scholarly journals Neutrophil transendothelial migration hotspots – mechanisms and implications

2021 ◽  
Vol 134 (7) ◽  
pp. jcs255653
Author(s):  
Max L. B. Grönloh ◽  
Janine J. G. Arts ◽  
Jaap D. van Buul
Keyword(s):  
Transendothelial Migration ◽  
Blood Stream ◽  
Substrate Stiffness ◽  
Physical Factors ◽  
Membrane Composition ◽  
Leukocyte Transendothelial Migration ◽  
Membrane Protrusions ◽  
Endothelial Junction ◽  
Current Paradigm

ABSTRACTDuring inflammation, leukocytes circulating in the blood stream exit the vasculature in a process called leukocyte transendothelial migration (TEM). The current paradigm of this process comprises several well-established steps, including rolling, adhesion, crawling, diapedesis and sub-endothelial crawling. Nowadays, the role of the endothelium in transmigration is increasingly appreciated. It has been established that leukocyte exit sites on the endothelium and in the pericyte layer are in fact not random but instead may be specifically recognized by migrating leukocytes. Here, we review the concept of transmigration hotspots, specific sites in the endothelial and pericyte layer where most transmigration events take place. Chemokine cues, adhesion molecules and membrane protrusions as well as physical factors, such as endothelial junction stability, substrate stiffness, the presence of pericytes and basement membrane composition, may all contribute to local hotspot formation to facilitate leukocytes exiting the vasculature. In this Review, we discuss the biological relevance of such hotspots and put forward multiple mechanisms and factors that determine a functional TEM hotspot.

scholarly journals Endocan regulates acute lung inflammation through control of leukocyte diapedesis

2019 ◽  
Vol 127 (3) ◽  
pp. 668-678 ◽  
Author(s):  
Alexandre Gaudet ◽  
Lucie Portier ◽  
Méline Prin ◽  
Marie-Christine Copin ◽  
Anne Tsicopoulos ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Inflammation ◽  
Distress Syndrome ◽  
Human Leukocyte ◽  
Transendothelial Migration ◽  
Acute Lung Inflammation ◽  
Leukocyte Transendothelial Migration

Acute respiratory distress syndrome is a severe form of respiratory failure, occurring in up to 20% of patients admitted to the intensive care unit with sepsis. Dysregulated leukocyte diapedesis is a major contributor to acute respiratory distress syndrome. Endocan is a circulating proteoglycan that binds to the leukocyte integrin leukocyte functional antigen-1 and blocks its interaction with its endothelial ligand, ICAM-1. The objective of this study was to evaluate the role of endocan in the control of acute lung inflammation. In vitro, endocan inhibited human leukocyte transendothelial migration as well as ICAM-1-dependent migration but had a very mild effect on ICAM-1-dependent adhesion. Endocan also acted as an inhibitor of transendothelial migration of mouse leukocytes. The effect of systemic administration of recombinant human endocan was assessed in a model of acute lung inflammation in BALB/c mice. Treatment with endocan 1 h after intratracheal LPS challenge reduced the alveolar inflammatory response, diminished histological features of acute lung injury, and improved respiratory function. These results highlight the anti-inflammatory role of human endocan and its protective effect against acute lung injury. NEW & NOTEWORTHY We show here that endocan inhibits ICAM-1-dependent human leukocyte transendothelial migration and ICAM-1-dependent adhesion. We also found that in BALB/c mice with tracheal LPS-induced acute lung injury treatment with recombinant human endocan reduces lung inflammation, notably through reduction of neutrophilic recruitment, and restores normal lung function. These results confirm the hypothesis that human endocan may have a protective effect against acute lung inflammation.

Participation of ABCA1 transporter in development of chronic obstructive pulmonary disease

2020 ◽  
Vol 28 (3) ◽  
pp. 360-370
Author(s):  
Stanislav N. Kotlyarov ◽  
Anna A. Kotlyarova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Significant Contribution ◽  
Modern Medicine ◽  
Lipid Homeostasis ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Reverse Transport ◽  
Current Paradigm

Despite all achievements of the modern medicine, the problem of chronic obstructive pulmonary disease (COPD) does not lose its relevance. The current paradigm suggests a key role of macrophages in inflammation in COPD. Macrophages are known to be heterogeneous in their functions. This heterogeneity is determined by their immunometabolic profile and also by peculiarities of lipid homeostasis of cells. Aim. To analyze the role of the ABCA1 transporter, a member of the ABC A subfamily, in the pathogenesis of COPD. The expression of ABCA1 in lung tissues is on the second place after the liver, which shows the important role of the carrier and of lipid homeostasis in the function of lungs. Analysis of the literature shows that participation of the transporter in inflammation consists in regulation of the content of cholesterol in the lipid rafts of the membranes, in phagocytosis and apoptosis. Conclusion. Through regulation of the process of reverse transport of cholesterol in macrophages of lungs, ABCA1 can change their inflammatory response, which makes a significant contribution to the pathogenesis of COPD.

