Cronobacter sakazakii induces necrotizing enterocolitis by regulating NLRP3 inflammasome expression via TLR4

Chen, Zhenhui; Zhang, Yiduo; Lin, Ruqin; Meng, Xiang‐Jin; Zhao, Wei; Shen, Wei; Fan, Huiying

doi:10.1099/jmm.0.001181

Cited by 27 publications

(25 citation statements)

References 33 publications

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“…Additionally, C. sakazakii induces NEC in which host cells present more abruptic (lysis) cell death characteristics than apoptosis (Chen et al . 2020); cellular aspects of this damage were demonstrated here with Hep2c and NCTC clone 929 cells, when treated with C292 filtrate. Cellular studies as well as morphological ones show that apoptosis is frequently observed af ter C. sakazakii and human cells interaction.…”

Section: Discussionmentioning

confidence: 60%

“…Clinical symptoms in infants are necrotizing enterocolitis (NEC), bacteraemia/septicaemia and meningitis (Forsythe 2018; Chen et al . 2020). These infections can be fatal, and even if the infant survives meningitis, they are likely to be neurologically damaged for life (Holý et al .…”

Section: Introductionmentioning

confidence: 99%

“…2019; Chen et al . 2020). The objective of this study was to evaluate and compare the cytotoxicity profile of a collection of five Cronobacter species isolated from foods and clinical specimens in Brazil in different cell lineages.…”

Section: Introductionmentioning

confidence: 99%

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Cytotoxicity profile of Cronobacter species isolated from food and clinical specimens in Brazil

Costa¹,

Siqueira²,

Guimarães³

et al. 2020

J Appl Microbiol

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Aims The objective of this study was to evaluate the cytotoxic activity of Cronobacter strains isolated from foods (n = 50) and clinical samples (n = 6) in Brazil and genotype selected strains (n = 18) using multi‐locus sequence typing (MLST) Methods and Results The cytotoxic activity of C. sakazakii (n = 29), C. dublinensis (n = 13), C. malonaticus (n = 6), C. turicensis (n = 6) and C. muytjensii (n = 2) was screened using Vero, RK13, Hep2c, NCTC clone 929 and BHK‐21 cell lines. Selected Cronobacter strains were assigned to C. sakazakii ST 21, C. turicensis ST 252, C. sakazakii ST 647, and three newly assigned STs: C. turicensis STs 738–740. The maximum death caused by non‐heat‐treated filtrates was 20·4, 86·2, 47·0 and 84·0%, in Vero, RK13, Hep2c and NCTC clone 929 cells, respectively. These were caused by C. sakazakii strains C291 and C292 (ST 494) which had been isolated during neonatal Cronobacter meningitis infection, and C110 (ST 395) isolated from flaxseed flour. Thermal treatment (100°C/20 min) significantly reduced the cytotoxicity activity in NCTC clone 929 and Vero cells (P ≤ 2 × 10−6), but not in RK13 (P = 0·12) and Hep2c (P = 0·85), indicating the cytotoxin(s) were probably proteinaceous. Electron microscopy revealed that cytotoxic compounds from C. sakazakii induced several cell death characteristics, including loss of cell–cell contact, microvilli reduction and cellular lysis. Autophagic vacuoles and mitochondrial damage were the most common ultrastructural features observed. Conclusions: It was concluded that Cronobacter strains, especially C. sakazakii, could produce heat‐labile cytotoxic compounds in cell filtrates. Significance and Impact of the Study This study providing insights into the pathogenesis of the Cronobacter genus. Cytotoxins were identified in excreted filtrates of C. sakazakii strains isolated from food and clinical specimens. The presence of Cronobacter strains that can produce cytotoxins in foods can be a potential threat to human health and highlight the need for high levels of hygiene.

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Section: Discussionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 99%

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Cytotoxicity profile of Cronobacter species isolated from food and clinical specimens in Brazil

Costa¹,

Siqueira²,

Guimarães³

et al. 2020

J Appl Microbiol

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“…NLRP3 inflammasome-mediated epithelial pyrotosis accelerates the development of atherosclerotic plaques and increases plaque size ( Wu et al., 2018 ; Zhang, Liu, et al., 2018 ). In certain diseases, the NLRP3 inflammasome mediated pyroptosis is associated with TLR4-mediated myeloid differentiation primary response protein 88/NF-κB including hepatic ischaemia/reperfusion injury ( El-Sisi et al., 2020 ) and necrotising enterocolitis ( Chen, Zhang, et al., 2020 ). TLR4-mediated myeloid differentiation primary response protein 88/NF-κB/NLRP3 inflammasome-induced pyroptosis is associated with the formation of gasdermin-D, a substrate of caspase-1 ( Chen, Zhang, et al., 2020 ; Liu, Yao, et al., 2020 ).…”

