| First Author | Liu H | Year | 2024 |
| Journal | Int Immunopharmacol | Volume | 128 |
| Pages | 111499 | PubMed ID | 38232535 |
| Mgi Jnum | J:344855 | Mgi Id | MGI:7580316 |
| Doi | 10.1016/j.intimp.2024.111499 | Citation | Liu H, et al. (2024) S100a10 deficiency in neutrophils aggravates ulcerative colitis in mice. Int Immunopharmacol 128:111499 |
| abstractText | BACKGROUND AND AIMS: S100a10 is a member of the S100 family of proteins, which plays a key role in the depression and tumor metastasis. However, the role of S100a10 is unclear in ulcerative colitis. METHODS: The effect of S100a10 was assessed using a murine ulcerative colitis model which was accompanied by parameters including body weight loss, disease activity index, histological score, colon weight and length. The quantity and role of immune cells was determined by flow cytometry and bone marrow chimeric mice. Neutrophils depletion, adoptive cell transfer and conditional knockout mice were used to ascertain which cells played the key role in ulcerative colitis. The function of neutrophils was evaluated by migration assay, phagocytosis assay, multiplex immunoassay and real-time PCR. RESULTS: In this study, our data showed that S100a10(-/-) mice were prone to ulcerative colitis induced by dextran sodium sulfate. Neutrophils number increased in colon of S100a10(-/-) mice after dextran sodium sulfate treatment significantly. Meanwhile, adoptive transfer of neutrophils from wild type mice partially decreased the susceptibility of S100a10(-/-) mice to dextran sodium sulfate. There was no difference in ulcerative colitis between the groups of S100a10(-/-) mice without neutrophils and wild type mice. Finally, we found that S100a10(-/-) neutrophils had stronger function in secretion and synthesis of inflammatory factor. CONCLUSIONS: In one word, these results suggest that S100a10 has a role in inhibiting the pathogenesis of ulcerative colitis through regulation of neutrophils function. |
