Environmental Pollution, Год журнала: 2022, Номер 309, С. 119789 - 119789
Опубликована: Июль 14, 2022
Язык: Английский
Environmental Pollution, Год журнала: 2022, Номер 309, С. 119789 - 119789
Опубликована: Июль 14, 2022
Язык: Английский
Frontiers in Nutrition, Год журнала: 2025, Номер 11
Опубликована: Фев. 13, 2025
Lung injury can lead to specific neurocognitive dysfunction, and the “triple-hit” phenomenon may be key theoretical mechanism for progressive impairment of lung injury-related cognitive impairment. The brain communicate biologically through immune regulation pathway, hypoxic neural circuit, mitochondrial microbial influence, which is called “lung-brain axis.” gut microbiota a highly complex community microorganisms that reside in with via “gut-lung dysregulation migration pathogenic bacteria lung, directly or indirectly regulate response their metabolites, cause aggravate injury. interact “gut-brain influence function behavior pathway mechanisms, hypothalamic–pituitary–adrenal (HPA) axis regulation. Based on axis” axis,” combined mechanisms caused by injury, we proposed hypothesis. It states pathophysiological changes trigger series events such as disorder, inflammatory responses, changes, activate “lung-gut thus forming leads development deterioration This hypothesis provides more comprehensive framework studying understanding dysfunction context review proposes existence an interactive tandem network information exchange among gut, brain, referred “gut-lung-brain further explores potential multiple interactions We found there are many numerous factors interaction within impact functions related mediated hypothesis, direct translocation microbes modulation, vagal nerve activity, HPA regulation, others. As research deepens, based it discovered therapy significantly change pathogenesis process also relieve therapeutically modulate behavior. perspective new idea follow-up treatment microbiota.
Язык: Английский
Процитировано
2Molecular Brain, Год журнала: 2025, Номер 18(1)
Опубликована: Фев. 17, 2025
Abstract Cardiac arrest (CA) is one of the most common illnesses worldwide. Post-CA brain injury (PCABI) a major cause death and poor recovery in CA patients current treatments are not very effective. The microbiome-gut-brain axis has been found to significantly affect ischemia injury. Furthermore, ischemic stroke patients, short-chain fatty acids (SCFA), especially sodium butyrate (SB), have observed promote neuroprotective effects by modulating inflammatory response microglial polarization cortex. However, precise mechanism SB on CA-induced remains elusive. Therefore, this research study established an oxygen–glucose deprivation reoxygenation (OGD/R) model using BV-2 HT22 cells simulate cerebral ischemia/reperfusion vitro potassium chloride-induced mouse mimic vivo. data revealed that markedly improved neurological scores reduced neuronal apoptosis. Moreover, it M1 microglia neuroinflammation mice. In addition, increased intestinal integrity alleviated systemic inflammation. 16S rDNA sequencing analysis indicated intervention mitigated gut microbiota dysbiosis SCFA depletion. It was also mice’s OGD/R-exposed BV2 had substantially levels MyD88, phosphorylated NF-κB p65, TLR4 proteins, which were after treatment. summary, can protect against ischemia–reperfusion controlling inhibit inflammation via TLR4/MyD88/NF-κB pathway.
Язык: Английский
Процитировано
2Microbiome, Год журнала: 2022, Номер 10(1)
Опубликована: Дек. 1, 2022
Mounting experimental evidence has shown that the gut microbiota plays a significant role in pathogenesis of mastitis, and clinical investigations have found occurrence mastitis is correlated with ruminal dysbiosis. However, underlying mechanism by which participates development remains unknown.In present study, we cows had marked systemic inflammation, was associated dysbiosis, especially enriched Proteobacteria rumen. Ruminal transplantation from (M-RMT) to mice induced symptoms recipient along increased mammary proinflammatory signature activation TLR4-cGAS-STING-NF-κB/NLRP3 pathways. M-RMT also mucosal inflammation impaired intestinal barrier integrity, leading endotoxemia inflammation. Moreover, showed mirrored disruption mice, as evidenced similar bacterial functions, were most parameters serum lipopolysaccharide (LPS) levels mice. Recurrent low-grade LPS treatment dysbiosis-induced caused severe Furthermore, dysbiosis-derived reduced host alkaline phosphatase activity activating neuraminidase (Neu), facilitates exposure E. coli-induced Conversely, calf or Neu inhibitor zanamivir alleviated mice.Our results suggest can cause aggravate pathogen-induced impairing anti-inflammatory enzymes, implies regulating prevent potential strategy for intervention. Video Abstract.
Язык: Английский
Процитировано
60The Science of The Total Environment, Год журнала: 2022, Номер 840, С. 156668 - 156668
Опубликована: Июнь 13, 2022
Язык: Английский
Процитировано
54Environmental Pollution, Год журнала: 2022, Номер 309, С. 119789 - 119789
Опубликована: Июль 14, 2022
Язык: Английский
Процитировано
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