016/j.mehy.2010.03.001. Epub 2010 Mar 23.
Seronegative spondylarthritides (SpAs) and inflammatory bowel disease (IBD) are disorders with a complex and elusive etiology. Current research has focused on downstream events and mechanisms of autoimmunity and inflammation but the primary etiologic factor is still unknown. We present a new hypothesis for the role of collagen into the pathogenesis of SpAs and IBD based on the assumption that they represent deferent phenotypes of the same disease. We gathered information on humans and animals which fit to the current evidence based concepts into their pathogenesis. We developed a logical hypothesis for the contribution of the individual's connective tissue profile among with the well known contribution of other genetic factors. The presence of a specific collagen or tissue matrix, which for abbreviation will be called the "soft collagen" (SC) is the basis for the pathogenesis of SpAs and the IBD. It seems that a triplet consisted of the "soft collagen", the genetic predisposition (such as the presence of HLA-B27, PSORS1 genes, NOD2/CARD mutations) and the triggering event (trauma or infection) are necessary for the development of these particular disorders. The "soft collagen" hypothesis may explain the pathogenesis as well as the various clinical aspects of these particular disorders which affect mostly young individuals.
血清阴性脊柱关节病（SpA）和炎症性肠病（IBD）是具有复杂且难以捉摸病因的疾病。目前的研究集中在自身免疫和炎症的下游事件和机制上，但主要病因仍不清楚。我们提出了一个关于胶原在 SpA 和 IBD 发病机制中的作用的新假设，该假设基于它们代表同一疾病的不同表型这一假设。我们收集了与目前基于证据的概念相适应的人类和动物信息，以纳入其发病机制。我们对个体结缔组织特征的贡献提出了一个合乎逻辑的假设，以及其他遗传因素的已知贡献。存在特定的胶原或组织基质，为方便起见，我们将其称为“软胶原”（SC），是 SpA 和 IBD 发病机制的基础。似乎由“软胶原”、遗传易感性（如 HLA-B27 的存在、PSORS1 基因、NOD2/CARD 突变）和触发事件（创伤或感染）组成的三联体是这些特定疾病发展所必需的。“软胶原”假说可以解释这些特定疾病的发病机制以及影响大多数年轻人的各种临床方面。
