Posttreatment With LYRM03 Protects Rats From Acute Lung Inflammation Induced by Lipopolysaccharide via Suppressing the NF-κB/MyD88/TLR4 Axis

Jiang, Qinghe; Wang, Shujuan; Shi, Yan

doi:10.1016/j.jss.2019.05.036

Cited by 7 publications

(4 citation statements)

References 11 publications

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“…Previous studies have shown that NF-κB and inhibitors of κB (IκB) combine and exist in the cytoplasm in an inactive form under normal physiological circumstances. The data showed that HPI in E. coli could reduce the content of IκB-α, which is similar to previous studies (Jiang et al 2019;Lan et al 2020). However, the overexpression of Ub can promote the degradation of IκB-α.…”

Section: Discussionsupporting

confidence: 91%

WITHDRAWN: Ubiquitin promotes Escherichia coli HPI-induced duodenitis through the TLR4/Myd88/NF-κB pathway

Zhao

Yang

Gao

et al. 2023

Preprint

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The high-pathogenicity island (HPI), carried by Yersinia pestis, is an essential pathogenic component of the virulence distributed in Escherichia coli (E. coli). As an NF-κB pathway activator, Ubiquitin (Ub) is crucial in the inflammatory response. However, the molecular mechanismsof Ub in the TLR4/Myd88/NF-κB signaling pathway induced by HPI in E. coliis still unclear. In our experiment, Ub was overexpressed usingsmall intestinal epithelial cells (in vitro), and BALB/c mouse models (in vivo) infected with E. coli HPI and analysed by using qPCR, ELISA, immunofluorescence, immunohistochemistry, and H&E staining assays. We demonstrated that E. coli HPI can promote the expression of TLR4, NF-κB, and Ub in. IPEC-J2 cells. Immunofluorescence and Immunohistochemistry analysis revealed that TLR4 and NF-κB key factor in the E. coli HPI group were expressed, and the NF-κB p65 protein translocated to the nucleus. Further research showed that the mRNA expression levels of TLR4, MyD88, NF-κB, IL-1β, and TNF-α were significantly increased in the Ub overexpression group and BALB/c mice group. H&E staining assay showed that Ub overexpression with IPEC-J2 cells have thecharacteristics of elongated, rounded, fragmented, duodenal villi diminished, and the surface was covered with many sloughed necrotic cells, indicating that exacerbating cell damage and duodenitis. Taken together, this study suggested that E. coliHPI can activate NF-κB via increasing the expression of Ub, andUb can exacerbate E. coli HPI-induced duodenitis through the TLR4/MyD88/NF-κB signaling pathway.

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Section: Discussionsupporting

confidence: 91%

WITHDRAWN: Ubiquitin promotes Escherichia coli HPI-induced duodenitis through the TLR4/Myd88/NF-κB pathway

Zhao

Yang

Gao

et al. 2023

Preprint

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“…Inflammation and apoptosis have been reported to play key roles in acute lung injury, which is often characterized by leukocyte infiltration, principally neutrophils and macrophages, in the lungs [ 21 , 22 ]. Accumulating evidence suggests that several pathological changes occur in the lungs after LPS treatment, including inflammation, oxidative stress, and apoptosis, which is a well-known experimental model to assess the effects of drugs on acute lung injury [ 23 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine ameliorates lipopolysaccharide-induced acute lung injury by inhibiting the PI3K/Akt/FoxO1 signaling pathway