Section: Signalling Pathways Of Nlrp3 Inflammasome Activation In Cerebrovascular Diseasesmentioning

confidence: 99%

“…The role of the PI3K/AKT pathway in stroke is well-known. It regulates downstream anti-apoptotic molecules and plays a protective role in rats after ischaemic stroke Lu et al, 2019;Meng et al, 2020;Wei et al, 2020;Yang et al, 2020). However, PI3K/AKT has not been associated with the NLRP3 inflammasome in cerebrovascular diseases.…”

Section: The Signal Pathway That Alleviates Cerebrovascular Diseasesmentioning

confidence: 99%

The Role of NLRP3 Inflammasome in Cerebrovascular Diseases Pathology and Possible Therapeutic Targets

et al. 2021

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Cerebrovascular diseases are pathological conditions involving impaired blood flow in the brain, primarily including ischaemic stroke, intracranial haemorrhage, and subarachnoid haemorrhage. The nucleotide-binding and oligomerisation (NOD) domain-like receptor (NLR) family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome is a protein complex and a vital component of the immune system. Emerging evidence has indicated that the NLRP3 inflammasome plays an important role in cerebrovascular diseases. The function of the NLRP3 inflammasome in the pathogenesis of cerebrovascular diseases remains an interesting field of research. In this review, we first summarised the pathological mechanism of cerebrovascular diseases and the pathological mechanism of the NLRP3 inflammasome in aggravating atherosclerosis and cerebrovascular diseases. Second, we outlined signalling pathways through which the NLRP3 inflammasome participates in aggravating or mitigating cerebrovascular diseases. Reactive oxygen species (ROS)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ROS/thioredoxin-interacting protein (TXNIP) and purinergic receptor-7 (P2X7R) signalling pathways can activate the NLRP3 inflammasome; activation of the NLRP3 inflammasome can aggravate cerebrovascular diseases by mediating apoptosis and pyroptosis. Autophagy/mitochondrial autophagy, nuclear factor E2-related factor-2 (Nrf2), interferon (IFN)-β, sirtuin (SIRT), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) reportedly alleviate cerebrovascular diseases by inhibiting NLRP3 inflammasome activation. Finally, we explored specific inhibitors of the NLRP3 inflammasome based on the two-step activation of the NLRP3 inflammasome, which can be developed as new drugs to treat cerebrovascular diseases.

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Bacteriocins attenuate Listeria monocytogenes–induced intestinal barrier dysfunction and inflammatory response

Wang,

Du,

et al. 2024

Appl Microbiol Biotechnol

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Bacteriocins have the potential to effectively improve food-borne infections or gastrointestinal diseases and hold promise as viable alternatives to antibiotics. This study aimed to explore the antibacterial activity of three bacteriocins (nisin, enterocin Gr17, and plantaricin RX-8) and their ability to attenuate intestinal barrier dysfunction and inflammatory responses induced by Listeria monocytogenes, respectively. Bacteriocins have shown excellent antibacterial activity against L. monocytogenes without causing any cytotoxicity. Bacteriocins inhibited the adhesion and invasion of L. monocytogenes on Caco-2 cells, lactate dehydrogenase (LDH), trans-epithelial electrical resistance (TEER), and cell migration showed that bacteriocin improved the permeability of Caco-2 cells. These results were attributed to the promotion of tight junction proteins (TJP) assembly, specifically zonula occludens-1 (ZO-1), occludin, and claudin-1. Furthermore, bacteriocins could alleviate inflammation by inhibiting the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways and reducing the secretion of interleukin-6 (IL-6), interleukin-1 β (IL-1β) and tumor necrosis factor α (TNF-α). Among three bacteriocins, plantaricin RX-8 showed the best antibacterial activity against L. monocytogenes and the most pronounced protective effect on the intestinal barrier due to its unique structure. Based on our findings, we hypothesized that bacteriocins may inhibit the adhesion and invasion of L. monocytogenes by competing adhesion sites. Moreover, they may further enhance intestinal barrier function by inhibiting the expression of L. monocytogenes virulence factors, increasing the expression of TJP and decreasing the secretion of inflammatory factors. Therefore, bacteriocins will hopefully be an effective alternative to antibiotics, and this study provides valuable insights into food safety concerns. Key points • Bacteriocins show excellent antibacterial activity against L. monocytogenes • Bacteriocins improve intestinal barrier damage and inflammatory response • Plantaricin RX-8 has the best protective effect on Caco-2 cells damage Graphical Abstract

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Cronobacter sakazakii induces necrotizing enterocolitis by regulating NLRP3 inflammasome expression via TLR4

Cited by 27 publications

References 33 publications

Cytotoxicity profile of Cronobacter species isolated from food and clinical specimens in Brazil

Cytotoxicity profile of Cronobacter species isolated from food and clinical specimens in Brazil

The Role of NLRP3 Inflammasome in Cerebrovascular Diseases Pathology and Possible Therapeutic Targets

Bacteriocins attenuate Listeria monocytogenes–induced intestinal barrier dysfunction and inflammatory response

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