scholarly journals Toll-like receptor 4-mediated necroptosis in the development of necrotizing enterocolitis

2021 ◽  
Author(s):  
Tianjing Liu ◽  
Haifeng Zong ◽  
Xiaoyu Chen ◽  
Sihang Li ◽  
Ziyun Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Necrotizing Enterocolitis ◽  
Pathological Process ◽  
List Type ◽  
Toll Like Receptor ◽  
Barrier Dysfunction ◽  
Toll Like Receptor 4 ◽  
Inflammatory Infiltration ◽  
Neonatal Necrotizing Enterocolitis

Abstract Background Dramatic intestinal epithelial cell death leading to barrier dysfunction is one of the mechanism of neonatal necrotizing enterocolitis (NEC), in which Toll-like receptor 4 (TLR4) plays a pivotal role. This study explored the role of necroptosis, a drastic way of cell death in NEC. Methods The expression of necroptotic proteins was tested in NEC intestinal tissue and compared with controls. NEC was induced in neonatal wild-type mice and a necroptosis inhibitor was given to investigate whether NEC could be relieved. The general condition, macroscopic scoring, and histological evaluations were performed. The expression of tight junction proteins, inflammatory cytokines, and necroptosis-related proteins was measured, and barrier function was examined. Then, NEC was induced in TLR4-knockout pups to confirm the role of TLR4 in necroptosis. Results Necroptotic proteins were significantly upregulated in both NEC patient and animal models, together with the expression of TLR4. NEC could be relieved and inflammatory infiltration was decreased by necrostatin-1s. TLR4-knockout mice showed milder tissue degradation and less necroptosis after NEC induction. Conclusions Necroptosis is an essential pathological process of NEC. TLR4 may be one stimulator of necroptosis in NEC. Inhibiting the intestinal cell necroptosis might be a useful strategy in the treatment of NEC. Impact Necroptosis is a key pathological process in NEC, which appears to involve TLR4. Anti-necroptosis treatment is a promising strategy that could significantly relieve the symptoms of NEC.

scholarly journals Toll-like receptor 4–mediated lymphocyte influx induces neonatal necrotizing enterocolitis

2015 ◽  
Vol 126 (2) ◽  
pp. 495-508 ◽  
Author(s):  
Charlotte E. Egan ◽  
Chhinder P. Sodhi ◽  
Misty Good ◽  
Joyce Lin ◽  
Hongpeng Jia ◽  
...  
Keyword(s):  
Necrotizing Enterocolitis ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Neonatal Necrotizing Enterocolitis

Role of toll-like receptor 4 in the regulation of the cell death pathway and neuroinflammation

2019 ◽  
Vol 148 ◽  
pp. 79-90
Author(s):  
Yafei Li ◽  
Li Zhang ◽  
Jun Tang ◽  
Xiaoyan Yang ◽  
Jichong Huang ◽  
...  
Keyword(s):  
Cell Death ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Cell Death Pathway

Chelidonine Attenuates Sepsis-Induced Acute Lung Injury via Suppressing Toll-like Receptor 4/Myeloid Differentiation Factor 88/Nuclear Factor-॔B Signaling Pathway in Newborn Mice

2020 ◽  
Vol 19 (1) ◽  
pp. 120-126
Author(s):  
Ayinuerguli Adili ◽  
Adilijiang Kari ◽  
Chuanlong Song ◽  
Abulaiti Abuduhaer
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Nuclear Factor Kappa B ◽  
Myeloid Differentiation ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Inflammatory Infiltration ◽  
Newborn Mice ◽  
Myeloid Differentiation Factor

We have examined the mechanism underlying amelioration of sepsis-induced acute lung injury by chelidonine in newborn mice. To this end, a sepsis model was established using cecal ligation and puncture in newborn mice. The sepsis-induced acute lung injury was associated with an increased inflammatory infiltration and pulmonary congestion, as well as abnormal alveolar morphology. The lung injury-associated increased tumor necrosis factor-α and interleukin-1β in bronchoalveolar lavage fluid and lung, the markers of inflammatory infiltration and pulmonary congestion, diminished by chelidonine treatment. Chelidonine administration also downregulated protein levels of toll-like receptor 4, myeloid differentiation factor 88, phosphorylated nuclear factor-kappa B, and nuclear factor-kappa B that are elevated in response to sepsis. In conclusion, chelidonine provides a potential therapeutic strategy for newborn mice with acute lung injury.

