scholarly journals Corrigendum to: Fungal Dysbiosis Aggravates Pouchitis in a Rat Model of Ileal Pouch Anal Anastomosis

2021 ◽  
Keyword(s):  
Rat Model ◽  
Ileal Pouch ◽  
Ileal Pouch Anal Anastomosis ◽  
Anal Anastomosis

Stasis Predisposes Ileal Pouch Inflammation in a Rat Model of Ileal Pouch-Anal Anastomosis

2010 ◽  
Vol 164 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Arthur F. Stucchi ◽  
Khaled O. Shebani ◽  
Karen L. Reed ◽  
Adam C. Gower ◽  
Michael F. Alapatt ◽  
...  
Keyword(s):  
Rat Model ◽  
Ileal Pouch ◽  
Ileal Pouch Anal Anastomosis ◽  
Anal Anastomosis

scholarly journals Intestinal Barrier Disruption in Ileal Pouchitis After Ileal Pouch-Anal Anastomosis in a Rat Model

2017 ◽  
Vol 23 (6) ◽  
pp. 923-931 ◽  
Author(s):  
Kai-Yu Li ◽  
Jian-Lin Wang ◽  
Yan-Yan Xu ◽  
Sen-Yang Gao ◽  
Ying-Ying Zhang ◽  
...  
Keyword(s):  
Rat Model ◽  
Ileal Pouch ◽  
Intestinal Barrier ◽  
Ileal Pouch Anal Anastomosis ◽  
Barrier Disruption ◽  
Anal Anastomosis

Fungal Dysbiosis Aggravates Pouchitis in a Rat Model of Ileal Pouch Anal Anastomosis

2020 ◽  
Vol 26 (12) ◽  
pp. 1831-1842
Author(s):  
Feng Zhu ◽  
Dengyu Feng ◽  
Chao Ding ◽  
Tenghui Zhang ◽  
Jianwei Chen ◽  
...  
Keyword(s):  
Rat Model ◽  
Nuclear Factor Kappa B ◽  
Ileal Pouch ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Ileal Pouch Anal Anastomosis ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Α Diversity ◽  
Anal Anastomosis

Abstract Background Although the interaction between gut microbiota and pouchitis after ileal pouch anal anastomosis (IPAA) for ulcerative colitis (UC) has been confirmed, evidence of commensal mycobiota in the etiology of pouchitis is still lacking. This study aimed to investigate the role of fungi in the pathogenesis of pouchitis. Methods Fecal samples were collected from UC patients with or without pouchitis after IPAA. Experimental pouchitis was induced by 5% dextran sulfate sodium for 7 consecutive days in a rat model of IPAA. Fungal dysbiosis was induced by 0.5% fluconazole (Flu), and commensal fungal recognition through dectin-1 was blocked by 5% laminarin. Fecal fungal composition was analyzed using internal transcribed spacer 2 sequencing. Severity of pouchitis and activation of the CARD9-nuclear factor kappa-B pathway was determined among different groups. Results Patients with pouchitis had a lower alpha (α) diversity in mycobiota composition and a higher abundance of Saccharomyces at the genus level compared with those with a normal pouch. In the rat model of pouchitis, Flu treatment decreased fungal burden but induced fungal dysbiosis, characterized by increased α diversity, a decreased relative abundance of Kazachstania, and increased Polythrincium and Saccharomyces. In addition, Flu treatment worsened dextran sulfate sodium pouchitis, as indicated by increased mortality, weight loss, higher histological score, and CD4+ cell infiltration. Laminarin also increased the severity of pouchitis. In the Flu and laminarin groups, the expression of interferon-γ, tumor necrosis factor-α, CARD9, and phosphorylated nuclear factor kappa-B inhibitor alpha was decreased. Conclusions Patients with pouchitis had altered fungal composition. Fungal dysbiosis or recognition deficiency by the host may exacerbate experimental pouchitis. Strategies targeting commensal mycobiota may provide therapeutic potential against pouchitis, especially for antibiotic-refractory patients.

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