P-350 The cross talk between hepatic macrophages and sinusoidal endotherial cells and the microcirculatory disturbances as the mechanism of development of endotoxin induced liver injury

1995 ◽  
Vol 3 ◽  
pp. S124
Author(s):  
S FUJITA
Keyword(s):  
Liver Injury ◽  
Cross Talk ◽  
Hepatic Macrophages ◽  
Microcirculatory Disturbances ◽  
The Cross

The cross-talk of NLRP3 inflammasome activation and necroptotic hepatocyte death in acetaminophen-induced mice acute liver injury

2020 ◽  
pp. 096032712096115
Author(s):  
L Li ◽  
S Shan ◽  
K Kang ◽  
C Zhang ◽  
R Kou ◽  
...  
Keyword(s):  
Liver Injury ◽  
Cross Talk ◽  
Nlrp3 Inflammasome ◽  
Time Course ◽  
Critical Role ◽  
Inflammasome Activation ◽  
Severe Liver ◽  
Drug Induced ◽  
The Cross ◽  
Apap Hepatotoxicity

Overdose acetaminophen (APAP) can result in severe liver injury, which is responsible for nearly half of drug-induced liver injury in western countries. Previous studies have found that there existed massive hepatocellular necrosis and severe inflammatory response in APAP-induced liver injury. However, the mechanistic linkage between necroptosis and NLRP3 inflammasome pathway in APAP-induced hepatotoxicity remains poorly understood. In order to investigate the relationship between inflammation and hepatocytes death in APAP hepatotoxicity, a time-course model for APAP hepatotoxicity in C57/BL6 mice was established by intraperitoneal (i.p) injection of 300 mg/kg APAP in this study. The activity of serum enzymes and pathological changes of APAP-treated mice were evaluated, and the critical molecules in necroptosis and NF-κB-NLRP3 inflammasome signaling pathway were determined by immunoblot and immunofluorescence analysis. The results demonstrated that APAP overdose resulted in a severe liver injury. Furthermore, the expression of critical molecules in NLRP3 inflammasome and necroptosis pathways peaked at 12–24 h, and then was decreased gradually, which is consistent with the pattern of pathological injury induced by APAP. Our further investigation found that the level of IL-1β in mouse liver was closely correlated with the level of phosphorylated MLKL following exposure to APAP. Furthermore, inhibition of necroptosis with necrostatin-1 significantly suppressed the activation of NLRP3 inflammasome signaling. Taken together, our results highlighted that the cross-talk between necroptosis and NLRP3 inflammasome played a critical role for promoting APAP-induced liver injury. Inhibition of the interaction of inflammation and necroptosis by pharmaceutical methods may represent a promising therapeutic strategy for APAP-induced liver injury.

The Role of Sensing Peptides in the Cross-talk between Microbiota and Human Cancer Cells

2018 ◽  
Vol 18 (18) ◽  
pp. 1567-1571
Author(s):  
Anna Lucia Tornesello ◽  
Luigi Buonaguro ◽  
Maria Lina Tornesello ◽  
Franco M. Buonaguro
Keyword(s):  
Cancer Cells ◽  
Cross Talk ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
The Cross

Effect of the cross-talk between autophagy and endoplasmic reticulum stress on Mn-induced alpha-synuclein oligomerization

2017 ◽  
Vol 33 (3) ◽  
pp. 315-324 ◽  
Author(s):  
Chang Liu ◽  
Dong-Ying Yan ◽  
Xuan Tan ◽  
Zhuo Ma ◽  
Can Wang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cross Talk ◽  
Alpha Synuclein ◽  
The Cross

scholarly journals LecRK-Ⅷ.2 mediates the cross-talk between sugar and brassinosteroid during hypocotyl elongation in Arabidopsis

2021 ◽  
Vol 1 (1) ◽  
pp. 55-63
Author(s):  
NingJie Hao ◽  
Xiaoxiao Zou ◽  
Xiaoxia Lin ◽  
Ruqiong Cai ◽  
Wenjun Xiao ◽  
...  
Keyword(s):  
Cross Talk ◽  
Hypocotyl Elongation ◽  
The Cross

scholarly journals Liver Injury and the Macrophage Issue: Molecular and Mechanistic Facts and Their Clinical Relevance

2021 ◽  
Vol 22 (14) ◽  
pp. 7249
Author(s):  
Siyer Roohani ◽  
Frank Tacke
Keyword(s):  
Bone Marrow ◽  
Liver Injury ◽  
Current Knowledge ◽  
Hepatocellular Cancer ◽  
Complete Recovery ◽  
Hepatic Macrophages ◽  
Liver Injuries ◽  
Microbial Products ◽  
Injured Liver

The liver is an essential immunological organ due to its gatekeeper position to bypassing antigens from the intestinal blood flow and microbial products from the intestinal commensals. The tissue-resident liver macrophages, termed Kupffer cells, represent key phagocytes that closely interact with local parenchymal, interstitial and other immunological cells in the liver to maintain homeostasis and tolerance against harmless antigens. Upon liver injury, the pool of hepatic macrophages expands dramatically by infiltrating bone marrow-/monocyte-derived macrophages. The interplay of the injured microenvironment and altered macrophage pool skews the subsequent course of liver injuries. It may range from complete recovery to chronic inflammation, fibrosis, cirrhosis and eventually hepatocellular cancer. This review summarizes current knowledge on the classification and role of hepatic macrophages in the healthy and injured liver.

Are neutrophil extracellular traps the link for the cross-talk between periodontitis and rheumatoid arthritis physiopathology?

Rheumatology ◽  
2021 ◽  
Author(s):  
Sicília Rezende Oliveira ◽  
José Alcides A de Arruda ◽  
Ayda Henriques Schneider ◽  
Valessa Florindo Carvalho ◽  
Caio Machado ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cross Talk ◽  
Neutrophil Extracellular Traps ◽  
Periodontal Therapy ◽  
Clinical Parameters ◽  
Extracellular Traps ◽  
Early Ra ◽  
The Cross ◽  
High Concentrations ◽  
The Impact

Abstract Objectives Neutrophil extracellular traps (NETs) play a role in the pathogenesis of periodontitis and rheumatoid arthritis (RA). However, it remains poorly understood whether NETs participate in the cross-talk between periodontitis and RA. Herein, we investigated the production of NETs in individuals with periodontitis and RA and its association with clinical parameters. The impact of periodontal therapy on RA and NET release was also assessed. Methods The concentration of NETs and cytokines was determined in the saliva and plasma of individuals with early RA (n = 24), established RA (n = 64), and individuals without RA (n = 76). The influence of periodontitis on the production of NETs and cytokines was also evaluated. Results Individuals with early RA had a higher concentration of NETs in saliva and plasma than individuals with established RA or without RA. Periodontitis resulted in an increase in the concentration of NETs of groups of individuals without RA and with early RA. The proportion of individuals with high concentrations of IL-6, IL-10 and GM-CSF was higher among individuals with periodontitis than among individuals without periodontitis. The concentrations of TNF-α, IL-6, IL-17/IL-25, and IL-28A were particularly high in individuals with early RA. Worse periodontal clinical parameters, RA onset and RA activity were significantly associated with circulating NETs. Periodontal therapy was associated with a reduction in the concentration of NETs and inflammatory cytokines and amelioration in periodontitis and RA. Conclusion This study reveals that NETs are a possible link between periodontitis and RA, with periodontal therapy resulting in a dramatic switch in circulating NET levels.

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