PD-L1 Regulates Inflammation in LPS-Induced Lung Epithelial Cells and Vascular Endothelial Cells by Interacting with the HIF-1α Signaling Pathway

Zhao, Shilong; Gao, Jing; Li, Jing; Wang, Shilei; Yuan, Congcong; Liu, Qiuhong

doi:10.1007/s10753-021-01474-3

Cited by 20 publications

(13 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the progression of pancreatitis in mice, LMT-28 treatment also reduced the expression of the proinflammatory cytokines IL-1β and TNF-α [11]. Furthermore, the levels of IL-1β and TNF-α in lung tissues from mice with sepsis were markedly decreased by LMT-28 [28]. As inflammatory biomarkers, the variations of IL-1β, IL-6, and TNF-α are the most commonly studied functional polymorphisms for periimplantitis and peri-implant bone loss [18,33,34].…”

Section: Discussionmentioning

confidence: 96%

“…LMT-28 is one type of IL-6 inhibitor and acts by binding directly to GP130 and selectively inhibiting IL-6-induced phosphorylation of GP130, which is a common receptor and signal transducer for the IL-6 family of cytokines. To date, it has been reported that LMT-28 was used to treat many diseases with positive results [25][26][27][28][29]. Several studies reported that LMT-28 played a crucial role in the improvement of inflammation in collagen-induced arthritis by inhibiting the IL-6/GP130 signaling pathway [12,26,30].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

A GP130-Targeting Small Molecule, LMT-28, Reduces LPS-Induced Bone Resorption around Implants in Diabetic Models by Inhibiting IL-6/GP130/JAK2/STAT3 Signaling

Liu

Yang

et al. 2023

Mediators of Inflammation

View full text Add to dashboard Cite

In this study, we examined the effect of the GP130-targeting molecule, LMT-28, on lipopolysaccharide- (LPS-) induced bone resorption around implants in diabetic models using in vitro and rat animal experiments. First, LMT-28 was added to osteoblasts stimulated by LPS and advanced glycation end products (AGEs), and nuclear factor-κB receptor-activating factor ligand (RANKL) and associated pathways were evaluated. Then, LMT-28 was administered by gavage at 0.23 mg/kg once every 5 days for 2 weeks to type 2 diabetic rats with peri-implantitis induced by LPS injection and silk ligature. The expression of IL-6 and RANKL was evaluated by immunohistochemistry, and the bone resorption around implants was evaluated by microcomputed tomography. The results showed that LMT-28 downregulated the expression of RANKL through the JAK2/STAT3 signaling pathway in osteoblasts stimulated by LPS and AGEs, reduced bone resorption around implants with peri-implantitis, decreased the expression of IL-6 and RANKL, and decreased osteoclast activity in type 2 diabetic rats. This study confirmed the ability of LMT-28 to reduce LPS-induced bone resorption around implants in diabetic rats.

show abstract

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

A GP130-Targeting Small Molecule, LMT-28, Reduces LPS-Induced Bone Resorption around Implants in Diabetic Models by Inhibiting IL-6/GP130/JAK2/STAT3 Signaling

Liu

Yang

et al. 2023

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…Pathological changes were observed and evaluated with a double-blind reference to the relevant literature [ 14 , 15 , 16 ]. The pathological evaluation of the organ focused on hyperplasia, alveolar hemorrhage and consolidation, tissue infiltration, neutrophil migration, congestion and edema, and the degree was divided into none, mild, moderate and severe.…”

Section: Methodsmentioning

confidence: 99%

“…Lung tissue homogenate and serum were taken, and the reactions between the antioxidant enzyme catalase (CAT) and Superoxide dismutase (SOD) were measured by Du-640 ultraviolet spectrophotometer according to the test kit manufacturer’s instructions [ 15 , 16 ].…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

High Concentration Hydrogen Mitigates Sepsis-Induced Acute Lung Injury in Mice by Alleviating Mitochondrial Fission and Dysfunction

