Mesenteric adipose tissue B lymphocytes promote intestinal injury in severe acute pancreatitis by mediating enteric pyroptosis.

BACKGROUND: Visceral adipose tissue (VAT) has been linked to the severe acute pancreatitis (SAP) prognosis, although the underlying mechanism remains unclear. It has been reported that pyroptosis worsens SAP. The present study aimed to verify whether mesenteric adipose tissue (MAT, a component of VAT) can cause secondary intestinal injury through the pyroptotic pathway. METHODS: Thirty-six male Sprague Dawley (SD) rats were divided into six different groups. Twelve rats were randomly divided into the SAP and control groups. We monitored the changes of MAT and B lymphocytes infiltration in MAT of SAP rats. Twelve SAP rats were injected with MAT B lymphocytes or phosphate buffer solution (PBS). The remaining twelve SAP rats were first injected with MAT B lymphocytes, and then with MCC950 (NLRP3 inhibitor) or PBS. We collected blood and tissue samples from pancreas, gut and MAT for analysis. RESULTS: Compared to the control rats, the SAP group showed inflammation in MAT, including higher expression of tumor necrosis factor (TNF-α) and interleukin-6 (IL-6), lower expression of IL-10, and histological changes. Flow cytometry analysis revealed B lymphocytes infiltration in MAT but not T lymphocytes and macrophages. The SAP rats also exhibited intestinal injury, characterized by lower expression of zonula occludens-1 (ZO-1) and occludin, higher levels of lipopolysaccharide and diamine oxidase, and pathological changes. The expression of NLRP3 and n-GSDMD, which are responsible for pyroptosis, was increased in the intestine of SAP rats. The injection of MAT B lymphocytes into SAP rats exacerbated the inflammation in MAT. The upregulation of pyroptosis reduced tight junction in the intestine, which contributed to the SAP progression, including higher inflammatory indicators and worse histological changes. The administration of MCC950 to SAP + MAT B rats downregulated pyroptosis, which subsequently improved the intestinal barrier and ameliorated inflammatory response of SAP. CONCLUSIONS: In SAP, MAT B lymphocytes aggravated local inflammation, and promoted the injury to the intestine through the enteric pyroptotic pathway.

Recurrence of Helicobacter pylori infection: incidence and influential factors.

BACKGROUND: Helicobacter pylori (H. pylori) eradication has been widely used. The recurrence rate of H. pylori after eradication and its related factors are gaining more and more attention. Our study aimed to determine the recurrence rate of H. pylori infection after successful eradication, and analyze its influential factors. METHODS: We prospectively studied 1050 patients with upper gastrointestinal symptoms who were diagnosed as H. pylori infection by gastroscopy and underwent eradication therapies from April 2013 to January 2014. The C-urea breath test (UBT) or Warthin-Starry (WS) staining was done at 8 to 12 weeks after the therapy. Patients with successful eradication were followed by repeated UBT or gastroscopy at one year and 3 years after therapy, as well as, questionnaire surveys. Recurrence was considered if the UBTs or WS staining of biopsy were positive. One-year and 3-year recurrence rates were calculated, and analyzed the differences between recurred patients and others in basic data, sociological characteristics, lifestyle. RESULTS: A total of 743 patients finished the 1-year follow-up, and the 1-year recurrence rate was 1.75%. Of the 607 patients who finished the 3-year follow-up, 28 patients recurred, and the 3-year recurrence rate was 4.61%. Analysis of variance showed that low-income, poor hygiene condition of dining out place, and receiving invasive diagnoses or treatments were significant risk factors for H. pylori infection recurrence. Logistic regression analysis demonstrated that the combination of invasive diagnoses or treatments, the level of income, and the hygiene standard of dining out place were significant and independent influential factors of the recurrence of H. pylori. CONCLUSIONS: The 1-year and 3-year recurrence rates of H. pylori infection after eradication therapy are 1.75% and 4.61%. Low-income, poor hygiene condition of dining out place, and a combination of invasive diagnoses or treatments are independent risk factors of H. pylori recurrence.