Effects of Probiotics on Preterm Infant Gut Microbiota Across Populations: A Systematic Review and Meta-Analysis.

Microbiota in early life is closely associated with the health of infants, especially premature ones. Probiotics are important drivers of gut microbiota development in preterm infants; however, there is no consensus regarding the characteristics of specific microbiota in preterm infants receiving probiotics. In this study, we performed a meta-analysis of 5 microbiome data sets (1816 stool samples from 706 preterm infants) to compare the gut microbiota of preterm infants exposed to probiotics with that of preterm infants not exposed to probiotics across populations. Despite study-specific variations, we found consistent differences in gut microbial composition and predicted functional pathways between the control and probiotic groups across different cohorts of preterm infants. The enrichment of Acinetobacter, Bifidobacterium, and Lactobacillus spp and the depletion of the potentially pathogenic bacteria Finegoldia, Veillonella, and Klebsiella spp. were the most consistent changes in the gut microbiota of preterm infants supplemented with probiotics. Probiotics drove microbiome transition into multiple preterm gut community types, and notably, preterm gut community type 3 had the highest α-diversity, with enrichment of Bifidobacterium and Bacteroides spp. At the functional level, the major predicted microbial pathways involved in peptidoglycan biosynthesis consistently increased in preterm infants supplemented with probiotics; in contrast, the crucial pathways associated with heme biosynthesis consistently decreased. Interestingly, Bifidobacterium sp. rather than Lactobacillus sp. gradually became dominant in gut microbiota of preterm infants using mixed probiotics, although both probiotic strains were administered at the same dosage. Taken together, our meta-analysis suggests that probiotics contribute to reshaping the microbial ecosystem of preterm infants at both the taxonomic and functional levels of the bacterial community. More standardized and relevant studies may contribute to better understanding the crosstalk among probiotics, the gut microbiota, and subsequent disease risk, which could help to give timely nutritional feeding guidance to preterm infants. This systematic review and meta-analysis was registered at PROSPERO (https://www.crd.york.ac.uk/PROSPERO/) as CRD42023447901.

Dietary Patterns and Gut Microbiota: The Crucial Actors in Inflammatory Bowel Disease.

It is widely believed that diet and the gut microbiota are strongly related to the occurrence and progression of inflammatory bowel disease (IBD), but the effects of the interaction between dietary patterns and the gut microbiota on IBD have not been well elucidated. In this article, we aim to explore the complex relation between dietary patterns, gut microbiota, and IBD. We first comprehensively summarized the dietary patterns associated with IBD and found that dietary patterns can modulate the occurrence and progression of IBD through various signaling pathways, including mammalian target of rapamycin (mTOR), mitogen-activated protein kinases (MAPKs), signal transducer and activator of transcription 3 (STAT3), and NF-κB. Besides, the gut microbiota performs a vital role in the progression of IBD, which can affect the expression of IBD susceptibility genes, such as dual oxidase 2 (DUOX2) and APOA-1 , the intestinal barrier (in particular, the expression of tight junction proteins), immune function (especially the homeostasis between effector and regulatory T cells) and the physiological metabolism, in particular, SCFAs, bile acids (BAs), and tryptophan metabolism. Finally, we reviewed the current knowledge on the interaction between dietary patterns and the gut microbiota in IBD and found that dietary patterns modulate the onset and progression of IBD, which is partly attributed to the regulation of the gut microbiota (especially SCFAs-producing bacteria and Escherichia coli). Faecalibacteria as "microbiomarkers" of IBD could be used as a target for dietary interventions to alleviate IBD. A comprehensive understanding of the interplay between dietary intake, gut microbiota, and IBD will facilitate the development of personalized dietary strategies based on the regulation of the gut microbiota in IBD and expedite the era of precision nutritional interventions for IBD.

Eriodictyol alleviates lipopolysaccharide-triggered oxidative stress and synaptic dysfunctions in BV-2 microglial cells and mouse brain.