The role of microRNA-33 as a key regulator in hepatic lipogenesis signaling and a potential serological biomarker for NAFLD with excessive dietary fructose consumption in C57BL/6N mice

2021 ◽  
Author(s):  
Jeong Hoon Pan ◽  
Hanvit Cha ◽  
Jingsi Tang ◽  
Seoyoon Lee ◽  
Suk Hee Lee ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Blood Stream ◽  
Hepatic Lipogenesis ◽  
Dietary Fructose

Fructose-induced hepatic miR-33 suppression lead to fatty liver via upregulation of SREBP1. Additionally, fructose-induced hepatic ferroptosis may cause a spill-over of miR-33 into blood stream, which could be a potential serological biomarker for fructose-induced NAFLD.

scholarly journals The Role of Gut, Vaginal, and Urinary Microbiome in Urinary Tract Infections: From Bench to Bedside

Diagnostics ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 7
Author(s):  
Tomislav Meštrović ◽  
Mario Matijašić ◽  
Mihaela Perić ◽  
Hana Čipčić Paljetak ◽  
Anja Barešić ◽  
...  
Keyword(s):  
Urinary Tract ◽  
Urinary Tract Infections ◽  
Subsequent Development ◽  
Potential Influence ◽  
Urinary Microbiome ◽  
Important Field ◽  
Tract Infections ◽  
The Relationship ◽  
Current Paradigm

The current paradigm of urinary tract infection (UTI) pathogenesis takes into account the contamination of the periurethral space by specific uropathogens residing in the gut, which is followed by urethral colonization and pathogen ascension to the urinary bladder. Consequently, studying the relationship between gut microbiota and the subsequent development of bacteriuria and UTI represents an important field of research. However, the well-established diagnostic and therapeutic paradigm for urinary tract infections (UTIs) has come into question with the discovery of a multifaceted, symbiotic microbiome in the healthy urogenital tract. More specifically, emerging data suggest that vaginal dysbiosis may result in Escherichia coli colonization and prompt recurrent UTIs, while urinary microbiome perturbations may precede the development of UTIs and other pathologic conditions of the urinary system. The question is whether these findings can be exploited for risk reduction and treatment purposes. This review aimed to appraise the three aforementioned specific microbiomes regarding their potential influence on UTI development by focusing on the recent studies in the field and assessing the potential linkages between these different niches, as well as evaluating the state of translational research for novel therapeutic and preventative approaches.

scholarly journals The emerging role of mechanical and topographical factors in the development and treatment of nervous system disorders: dark and light sides of the force

2021 ◽  
Author(s):  
Natalia Bryniarska-Kubiak ◽  
Andrzej Kubiak ◽  
Małgorzata Lekka ◽  
Agnieszka Basta-Kaim
Keyword(s):  
Nervous System ◽  
Physical Factors ◽  
Nervous System Diseases ◽  
Therapeutic Approaches ◽  
System Disease ◽  
New Therapeutic Approaches ◽  
The Subject ◽  
Topographical Factors ◽  
New Treatment

AbstractNervous system diseases are the subject of intensive research due to their association with high mortality rates and their potential to cause irreversible disability. Most studies focus on targeting the biological factors related to disease pathogenesis, e.g. use of recombinant activator of plasminogen in the treatment of stroke. Nevertheless, multiple diseases such as Parkinson’s disease and Alzheimer’s disease still lack successful treatment. Recently, evidence has indicated that physical factors such as the mechanical properties of cells and tissue and topography play a crucial role in homeostasis as well as disease progression. This review aims to depict these factors’ roles in the progression of nervous system diseases and consequently discusses the possibility of new therapeutic approaches. The literature is reviewed to provide a deeper understanding of the roles played by physical factors in nervous system disease development to aid in the design of promising new treatment approaches. Graphic abstract

The role of physical factors in the complex therapy of patients with rheumatoid arthritis

1985 ◽  
Vol 66 (4) ◽  
pp. 318-318
Author(s):  
L. V. Chernetsova ◽  
A. G. Ibragimova
Keyword(s):  
Rheumatoid Arthritis ◽  
Comparative Analysis ◽  
Drug Therapy ◽  
Electromagnetic Waves ◽  
Physical Factors ◽  
Complex Therapy ◽  
Decimeter Range

The comparative analysis of treatment of 76 patients with rheumatoid arthritis using electromagnetic waves of the decimeter range and lithium electrophoresis, depending on the activity of the process and the type of drug therapy.

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