Cui

Zhang

2021

J Anesth

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Purpose Dexmedetomidine (DEX) has been associated with inflammation, oxidative stress, and apoptosis, but its effects on lipopolysaccharide (LPS)-induced lung injury remain uncertain. The present study explored the effects of DEX on LPS-induced lung injury and studied the possible molecular mechanisms by testing the effects of the phosphoinositide-3 kinase (PI3K) inhibitor LY294002 and BEZ235. Methods Seventy C57BL/6 mice were randomly divided into the control, LPS, LPS + DEX, LPS + LY294002, LPS + BEZ235, LPS + DEX + LY294002, and LPS + DEX + BEZ235groups. Lung samples were collected 48 h after LPS treatment. Results DEX significantly inhibited LPS-induced increases in the lung weight/body weight ratio and lung wet/dry weight ratio, decreased inflammatory cell infiltration, and decreased the production of proinflammatory factors, such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α)in the lungs. DEX also markedly attenuated the increases in malondialdehyde 5 (MDA 5) and inositol-dependent enzyme a (IRE-a), attenuated the decrease in superoxide dismutase 1(SOD-1), reversed the low expression of B-cell lymphoma-2 (Bcl-2), and the high expressions of Bax and Caspase-3. DEX also decreased the expression of phosphorylated PI3K and phosphorylated Akt and increased the expression of phosphorylated forkhead box-O transcription factor 1 (FoxO1). More interestingly, LY294002 or BEZ235 pretreatment significantly abolished the inhibitory effects of DEX on LPS-induced lung inflammation, oxidative stress, and apoptosis. Conclusions These data suggest that DEX ameliorates LPS-induced acute lung injury partly through the PI3K/Akt/FoxO1 signaling pathway.

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“…MyD88 is an important junction protein for TLR4 to transmit signals, and is one of the downstream signal proteins of TLR4 signaling pathway. The death domain of MyD88 binds to the death domain of interleukin receptor-related kinase (IRAK), resulting in the phosphorylation of IRAK itself, resulting in the activation of NF-κB [ 25 ]. The activation of NF-κB is involved in many processes such as inflammatory response, oxidative stress and apoptosis [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

The Preventive Effects of Lactobacillus casei on Acute Lung Injury Induced by Lipopolysaccharide

Zhao

Mao

et al. 2021

Indian J Microbiol

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Lactobacillus has been reported to inhibit acute lung injury (ALI). However, the molecular mechanism of Lactobacillus casei ( L. casei ) in preventing ALI has not been identified, so we investigated whether L. casei pretreatment could inhibit the activation of TLR4/MyD88/NF-κB signaling pathway following ALI. ALI model was established by intraperitoneal injection of 2 mg/kg lipopolysaccharide (LPS) to female BALB/c mice. In L. casei LC2W group, mice were intragastrically administrated L. casei LC2W for a week, before the ALI modeling. The serum of normal BALB/c mice after intragastric administration of L. casei LC2W was used for in vitro cell assays. The serum was pre-incubated with mouse macrophage cell line (RAW264.7) and human lung cell line (HLF-A), then LPS was added to co-incubate. Compared with ALI model group, L. casei LC2W pretreatment significantly reduced lung pathological damage, the number of neutrophils and total cells in bronchoalveolar lavage fluid. Besides, L. casei LC2W pretreatment could significantly reverse the abnormal expression of ICAM-1, IL-6, TNF-α and IL-10 in lung tissue and serum, plus, L. casei LC2W significantly reduced the phosphorylation levels of IRAK-1 and NF-κB p65. In vitro, the serum decreased the up-regulation of IL-6 and TNF-α in cell lines induced by LPS. In conclusion, L. casei LC2W intragastric administration pretreatment could significantly improve LPS-induced ALI in mice, probably through circulation to reach the lungs so as to inhibit the inflammatory response induced by activation of TLR4/MyD88/NF-κB signaling pathway.

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Posttreatment With LYRM03 Protects Rats From Acute Lung Inflammation Induced by Lipopolysaccharide via Suppressing the NF-κB/MyD88/TLR4 Axis

Cited by 7 publications

References 11 publications

WITHDRAWN: Ubiquitin promotes Escherichia coli HPI-induced duodenitis through the TLR4/Myd88/NF-κB pathway

WITHDRAWN: Ubiquitin promotes Escherichia coli HPI-induced duodenitis through the TLR4/Myd88/NF-κB pathway

Dexmedetomidine ameliorates lipopolysaccharide-induced acute lung injury by inhibiting the PI3K/Akt/FoxO1 signaling pathway

The Preventive Effects of Lactobacillus casei on Acute Lung Injury Induced by Lipopolysaccharide

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