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Enterococcus faecalis-derived lactate mediated suppression of NF-κB and ERK pathways in macrophages to promote polymicrobial wound infection

ABSTRACT: Enterococcus faecalis-derived lactate mediated suppression of NF-κB and ERK pathways in macrophages to promote polymicrobial wound infection

PROVIDER: PRJNA780609 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16953215_1.fastq.gz	Fastqsanger.gz
	SRR16953215_2.fastq.gz	Fastqsanger.gz
	SRR16953216_1.fastq.gz	Fastqsanger.gz
	SRR16953216_2.fastq.gz	Fastqsanger.gz
	SRR16953217_1.fastq.gz	Fastqsanger.gz

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Enterococcus faecalis-derived lactate mediated suppression of NF-κB and ERK pathways in macrophages to promote polymicrobial wound infection

Project description:Enterococcus faecalis, a member of the human gastrointestinal microbiota, is a Gram-positive, opportunistic pathogen associated with hospital-acquired wound, bloodstream, and urinary tract infections. E. faecalis can suppress or evade immune-mediated clearance by macrophages to promote persistent infection, although the exact mechanisms and bacterial factor(s) involved are not well-defined. In this study, we examined E. faecalis factor(s) involved in suppressing macrophage activation, as well the macrophage pathways modulated by E. faecalis to suppress activation. We observed that E. faecalis prevents ERK and p65 phosphorylation and reduces MyD88 expression leading to a reduction in NF-κB activity. We identified E. faecalis lactate dehydrogenase, which is important for lactic acid production by E. faecalis, to be necessary for macrophage suppression and demonstrated that E. faecalis lactate dehydrogenase-mediated immune suppression promotes E. coli survival during polymicrobial wound infection. Taken together, these results suggest that that E. faecalis-derived lactic acid is involved in macrophage subversion and may help to promote the virulence of co-infecting bacteria.

2024-11-01 | GSE188916 | GEO

L-Chiral Hydrogel Accelerates Wound Healing via Lactate-Mediated RNF123 K57 Lactylation

Project description:Chronic wounds, characterized by delayed healing and persistent inflammation, represent a major clinical burden with limited effective therapies. Inspired by the stereoselective interactions in biological systems, we developed an L-chiral hydrogel composed of self-assembled helical nanofibers from L-histidine derivatives, which preferentially enriches lactate to promote wound repair. Compared to D-chiral and racemic hydrogels, the L-chiral hydrogel significantly accelerated wound closure in rat models, achieving nearly 90% healing by day 14 and reducing healing time to 16-17 days. Transcriptomic and metabolomic analyses revealed enhanced wound response pathways and elevated lactate levels in the L-chiral group. Mechanistically, enriched lactate induced K57 lactylation of RNF123, mediated by AARS1, altering RNF123 conformation and weakening its binding to UBAC1. This modification enhanced ubiquitination and processing of NF-κB p105 into p50, inhibiting the NF-κB pathway and promoting angiogenesis via enhanced endothelial cell migration, tube formation, and sprouting. Rescue experiments with lactate inhibitor Oxamate and exogenous lactate confirmed the lactate-dependent mechanism. This study not only demonstrates a drug-free chiral biomaterial for efficient wound healing but also unveils the molecular role of lactate-mediated lactylation in mechanoregulating inflammation and vascularization, offering new insights for regenerative medicine.

2025-10-17 | GSE308113 | GEO

Cold Atmospheric Plasma Jet Activated Medium Promotes Wound Healing through CK2-mediated ERK and AKT signaling pathways

Project description:In this study, we aimed to explore the molecular mechanisms of wound healing affected by CAPJ using the parallel MS-based proteome and phosphoproteome. The keratinocyte, HaCaT, was used as cell mode to treat CAPJ indirectly by employing plasma activated medium (PAM) which was culture medium explored to He/Ar-generated CAPJ following previous study’s procedures. The datasets were integrated and systematically analyzed to dissect molecular and signaling pathway alternation in keratinocytes during PAM intervention. The results showed that PAM treatment significantly activated ERK, CK2 and AKT kinases and the phosphorylation-dependent signaling pathways of PI3K/AKT/mTOR and MEK/ERK were multiaxially disturbed, in which CK2 was suggested to play a coordination role between these two pathways. Collectively, this knowledge allows for a better understanding of how CAPJ regulates keratinocyte signaling during wound closure, and provides new insights into the development of clinical skin wound treatments.

