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Lactobacillus salivarius UCC118™ Dampens Inflammation and Promotes Microbiota Recovery to Provide Therapeutic Benefit in a DSS-Induced Colitis Model

唾液乳杆菌 结肠炎 失调 炎症性肠病 益生菌 乳酸菌 免疫学 双歧杆菌 炎症 微生物学 肠道菌群 医学 生物 疾病 细菌 内科学 遗传学
作者
Namrata Iyer,Michelle A. Williams,Amy O’Callaghan,Elaine Dempsey,Raúl Cabrera‐Rubio,Mathilde Raverdeau,Fiona Crispie,Paul D. Cotter,Sinéad C. Corr
出处
期刊:Microorganisms [Multidisciplinary Digital Publishing Institute]
卷期号:10 (7): 1383-1383 被引量:20
标识
DOI:10.3390/microorganisms10071383
摘要

The use of probiotics such as Lactobacillus and Bifidobacterium spp. as a therapeutic against inflammatory bowel disease (IBD) is of significant interest. Lactobacillus salivarus strain UCC118TM is a commensal that has been shown to possess probiotic properties in vitro and anti-infective properties in vivo. However, the usefulness of UCC118 TM as a therapeutic against colitis remains unclear. This study investigates the probiotic potential of Lactobacillus salivarius, UCC118™ in a mouse model of colitis. DSS-induced colitis was coupled with pre-treatment or post-treatment with UCC118TM by daily oral gavage. In the pre-treatment model of colitis, UCC118TM reduced the severity of the disease in the early stages. Improvement in disease severity was coupled with an upregulation of tissue IL-10 levels and increased expression of macrophage M2 markers. This anti-inflammatory activity of UCC118TM was further confirmed in vitro, using a model of LPS-treated bone marrow-derived macrophages. Taken together, these results suggest that UCC118TM may promote the resolution of inflammation. This was supported in a mouse model of established DSS-induced colitis whereby UCC118TM treatment accelerated recovery, as evidenced by weight, stool, histological markers and the recovery of microbiome-associated dysbiosis with an increased abundance of beneficial commensal species. These results demonstrate the potential of Lactobacillus salivarius UCC118TM as a probiotic-based therapeutic strategy to promote health through the upregulation of anti-inflammatory IL-10 and protect against dysbiosis during IBD.
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