STAT5 promotes chronic pancreatitis by enhancing GM-CSF-dependent neutrophil augmentation,Journal of Leukocyte Biology

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STAT5 promotes chronic pancreatitis by enhancing GM-CSF-dependent neutrophil augmentation
Journal of Leukocyte Biology ( IF 3.6 ) Pub Date : 2021-06-28 , DOI: 10.1002/jlb.3ma1020-647r
Yuli Lin _{1,

2} , Yusheng Chen ₃ , Wenxue Feng ₄ , Junfeng Zhang ₅ , Rong Hua ₅ , Bo Yin ₄ , Xuguang Yang ₁

Affiliation

Chronic pancreatitis (CP) is a continuing or relapsing inflammatory disease of the pancreas, characterized by fibrosis of the whole tissue. The regulatory mechanisms of the immune microenvironment in the pathogenesis of CP are still not clear. Immune cells, especially myeloid cells, play an important role in the pathogenesis of pancreatitis. Understanding the regulatory mechanisms of immune infiltration has a significant impact on CP intervention. Here, we demonstrated that transcription factor STAT5 was involved in and critical for the progression of CP. Inflammatory stress could significantly increase the expression and activation of STAT5 during CP. STAT5 deficiency or inhibition contributed to alleviating pancreatic inflammation and fibrosis in CP mice. The increased neutrophil infiltration, mediated by up-regulated GM-CSF, was responsible for the pancreatitis-promoting activity of STAT5. Our investigation highlighted the importance of STAT5 in regulating the immune microenvironment of CP. Targeting STAT5 may hold distinct promise for clinical treatment to alleviate CP.

中文翻译：

STAT5 通过增强 GM-CSF 依赖性中性粒细胞增加促进慢性胰腺炎

慢性胰腺炎 (CP) 是一种持续性或复发性胰腺炎性疾病，其特征是整个组织的纤维化。免疫微环境在CP发病中的调控机制尚不清楚。免疫细胞，尤其是髓细胞，在胰腺炎的发病机制中起重要作用。了解免疫浸润的调控机制对 CP 干预具有重要影响。在这里，我们证明转录因子 STAT5 参与 CP 的进展并且对 CP 的进展至关重要。炎症应激可显着增加 CP 期间 STAT5 的表达和激活。STAT5 缺乏或抑制有助于减轻 CP 小鼠的胰腺炎症和纤维化。由上调的 GM-CSF 介导的中性粒细胞浸润增加，负责 STAT5 的胰腺炎促进活性。我们的研究强调了 STAT5 在调节 CP 免疫微环境中的重要性。靶向 STAT5 可能对减轻 CP 的临床治疗有明显的希望。

更新日期：2021-07-28

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