Zhao

Sun

Cui

et al. 2023

JPM

View full text Add to dashboard Cite

Background: Multiple organ failure (MOF) is the main cause of early death in septic shock. Lungs are among the organs that are affected in MOF, resulting in acute lung injury. A large number of inflammatory factors and stress injury in sepsis can lead to alterations in mitochondrial dynamics. Numerous studies have confirmed that hydrogen can alleviate sepsis in the animal model. The purpose of this experiment was to explore the therapeutic effect of high concentration (67%) hydrogen on acute lung injury in septic mice and its mechanism. Methods: The moderate and severe septic models were prepared by cecal ligation and puncture. Hydrogen with different concentrations was inhaled for one hour at 1 h and 6 h after the corresponding surgery. The arterial blood gas of mice during hydrogen inhalation was monitored in real time, and the 7-day survival rate of mice with sepsis was recorded. The pathological changes of lung tissues and functions of livers and kidneys were measured. The changes of oxidation products, antioxidant enzymes and pro-inflammatory cytokines in lungs and serums were detected. Mitochondrial function was measured. Results: The inhalation of 2% or 67% hydrogen improves the 7-day survival rate and reduces acute lung injury as well as liver and kidney injury in sepsis. The therapeutic effect of 67% hydrogen inhalation on sepsis was related to increasing antioxidant enzyme activity, reducing oxidation products and pro-inflammatory cytokines in lungs and serums. Compared with the Sham group, mitochondrial dysfunction was alleviated in hydrogen groups. Conclusions: Hydrogen inhalation by high or low concentration can both significantly improve sepsis; however, a high concentration demonstrates a better protective effect. High concentration hydrogen inhalation can significantly improve the mitochondrial dynamic balance and reduce the lung injury in septic mice.

show abstract

Reactive Oxygen Species‐Activated CO Versatile Nanomedicine with Innate Gut Immune and Microbiome Remodeling Effects for Treating Inflammatory Bowel Disease

Zeng

Fan

Zhou

et al. 2023

Adv Funct Materials

View full text Add to dashboard Cite

Abnormal activation of the gut mucosal immune system and a highly dysregulated gut microbiota play essential roles in the progression of inflammatory bowel disease (IBD). The clinical treatment of IBD remains highly challenging, with first‐line drugs showing limited efficacy and significant side effects. A reactive oxygen species (ROS)‐activated CO versatile nanomedicine (CMPs) capable of remodeling the gut immune‐microbiota microenvironment via potent anti‐oxidant, anti‐inflammatory, and antimicrobial effects is developed. CORM‐401‐loaded mannose‐modified peptide dendrimer nanogel: CMPs preferentially congregate on the surface of damaged colon mucosa after rectal administration and are subsequently internalized by activated immune cells. CORM‐401 can release numerous CO molecules in response to high ROS levels in cells and at the site of IBD, resulting in multiple therapeutic effects. In vitro and in vivo studies have demonstrated that CMPs scavenge ROS, suppress inflammatory responses, eliminate pathogens, and alleviate colitis in mouse models. RNA sequencing reveals that CMPs successfully remodel gut mucosal immune homeostasis by scavenging ROS, inhibiting NF‐κB/p38MAPK, activating PI3K‐Akt, and inhibiting HIF‐1‐induced glycolysis. 16S ribosomal RNA sequencing shows that CMPs can remodel the gut flora composition by restraining detrimental bacteria and augmenting beneficial bacteria. This study develops a promising and versatile nanomedicine for the management of IBD.

show abstract

PD-L1 Regulates Inflammation in LPS-Induced Lung Epithelial Cells and Vascular Endothelial Cells by Interacting with the HIF-1α Signaling Pathway

Cited by 20 publications

References 37 publications

A GP130-Targeting Small Molecule, LMT-28, Reduces LPS-Induced Bone Resorption around Implants in Diabetic Models by Inhibiting IL-6/GP130/JAK2/STAT3 Signaling

A GP130-Targeting Small Molecule, LMT-28, Reduces LPS-Induced Bone Resorption around Implants in Diabetic Models by Inhibiting IL-6/GP130/JAK2/STAT3 Signaling

High Concentration Hydrogen Mitigates Sepsis-Induced Acute Lung Injury in Mice by Alleviating Mitochondrial Fission and Dysfunction

Reactive Oxygen Species‐Activated CO Versatile Nanomedicine with Innate Gut Immune and Microbiome Remodeling Effects for Treating Inflammatory Bowel Disease

Contact Info

Product

Resources

About