Oxidative stress takes part in the development of the neurodegenerative disease. Eriodictyol, a flavonoid, commonly presents in citrus fruits, which was well-known for its various bioactivities. The purpose of this study was to investigate the neuroprotective effects of eriodictyol on lipopolysaccharide (LPS)-induced neuroinflammation, oxidative stress, synaptic dysfunctions, and the potential mechanisms involved. We found that eriodictyol explicitly restored LPS-triggered the decrease of cell viability and the mitochondrial potential as well as inflammation responses via mitogen-activated protein kinases (MAPKs) and nuclear factor κB (NF-κB) pathways regulated by reactive oxygen species (ROS). Besides, eriodictyol alleviated LPS-induced oxidative stress via NF-E2-Related factor2/Kelch-like ECH-associated protein 1 (Nrf2/Keap1) pathway in vivo and in vitro. Furthermore, eriodictyol reduced LPS-elicited synaptic dysfunctions via increasing the expression of silent information regulator 1 (Sirt1). Overall, eriodictyol protects LPS-triggered oxidative stress, neuroinflammation, and synaptic dysfunctions partially through MAPKs, NF-κB mediated by ROS, Sirt1, and Nrf2/Keap1 signal pathways, which further supports that eriodictyol is a potentially nutritional preventive strategy for oxidative stress-related neurodegenerative diseases.

Eriodictyol Attenuates LPS-Induced Neuroinflammation, Amyloidogenesis, and Cognitive Impairments via the Inhibition of NF-κB in Male C57BL/6J Mice and BV2 Microglial Cells.

Eriodictyol, a natural flavonoid mainly distributed in citrus fruits and peanut, has been well-documented with possession of excellent anti-inflammatory, antioxidant, and anticancer bioactivities. This work focus on the protective effects of eriodictyol on LPS-induced neuroinflammation, amyloidogenesis, cognitive impairment, and the potential mechanisms involved. Behavioral tests and histological examinations showed that eriodictyol significantly prevented the memory and neuronal damage triggered by LPS. Consistently, eriodictyol (100 mg/kg) reduced the formation of Aß1-42 by 28.37 ± 16.71 pg/mL compared to the LPS group. In addition, high dose eriodictyol (100 mg/kg) also equilibrated the cholinergic system via suppressing AChE activity (0.1996 ± 0.0831 U/mgprot) and elevating ChAT activity (41.81 ± 24.72 U/g) as well as ACh level (5.093 ± 3.531 µg/mgprot) compared to the LPS group. Western blot results indicated that compared to the LPS group, eriodictyol suppressed LPS-induced glial overactivation (84.29% ± 27.21%) and regulated inflammatory mediators and cytokines by inhibiting the NF-κB and MAPK pathways. These results indicated that eriodictyol alleviated amyloidogenesis and memory impairment triggered by LPS via inhibiting TLR4, MAPKs, and PI3K/Akt, and activating Sirt1 pathways and thus blocking downstream translocation of NF-κB, which offers a potential nutritional preventive strategy for neuroinflammation diseases such as Alzheimer's disease (AD).

1,3-Dichloro-2-propanol evokes inflammation and apoptosis in BV-2 microglia via MAPKs and NF-κB signaling pathways mediated by reactive oxygen species.

1,3-dichloro-2-propanol (1,3-DCP) is a widely concerned food processing contaminant which has been investigated for decades. While the neurotoxicity of 1,3-DCP and related mechanisms are still elusive. Herein, the effect of 1,3-DCP on neurotoxicity was investigated using BV-2 microglia cells. 1,3-DCP significantly decreased cell viability from 78.6% to 59.2% at doses between 2 and 20 mM. AO/EB and JC-1 staining indicated that 1,3-DCP induced apoptosis by means of the decrease of mitochondrial membrane potential. Meanwhile, western blot showed that 1,3-DCP stimulated inflammation of BV-2 cells through phosphorylation of MAPKs and activation of NF-κB pathways mediated by reactive oxygen species (ROS). Furthermore, the degree of inflammation and apoptosis has eased through MAPKs and NF-κB pathways with cells pretreated by N-acetylcysteine (NAC). Overall, these results presented here suggested that 1,3-DCP has neurotoxic effect on BV-2 microglia mainly via MAPKs and NF-κB pathways mediated by ROS.