2025-02-22 | PXD050065 | JPOST Repository

Autologous microgratf accelerates endogenous wound healing response through ERK-induced cell migration.

Project description:Defective fibroblast migration cause delayed wound healing (WH) and chronic skin lesions. Autologous micrograft (AMG) therapies have recently emerged as a new effective treatment able to improve wound healing capacity. However, the molecular mechanisms connecting their beneficial outcomes with the wound healing process are still unrevealed. Here, we show that AMG modulates primary fibroblast migration and accelerates skin re-epithelialization without affecting cell proliferation. We demonstrate that AMG is enriched in a pool of WH-associated growth factors that may provide the initiation signal for faster endogenous wound healing response. This, in turn leads to increased cell migration rate by elevating activity of ERK and subsequent activation of matrix metalloproteinase expression and their extracellular enzymatic activity. Moreover, AMG-treated wounds showed increased granulation tissue formation and organized collagen content. Overall, we shed light on AMG molecular mechanism supporting its potential to trigger highly improved wound healing process.

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Project description:Wound healing is associated with high rates of cell replication and lactate accumulation even under normoxic and hyperoxic conditions. Lactate accounts for various effects in tissue regeneration, such as collagen synthesis, angiogenesis, modulation of cytokine patterns and as recently shown for stem cell homing. Its influence on genes involved in cell replication has not been shown yet. Therefore, the effect of lactate considering genes involved in different cellular processes was investigated. Human umbilical vein endothelial cells (HUVEC) were cultured and incubated with lactate for different periods of time. Gene expression analysis was performed using custom-designed oligonucleotide microarrays. Keywords: Human gene expression study Reference design with Cy3 labeled uniRNA and Cy5 labeled sample RNA.

2010-05-15 | E-GEOD-11458 | biostudies-arrayexpress

FGF19 facilitates colorectal cancer metastasis through FGFR4-ERK-NF-κB signaling pathway

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L-Chiral Hydrogel Accelerates Wound Healing via Lactate-Mediated RNF123 K57 Lactylation

Project description:L-Chiral Hydrogel Accelerates Wound Healing via Lactate-Mediated RNF123 K57 Lactylation

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Autologous microgratf accelerates endogenous wound healing response through ERK-induced cell migration.

Project description:Autologous microgratf accelerates endogenous wound healing response through ERK-induced cell migration.

| PRJNA509935 | ENA

Lactate modulates gene expression in human mesenchymal stem cells

2010-05-16 | GSE11458 | GEO

Polymicrobial sepsis-induced Myocardial Depression Transcriptional Profile

Project description:To describe the transcriptional changes associated with polymicrobial-sepsis induced myocardial depression in wild type and iNOS deficient mice. Keywords: myocardium, contractility, differential gene expression, nitric oxide synthase, infection We compared the transcriptional profile of C57/BL6 WT mice and congenic B6 129P2-Nos2tm1Lau/J mice after 48 hrs of polymicrobial sepsis induced by caecal ligation and perforation. 48 hours after surgery, mice were anaesthetised (intraperitoneal 100 mg/kg ketamine and 10 mg/kg xylazine). The right common carotid artery was cannulated (Millar Mikro-Tip pressure transducing catheter: 1.4F sensor, 2F catheter; Houston TX). Pressure tracings from the aorta and left ventricle were recorded (SonoLAB software; Sonometrics Corp., London Ontario Canada) and analysed using Cardiosoft and Origin 6.0 (Sonometrics Corp., and Microcal Software, Northampton MA). The heart was removed, emptied of blood, and snap frozen.

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