Lactobacillus acidophilus KLDS 1.0738 inhibits TLR4/NF‐κB inflammatory pathway in β‐lactoglobulin‐induced macrophages via modulating miR‐146a

嗜酸乳杆菌 TLR4型 炎症 巨噬细胞 NF-κB 信号转导 过敏 受体 细胞因子 免疫学 化学 生物 微生物学 医学 体外 细胞生物学 益生菌 细菌 生物化学 遗传学
作者
Aili Li,Jiajie Yang,Chao Zhang,Houyu Chi,Congwei Zhang,Tongtong Li,Jingjing Zhang,Peng Du
出处
期刊:Journal of Food Biochemistry [Wiley]
卷期号:45 (10): e13662-e13662 被引量:15
标识
DOI:10.1111/jfbc.13662
摘要

Our previous study has confirmed that Lactobacillus acidophilus KLDS 1.0738 (La KLDS 1.0738) could alleviate β-lactoglobulin (β-Lg)-induced allergic inflammation. This study further explored its molecular regulation mechanism through an in vitro macrophage model. β-Lg-induced macrophages were treated with strains of viable or non-viable L. acidophilus and Toll-like receptor 4 (TLR4) inhibitor or miR-146a inhibitor. Our results revealed that β-Lg stimulation led to the increased expression of TLR4/NF-κB signal pathway in macrophages. Similar to TLR4 inhibitor treatment, La KLDS 1.0738 interventions significantly reduced the allergic inflammation by inhibition of TLR4 pathway, which was superior to the commercial L. acidophilus GMNL-185 strains (La GMNL-185) or the control, especially in living L. acidophilus-treated group. Furthermore, La KLDS 1.0738 strains could remarkably reduce transduction of TLR4 and inflammatory cytokine production, which was closely associated with up-regulation of miR-146a levels. MiR-146a inhibitor attenuated the alleviative effect of La KLDS 1.0738, indicating miR-146a might be a crucial mediator of L. acidophilus strains to reduce β-Lg-induced inflammation in macrophages through TLR4 pathway. In conclusion, these observations highlighted that probiotics might regulate host miRNA levels to down-regulate TLR4/NF-κB-dependent inflammation. PRACTICAL APPLICATIONS: Cow's milk allergy (CMA) is one of the most common diseases of food allergy, which has a high prevalence in infants and young children. La KLDS 1.0738 has been shown to be effective in alleviating β-Lg-induced allergic inflammation. Our study further found that treatment with La KLDS 1.0738 could suppress the TLR4/NF-κB signaling pathway via modulating miR-146a expression, thereby reducing the overexpression of downstream inflammatory factors. This study not only elucidates the specific pathway of La KLDS 1.0738 to relieve allergic inflammation, but also provides a new insight into the molecular mechanism for the remission and treatment of CMA by probiotics.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
小丸子发布了新的文献求助10
刚刚
逆时针完成签到,获得积分10
1秒前
1秒前
小刘不牛完成签到,获得积分10
1秒前
科研通AI2S应助王晓采纳,获得10
1秒前
1176517761完成签到,获得积分20
2秒前
lulu1234完成签到,获得积分10
2秒前
wisdom完成签到,获得积分10
3秒前
3秒前
英俊的铭应助橙橙妈妈采纳,获得10
3秒前
3秒前
SciGPT应助淡淡的安双采纳,获得10
3秒前
春锅锅完成签到,获得积分10
3秒前
陙兂完成签到,获得积分10
4秒前
5秒前
5秒前
5秒前
胡东东发布了新的文献求助10
5秒前
yyyy完成签到,获得积分10
5秒前
5秒前
5秒前
君洛宇发布了新的文献求助10
6秒前
爆米花应助阔达的傲MUMU采纳,获得10
6秒前
胡思发布了新的文献求助10
6秒前
6秒前
酒洲完成签到,获得积分10
6秒前
小十七果发布了新的文献求助10
7秒前
牧愚完成签到,获得积分10
7秒前
Lucas应助yueoho采纳,获得10
7秒前
7秒前
六六发布了新的文献求助10
7秒前
科研通AI6.4应助0011采纳,获得10
8秒前
8秒前
隐形曼青应助外向念之采纳,获得10
9秒前
xie完成签到,获得积分10
9秒前
stepwise发布了新的文献求助10
9秒前
9秒前
11完成签到,获得积分10
9秒前
脑洞疼应助FeMoco采纳,获得10
9秒前
花怂怂完成签到 ,获得积分10
10秒前
高分求助中
GL 2 A method for assessing the in-place cleanability of food processing equipment, Fourth Edition, December 2023 3000
Annie Ernaux: De la perte au corps glorieux 600
Writing Systems 500
类器官构建与应用:从基础到前沿 500
Electric Vehicle Powertrains Design Fundamentals, Components, and Applications 400
Handbook on Planning and Climate Change Adaptation 400
Optical Coating Design with the Essential Macleod 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6809063
求助须知:如何正确求助?哪些是违规求助? 8525500
关于积分的说明 18148353
捐赠科研通 6133753
什么是DOI,文献DOI怎么找? 3029040
邀请新用户注册赠送积分活动 2005616
关于科研通互助平台的介绍 2003139