Probiotics VSL#3 protect against development of visceral pain in murine model of irritable bowel syndrome.
Probiotics VSL#3 protect against development of visceral pain in murine model of irritable bowel syndrome.
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DOI：
10.1371/journal.pone.0063893
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Fiorucci S
中科院分区：
文献类型：
--
作者：
Distrutti E;Cipriani S;Mencarelli A;Renga B;Fiorucci S
肠易激综合征（IBS）与炎症后和应激相关因素有关，这些因素导致内脏事件感知的变化。益生菌可能有效治疗IBS症状。在此，我们研究了生命早期给予VSL#3（一种8种益生菌菌株的混合物）是否可预防由新生儿母体分离（NMS）（一种IBS大鼠模型）驱动的内脏超敏反应的发生。雄性NMS幼仔从第3天至第60天经口给予安慰剂或VSLI #3，而正常、未分离大鼠用作对照。出生60天后，通过评估腹部退缩反射（评分0-4）来测量由结直肠扩张（CRD）引起的疼痛感觉。通过使用Agilent全大鼠基因组寡核苷酸微阵列平台评估结肠基因表达，并通过真实的时间PCR确认。与对照组大鼠相比，NMS大鼠表现出痛觉过敏和异常性疼痛。VSLI #3对CRD诱导的疼痛具有强效镇痛作用，且不改变结直肠顺应性。微阵列分析表明，NMS诱导参与疼痛传递和炎症的基因亚组（CCL 2、NOS 3、THP 1、NTRK 1、CCR 2、BDRKRB 1、IL-10、TNFRSF 1B、TRPV 4、CNR 1和OPRL 1）表达的稳健变化。TPH 1，色氨酸羟化酶1，IBS治疗中一种经验证的靶基因，通过NMS显著上调，该效应通过VSLI #3干预逆转。生命早期给予VSLI #3可降低IBS模型中的内脏疼痛感知，并重置介导疼痛和炎症的基因亚群的结肠表达。表达微阵列数据库的登录号为GSE 38942（http：www.ncbi.nlm.nih.gov/geo/query/acc.cgi? acc= GSE 38942）。
Irritable bowel syndrome (IBS) is linked to post-inflammatory and stress-correlated factors that cause changes in the perception of visceral events. Probiotic bacteria may be effective in treating IBS symptoms. Here, we have investigated whether early life administration of VSL#3, a mixture of 8 probiotic bacteria strains, protects against development of visceral hypersensitivity driven by neonatal maternal separation (NMS), a rat model of IBS. Male NMS pups were treated orally with placebo or VSL#3 from days 3 to 60, while normal, not separated rats were used as controls. After 60 days from birth, perception of painful sensation induced by colorectal distension (CRD) was measured by assessing the abdominal withdrawal reflex (score 0–4). The colonic gene expression was assessed by using the Agilent Whole Rat Genome Oligo Microarrays platform and confirmed by real time PCR. NMS rats exhibited both hyperalgesia and allodynia when compared to control rats. VSL#3 had a potent analgesic effect on CRD-induced pain without changing the colorectal compliance. The microarray analysis demonstrated that NMS induces a robust change in the expression of subsets of genes (CCL2, NOS3, THP1, NTRK1, CCR2, BDRKRB1, IL-10, TNFRSF1B, TRPV4, CNR1 and OPRL1) involved in pain transmission and inflammation. TPH1, tryptophan hydroxylase 1, a validated target gene in IBS treatment, was markedly upregulated by NMS and this effect was reversed by VSL#3 intervention. Early life administration of VSL#3 reduces visceral pain perception in a model of IBS and resets colonic expression of subsets of genes mediating pain and inflammation. Accession number of repository for expression microarray data is GSE38942 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE38942).
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影响因子：
3.7
作者：
Evrard B;Coudeyras S;Dosgilbert A;Charbonnel N;Alamé J;Tridon A;Forestier C
通讯作者：
Forestier C
影响因子：
29.4
作者：
Brown PM;Drossman DA;Wood AJ;Cline GA;Frazier KS;Jackson JI;Bronner J;Freiman J;Zambrowicz B;Sands A;Gershon MD
通讯作者：
Gershon MD
DOI：
10.1097/mpg.0b013e3181ca4d95
发表时间：
2010-07-01
影响因子：
2.9
作者：
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通讯作者：
Setty, Mala
影响因子：
29.4
作者：
Gionchetti, P;Rizzello, F;Campieri, M
通讯作者：
Campieri, M
影响因子：
9.3
作者：
Distrutti, Eleonora;Mencarelli, Andrea;Fiorucci, Stefano
通讯作者：
Fiorucci, Stefano