Potential role of NF-κB pathway in the immuno-inflammatory responses during human cystic echinococcosis

Acta Tropica ◽  
2020 ◽  
Vol 203 ◽  
pp. 105306 ◽  
Author(s):  
Sarah Tilioua ◽  
Dalila Mezioug ◽  
Zine-Charaf Amir-Tidadini ◽  
Yacine-Miloud Medjdoub ◽  
Chafia Touil-Boukoffa
Keyword(s):  
Cystic Echinococcosis ◽  
Potential Role ◽  
Inflammatory Responses ◽  
Human Cystic Echinococcosis

Effect of mebendazole on human cystic echinococcosis: the role of dosage and treatment duration

1999 ◽  
Vol 93 (4) ◽  
pp. 357-365 ◽  
Author(s):  
K. Vutova ◽  
G. Mechkov ◽  
P. Vachkov ◽  
R. Petkov ◽  
P. Georgiev ◽  
...  
Keyword(s):  
Cystic Echinococcosis ◽  
Treatment Duration ◽  
Human Cystic Echinococcosis

scholarly journals Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis

2019 ◽  
Author(s):  
Kurt T. K. Giuliani ◽  
Andrew J. Kassianos ◽  
Helen Healy ◽  
Pedro F. H. Gois
Keyword(s):  
Nlrp3 Inflammasome ◽  
Potential Role ◽  
Inflammatory Responses ◽  
Receptor Protein ◽  
Interleukin 18 ◽  
Nucleotide Binding Domain ◽  
Renal Vasoconstriction ◽  
Pigment Nephropathy ◽  
Inflammatory Caspases

Pigment nephropathy is an acute decline in renal function following the deposition of endogenous haem-containing proteins in the kidneys. Haem pigments such as myoglobin and haemoglobin are filtered by glomeruli and absorbed by the proximal tubules. They cause renal vasoconstriction, tubular obstruction, increased oxidative stress and inflammation. Haem is associated with inflammation in sterile and infectious conditions, contributing to the pathogenesis of many disorders such as rhabdomyolysis and haemolytic diseases. In fact, haem appears to be a signaling molecule that is able to activate the inflammasome pathway. Recent studies highlight a pathogenic function for haem in triggering inflammatory responses through the activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome. Among the inflammasome multiprotein complexes, the NLRP3 inflammasome has been the most widely characterized as a trigger of inflammatory caspases and the maturation of interleukin-18 and -1β. In the present review, we discuss the latest evidence on the importance of inflammasome-mediated inflammation in pigment nephropathy. Finally, we highlight the potential role of inflammasome inhibitors in the prophylaxis and treatment of pigment nephropathy.

scholarly journals Microbial-Driven Immunological Memory and Its Potential Role in Microbiome Editing for the Prevention of Colorectal Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Laure Campillo-Gimenez ◽  
David Rios-Covian ◽  
Jesus Rivera-Nieves ◽  
Hiroshi Kiyono ◽  
Hiutung Chu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Potential Role ◽  
Microbial Consortium ◽  
Inflammatory Responses ◽  
Microbial Interactions ◽  
Intestinal Microbiome ◽  
Immune Memory ◽  
Mucosal Lymphocyte ◽  
Made In

Over the last several years, many advances have been made in understanding the role of bacteria in the pathogenesis of gastrointestinal cancers. Beginning with Helicobacter pylori being recognized as the first bacterial carcinogen and the causative agent of most gastric cancers, more recent studies have examined the role of enteric microbes in colorectal cancer. In the digestive tract, these communities are numerous and have a complex interrelationship with local immune/inflammatory responses that impact the health of the host. As modifying the microbiome in the stomach has decreased the risk of gastric cancer, modifying the distal microbiome may decrease the risk of colorectal cancers. To date, very few studies have considered the notion that mucosal lymphocyte-dependent immune memory may confound attempts to change the microbial components in these communities. The goal of this review is to consider some of the factors impacting host-microbial interactions that affect colorectal cancer and raise questions about how immune memory responses to the local microbial consortium affect any attempt to modify the composition of the intestinal microbiome.

scholarly journals Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis

2019 ◽  
Vol 20 (8) ◽  
pp. 1997 ◽  
Author(s):  
Kurt T. K. Giuliani ◽  
Andrew J. Kassianos ◽  
Helen Healy ◽  
Pedro H. F. Gois
Keyword(s):  
Nlrp3 Inflammasome ◽  
Potential Role ◽  
Inflammatory Responses ◽  
Receptor Protein ◽  
Nucleotide Binding Domain ◽  
Renal Vasoconstriction ◽  
Signalling Molecule ◽  
Pigment Nephropathy ◽  
Inflammatory Caspases

Pigment nephropathy is an acute decline in renal function following the deposition of endogenous haem-containing proteins in the kidneys. Haem pigments such as myoglobin and haemoglobin are filtered by glomeruli and absorbed by the proximal tubules. They cause renal vasoconstriction, tubular obstruction, increased oxidative stress and inflammation. Haem is associated with inflammation in sterile and infectious conditions, contributing to the pathogenesis of many disorders such as rhabdomyolysis and haemolytic diseases. In fact, haem appears to be a signalling molecule that is able to activate the inflammasome pathway. Recent studies highlight a pathogenic function for haem in triggering inflammatory responses through the activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome. Among the inflammasome multiprotein complexes, the NLRP3 inflammasome has been the most widely characterized as a trigger of inflammatory caspases and the maturation of interleukin-18 and -1β. In the present review, we discuss the latest evidence on the importance of inflammasome-mediated inflammation in pigment nephropathy. Finally, we highlight the potential role of inflammasome inhibitors in the prophylaxis and treatment of pigment nephropathy.

scholarly journals Tissue-specific control of galectin-1-driven circuits during inflammatory responses

