establishment-mouse-severe-acute-pancreatitis-model-using-retrograde

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

The prevalence of acute pancreatitis (AP), especially severe acute pancreatitis (SAP), is increasing in younger age groups annually. However, there is a ...

The First Affiliated Hospital of Soochow University

Immune checkpoint blockade (ICB) has shown long-term survival benefits, but only in a small fraction of cancer patients. Recent studies suggest that improved vessel perfusion by ICB positively correlates with its therapeutic outcomes. However, the underlying mechanism of such a process remains unclear. Here, we show that anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA4) treatment-induced tumor vessel normalization was accompanied by an increased infiltration of eosinophils into breast tumors. Eosinophil accumulation was positively correlated with the responsiveness of a breast tumor to anti-CTLA4 therapy. Depletion of eosinophils subsequently negated vessel normalization, reduced antitumor immunity and attenuated tumor growth inhibition by anti-CTLA4 therapy. Moreover, intratumoral accumulation of eosinophils relied on T lymphocytes and interferon γ production. Together, these results suggest that eosinophils partially mediate the antitumor effects of CTLA4 blockade through vascular remodeling. Our findings uncover an unidentified role of eosinophils in anti-CTLA4 therapy, providing a potential new target to improve ICB therapy and to predict its efficacy.

CTLA4 blockade promotes vessel normalization in breast tumors via the accumulation of eosinophils.

This study aims to investigate the effects of albendazole on pancreatic cancer cells and to explore the possible mechanisms involved. MTT, colony formation, wound healing and Transwell assays and immunocytochemistry analyses of proliferation antigen Ki-67 were employed to evaluate the role of albendazole in pancreatic cancer cell line proliferation and migration. Moreover, flow cytometry cell apoptosis evaluation was used for mechanism analysis. Finally, the in-vivo effects of albendazole were examined in an in-vivo nude mouse xenograft model. Compared to the control treatment, albendazole significantly decreased the growth of the pancreatic cancer cell lines SW1990 and PANC-1 in a time- and dose-dependent manner, as evidenced by decreased MTT absorbance, colony number and Ki-67 levels. Furthermore, albendazole decreased cell migration in 2- and 3-dimensional models in a dose-dependent manner. In addition, albendazole increased the apoptotic cell ratio in a dose-dependent manner. Finally, the in-vivo results confirmed that albendazole could decrease tumor growth. We demonstrated the inhibitory effects of albendazole on pancreatic cell proliferation and migration in vitro and in vivo, which indicate that albendazole might serve as a novel treatment modality for pancreatic cancer.

Haifeng Chen

Department of Gastroenterology

The First Affiliated Hospital of Soochow University

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Haifeng Chen

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Gastroenterology

The First Affiliated Hospital of Soochow University

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct

Department of Gastroenterology