scholarly journals Detrimental Role of Heat Shock Protein 60&70 and Toll-like Receptor 4 in Skeletal Muscle Ischaemia In Vitro

2013 ◽  
Vol 57 (5) ◽  
pp. 77S
Author(s):  
Ali Navi ◽  
Rebekah Yu ◽  
Xu Shi-Wen ◽  
Sidney Shaw ◽  
George Hamilton ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Muscle Ischaemia

Intestinal Lesions Containing Coronavirus-like Particles in Neonatal Necrotizing Enterocolitis: An Ultrastructural Analysis

PEDIATRICS ◽  
1984 ◽  
Vol 73 (2) ◽  
pp. 218-224
Author(s):  
S. Rousset ◽  
O. Moscovici ◽  
P. Lebon ◽  
J. P. Barbet ◽  
P. Helardot ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Small Intestine ◽  
Necrotizing Enterocolitis ◽  
Intestinal Mucosa ◽  
Light And Electron Microscopy ◽  
Anaerobic Bacteria ◽  
Intestinal Lesions ◽  
Maternity Hospitals ◽  
Neonatal Necrotizing Enterocolitis

Since the outbreaks of neonatal necrotizing enterocolitis occurring in maternity hospitals of Paris and suburbs in 1979-1980, it has been possible to examine by light and electron microscopy gut specimens from ten newborns with this illness. Coronavirus-like particles, enclosed in intracytoplasmic vesicles of damaged epithelial cells of the intestinal mucosa, were observed in the small intestine, appendix, and colon. The ultrastructural study, supported by bacteriologic findings, suggests the role of coronavirus-like particles in the appearance of the lesions. Secondary proliferation of mainly anaerobic bacteria, probably responsible for pneumatosis, may aggravate the disease.

Contrasting effects of the Toll-like receptor 4 in determining ovarian follicle endowment and fertility in female adult mice

Zygote ◽  
2021 ◽  
pp. 1-7
Author(s):  
Júlio Panzera Gonçalves ◽  
Breno Augusto Magalhães ◽  
Paulo Henrique Almeida Campos-Junior
Keyword(s):  
Ovarian Follicle ◽  
Cumulus Cells ◽  
Toll Like Receptor ◽  
Female Reproduction ◽  
Toll Like Receptor 4 ◽  
Genetic Ablation ◽  
Adult Mice ◽  
Cumulus Oocyte Complex ◽  
Estrous Cyclicity

Abstract Toll-like receptor 4 (TLR4) is best known for its role in bacteria-produced lipopolysaccharide recognition. Regarding female reproduction, TLR4 is expressed by murine cumulus cells and participates in ovulation and in cumulus–oocyte complex (COC) expansion, maternal–fetal interaction and preterm labour. Despite these facts, the role of TLR4 in ovarian physiology is not fully understood. Therefore, the aim of the present study was to investigate the effects of TLR4 genetic ablation on mice folliculogenesis and female fertility, through analysis of reproductive crosses, ovarian responsiveness and follicular quantification in TLR4−/− (n = 94) and C57BL/6 mice [wild type (WT), n = 102]. TLR4-deficient pairs showed a reduced number of pups per litter (P = 0.037) compared with WT. TLR4−/− mice presented more primordial, primary, secondary and antral follicles (P < 0.001), however there was no difference in estrous cyclicity (P > 0.05). A lower (P = 0.006) number of COC was recovered from TLR4−/− mice oviducts after superovulation, and in heterozygous pairs, TLR4−/− females also showed a reduction in the pregnancy rate and in the number of fetuses per uterus (P = 0.007) when compared with WT. Altogether, these data suggest that TLR4 plays a role in the regulation of murine folliculogenesis and in determining ovarian endowment. TLR4 deficiency may affect ovulation and pregnancy rates, potentially decreasing fertility, therefore the potential side effects of its blockade have to be carefully investigated.

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