Glycobiology ◽  
2021 ◽  
Author(s):  
Anabela M Cutine ◽  
Camila A Bach ◽  
Florencia Veigas ◽  
Joaquín P Merlo ◽  
Lorena Laporte ◽  
...  
Keyword(s):  
Potential Role ◽  
Inflammatory Responses ◽  
Binding Protein ◽  
Experimental Models ◽  
Tissue Specific ◽  
Inflammatory Conditions ◽  
Evolutionarily Conserved ◽  
And Function ◽  
Specific Control

Abstract The relevance of glycan-binding protein in immune tolerance and inflammation has been well established, mainly by studies of C-type lectins, siglecs and galectins both in experimental models and patient samples. Galectins, a family of evolutionarily conserved lectins, are characterized by sequence homology in the carbohydrate-recognition domain (CRD), atypical secretion via an ER-Golgi-independent pathway and the ability to recognize β-galactoside-containing saccharides. Galectin-1 (Gal-1), a prototype member of this family displays mainly anti-inflammatory and immunosuppressive activities, although, similar to many cytokines and growth factors, it may also trigger paradoxical pro-inflammatory effects under certain circumstances. These dual effects could be associated to tissue-, time- or context-dependent regulation of galectin expression and function, including particular pathophysiologic settings and/or environmental conditions influencing the structure of this lectin, as well as the availability of glycosylated ligands in immune cells during the course of inflammatory responses. Here, we discuss the tissue-specific role of Gal-1 as a master regulator of inflammatory responses across different pathophysiologic settings, highlighting its potential role as a therapeutic target. Further studies designed at analyzing the intrinsic and extrinsic pathways that control Gal-1 expression and function in different tissue microenvironments may contribute to design tailored therapeutic strategies aimed at positively or negatively modulate this glycan-binding protein in pathologic inflammatory conditions.

scholarly journals GBP1 exerts inhibitory effects on acute viral myocarditis by inhibiting the inflammatory response of macrophages in mice

2019 ◽  
Vol 97 (4) ◽  
pp. 454-462
Author(s):  
Ya-Nan Zhao ◽  
Guang-Jun Xu ◽  
Ping Yang
Keyword(s):  
Potential Role ◽  
Inflammatory Responses ◽  
Viral Myocarditis ◽  
Serum Levels ◽  
Cardiomyocyte Apoptosis ◽  
Inhibitory Effects ◽  
Tnf Α ◽  
Cox 2 ◽  
Lower Expression

Viral myocarditis (VMC) is a condition that could potentially progress to dilated cardiomyopathy or congestive heart failure, making it the leading cause of the untimely death in young adults. Interferon-induced GBP1 encodes much of the GTPase induced by interferon gamma in many eukaryotic cells. However, little is known regarding the effect of GBP1 on acute VMC (AVMC). Hence, this aim of this study was to assess the effect of GBP1 on AVMC. Once the AVMC mouse models were established, the functional role of GBP1 was determined in AVMC. Serum levels of IL-6, TNF-α, and TGF-β, and expression levels of GBP1, MIF, iNOS, and COX-2 were detected, together with the viability and apoptosis of cardiomyocytes. AVMC mice presented with increased levels of TGF-β, IL-6, TNF-α, MIF, iNOS, and COX-2, as well as cell apoptosis, but lower expression of GBP1 and viability of cardiomyocytes. Restored GBP1 or depleted macrophages resulted in decreased levels of TGF-β, IL-6, TNF-α, MIF, iNOS, and COX-2, as well as cardiomyocyte apoptosis, while increasing cardiomyocyte viability. In conclusion, our results highlight the potential role of GBP1 in inhibiting AVMC development. The experimental results indicate that GBP1 up-regulation and macrophage depletion can alleviate AVMC-related cardial damage by inhibiting inflammatory responses and cardiomyocyte apoptosis while increasing cardiomyocyte viability.

The potential role of toll-like receptor 4 Asp299Gly polymorphism and its association with recurrent cystic echinococcosis in postoperative patients

2018 ◽  
Vol 117 (6) ◽  
pp. 1717-1727 ◽  
Author(s):  
Jafar Noori ◽  
Adel Spotin ◽  
Ehsan Ahmadpour ◽  
Mahmoud Mahami-Oskouei ◽  
Homayoun Sadeghi-Bazargani ◽  
...  
Keyword(s):  
Cystic Echinococcosis ◽  
Potential Role ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals The Oral Microbiome in Pediatric IBD: A Source of Pathobionts or Biomarkers?

2021 ◽  
Vol 8 ◽  
Author(s):  
Khalid Elmaghrawy ◽  
Séamus Hussey ◽  
Gary P. Moran
Keyword(s):  
Potential Role ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Oral Bacteria ◽  
Oral Microbiome ◽  
Gi Tract ◽  
Clinical Indicator ◽  
Microbial Dysbiosis ◽  
Oral Microbes

The oral cavity is continuous with the gastrointestinal tract and in children, oral health may be closely linked with the overall health of the GI tract. In the case of pediatric Crohn's disease (CD), oral manifestations are an important clinical indicator of intestinal disease. Recent studies of the microbiome in IBD suggest that translocation of oral microbes to the gut may be a common feature of the microbial dysbiosis which is a signature of both CD and ulcerative colitis (UC). Murine studies suggest that translocation of oral bacteria and yeasts to the lower GI tract may trigger inflammation in susceptible hosts, providing a mechanistic link to the development of IBD. Conversely, some studies have shown that dysbiosis of the oral microbiome may occur, possibly as a result of inflammatory responses and could represent a useful source of biomarkers of GI health. This review summarizes our current knowledge of the oral microbiome in IBD and presents current hypotheses on the potential role of this community in the pathogenesis of these diseases.

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