PRJNA223341
Bacterial 16S rRNA tag-encoded 16S rRNA pyrosequencing
Mice deficient of plasminogen (plgtm1Bug), the proenzyme form of plasmin, which exhibits it’s key role in the degradation of fibrin polymers, are widely used in a wound healing model within biomedical research. However, they suffer from colitis and rectal prolapses. The aim of this study was to elucidate by histopathology, sequencing of the gut microbiota and cytokine measurement in plgtm1Bug as well as wild type mice the nature of this colitis, and to which extent it, as other forms of colitis in mice, is due to an immunological reaction towards the gut microbiota. Compared to the wild type plgtm1Bug mice exhibited delayed wound healing, and they could clearly be divided into three distinct groups with different wound healing times. The histology of the colon lesions in plgtm1Bug mice was characterized by the accumulation of fibrin and formation of cysts in the colon epithelium, and normal numbers of goblet cell and neutrophil granulocytes. Lesions were located only in the intermediate and distal parts of the colon, and not at all in the proximal part of the colon, indicating that the texture of colon content might influence the development of the lesions rather than the gut microbiota to which none of the parameters monitored correlated. This was accompanied by a cytokine profile indicative of chronic tissue damage. It is concluded that the colitis in plgtm1Bug mice mostly seems to be related to a mechanical tissue damage caused by the gut contents, and therefore future studies may include housing the mice on bedding being less traumatic.