Lactobacillus rhamnosus modulates murine neonatal gut microbiota and inflammation caused by pathogenic Escherichia coli.

IF 4 2区 生物学 Q2 MICROBIOLOGY BMC Microbiology Pub Date : 2024-11-06 DOI:10.1186/s12866-024-03598-6
Hao Xuan, Shahid Umar, Cuncong Zhong, Wei Yu, Ishfaq Ahmed, Joshua L Wheatley, Venkatesh Sampath, Susana Chavez-Bueno
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引用次数: 0

Abstract

Background: Pathogenic Escherichia coli strains produce neonatal septicemia after colonizing the neonatal gut. While the probiotic Lactobacillus rhamnosus GG (LGG) effectively reduces neonatal sepsis, LGG's effects on the neonatal intestinal microbiota alterations and inflammation triggered by E. coli are incompletely understood. We hypothesized that LGG significantly modulates the specific neonatal gut microbial populations changes and the inflammatory response elicited by the enteral introduction of septicemia-producing E. coli. To test this hypothesis, newborn rats were pretreated orally with LGG or placebo prior to infection with the neonatal E. coli septicemia clinical isolate SCB34. Amplicon 16S rRNA gene sequencing was performed on intestinal samples. Intestinal injury and expression of inflammatory mediators and apoptosis were determined.

Results: Alpha diversity of gut microbiota was greater in SCB34-infected pups in comparison to sham-infected pups, these changes were not modified by LGG pretreatment. Beta diversity analyses also showed differences between SCB34-infected vs. uninfected pups. LGG pretreatment before SCB34 infection did not result in significant beta diversity changes compared to placebo. Moreover, individual genera and species abundance analyses by linear discriminant analysis effect size (LEfSe) showed significant changes in Gram-negative, Gram-positive, and anaerobic populations resulting from LGG pretreatment and SCB34 infection. LGG significantly suppressed the expression of inflammatory cytokines but did not attenuate SCB34-induced apoptosis or histologic injury.

Conclusions: LGG modulates clinically significant microbiota features and inflammation triggered by pathogenic E. coli intestinal infection shortly after birth. This new knowledge can potentially be harnessed to design novel interventions against gut-derived neonatal sepsis.

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鼠李糖乳杆菌可调节小鼠新生儿肠道微生物群和致病性大肠杆菌引起的炎症。
背景:致病性大肠杆菌菌株在新生儿肠道定植后会导致新生儿败血症。虽然益生菌鼠李糖乳杆菌 GG(LGG)能有效减少新生儿败血症,但人们对 LGG 对新生儿肠道微生物区系改变和大肠杆菌引发的炎症的影响还不完全了解。我们假设 LGG 能显著调节特定的新生儿肠道微生物种群变化以及肠道引入产败血病大肠杆菌引起的炎症反应。为了验证这一假设,在新生大鼠感染新生大肠杆菌败血症临床分离物 SCB34 之前,先口服 LGG 或安慰剂。对肠道样本进行了扩增 16S rRNA 基因测序。结果表明:肠道微生物群的α多样性较高:结果:与假感染幼崽相比,SCB34 感染幼崽肠道微生物群的α多样性更高,LGG 预处理不会改变这些变化。贝塔多样性分析也显示出 SCB34 感染幼鼠与未感染幼鼠之间的差异。与安慰剂相比,SCB34感染前的LGG预处理不会导致β多样性发生显著变化。此外,通过线性判别分析效应大小(LEfSe)进行的单个菌属和菌种丰度分析表明,LGG 预处理和 SCB34 感染会导致革兰氏阴性菌、革兰氏阳性菌和厌氧菌群发生显著变化。LGG 能明显抑制炎症细胞因子的表达,但不能减轻 SCB34 诱导的细胞凋亡或组织损伤:结论:LGG 可调节出生后不久由致病性大肠杆菌肠道感染引发的具有临床意义的微生物群特征和炎症。这一新知识可用于设计新型干预措施,预防新生儿肠源性败血症。
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来源期刊
BMC Microbiology
BMC Microbiology 生物-微生物学
CiteScore
7.20
自引率
0.00%
发文量
280
审稿时长
3 months
期刊介绍: BMC Microbiology is an open access, peer-reviewed journal that considers articles on analytical and functional studies of prokaryotic and eukaryotic microorganisms, viruses and small parasites, as well as host and therapeutic responses to them and their interaction with the environment.
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