scholarly journals The Potential Interplay of Adipokines with Toll-Like Receptors in the Development of Hepatocellular Carcinoma

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Shen-Nien Wang ◽  
Sen-Te Wang ◽  
King Teh Lee
Keyword(s):  
Hepatocellular Carcinoma ◽  
Chronic Inflammation ◽  
Metabolic Diseases ◽  
Viral Infections ◽  
Inflammatory Diseases ◽  
Epidemiological Data ◽  
Potential Interaction ◽  
Potential Contribution ◽  
Toll Like Receptors

Toll-like receptors (TLRs) are not only crucial to the initiation of the immune system, but also play a key role in several human inflammatory diseases. Hepatocellular carcinoma (HCC) is among those human cancers, which arise from sites of chronic inflammation. Therefore, a number of studies have explored the potential contribution of TLRs to HCC occurrence, which is initiated by exposure to chronic hepatic inflammation of different etiologies (including ethanol, and chronic B and C viral infections). Recent epidemiological data have shown the association of obesity and HCC development. Given the fact that adipose tissues can produce a variety of inflammation-related adipokines, obesity has been characterized as a state of chronic inflammation. Adipokines are therefore considered as important mediators linking inflammation to several metabolic diseases, including cancers. More recently, many experts have also shown the bridging role of TLRs between inflammation and metabolism. Hopefully, to retrieve the potential interaction between TLRs and adipokines in carcinogenesis of HCC will shed a new light on the therapeutic alternative for HCC. In this paper, the authors first review the respective roles of TLRs and adipokines, discuss their mutual interaction in chronic inflammation, and finally anticipate further investigations of this interaction in HCC development.

The role of gut microbiota in intestinal and liver diseases

2018 ◽  
Vol 53 (3) ◽  
pp. 271-280 ◽  
Author(s):  
Tomas Hrncir ◽  
Lucia Hrncirova ◽  
Miloslav Kverka ◽  
Helena Tlaskalova-Hogenova
Keyword(s):  
Gut Microbiota ◽  
Liver Diseases ◽  
Metabolic Diseases ◽  
Environmental Changes ◽  
Inflammatory Diseases ◽  
Food Additives ◽  
Epidemiological Data ◽  
Immune Mediated ◽  
Intestinal Immune System

The world-wide incidence of many immune-mediated and metabolic diseases, including those of the intestines and liver, is steadily increasing. Gut microbiota plays a central role in the pathogenesis of these diseases as it mediates environmental changes to the intestinal immune system. Various environmental factors including diet, food additives and medication also trigger the compositional and functional alterations of microbiota, that is, dysbiosis, and this dysbiosis is closely associated with many chronic inflammatory diseases. However, the causal relationship remains unclear for the majority of these diseases. In this review, we discuss essential epidemiological data, known pathogenetic factors including those of genetic and environmental nature, while mainly focusing on the role of gut microbiota in the development of selected intestinal and liver diseases. Using specific examples, we also briefly describe some of the most widely-used animal models including gnotobiotic models and their contribution to the research of pathogenetic mechanisms of the host–microbiota relationship.

Role of Exosomes in the Exchange of Spermatozoa after Leaving the Seminiferous Tubule: A Review

2020 ◽  
Vol 21 (5) ◽  
pp. 330-338
Author(s):  
Luming Wu ◽  
Yuan Ding ◽  
Shiqiang Han ◽  
Yiqing Wang
Keyword(s):  
Drug Delivery ◽  
Plasma Membrane ◽  
Seminiferous Tubule ◽  
Metabolic Diseases ◽  
Inflammatory Diseases ◽  
Multivesicular Bodies ◽  
Extensive Search ◽  
Neurological Research ◽  
The One

Background: Exosomes are extracellular vesicles (EVs) released from cells upon fusion of an intermediate endocytic compartment with the plasma membrane. They refer to the intraluminal vesicles released from the fusion of multivesicular bodies with the plasma membrane. The contents and number of exosomes are related to diseases such as metabolic diseases, cancer and inflammatory diseases. Exosomes have been used in neurological research as a drug delivery tool and also as biomarkers for diseases. Recently, exosomes were observed in the seminal plasma of the one who is asthenozoospermia, which can affect sperm motility and capacitation. Objective: The main objective of this review is to deeply discuss the role of exosomes in spermatozoa after leaving the seminiferous tubule. Methods: We conducted an extensive search of the literature available on relationships between exosomes and exosomes in spermatozoa on the bibliographic database. Conclusion: : This review thoroughly discussed the role that exosomes play in the exchange of spermatozoa after leaving the seminiferous tubule and its potential as a drug delivery tool and biomarkers for diseases as well.

scholarly journals The role of selected mechanisms of innate immunity in the pathogenesis of diabetes

2021 ◽  
Vol 11 (9) ◽  
pp. 544-549
Author(s):  
Paulina Trojanowska ◽  
Magdalena Chrościńska-Krawczyk ◽  
Alina Trojanowska ◽  
Ewa Tywanek ◽  
Jakub Wronecki ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Metabolic Diseases ◽  
Inflammatory Diseases ◽  
The Body ◽  
Low Grade ◽  
Intracellular Space ◽  
Cytoplasmic Proteins

Understanding the important role of the non-specific immune response in protecting the body against the development of numerous diseases has become partially possible after the discovery of several classes of pattern recognition receptors (PRR), such as Toll-like or NOD-like receptors. A group of cytoplasmic proteins called the inflammasome, which detect PAMP and DAMP through the PRR receptors, is able to activate pro-inflammatory cytokines and trigger an acute inflammatory reaction both in the extracellular and intracellular space. Low-grade systemic and local inflammation contributes to the development and progression of various conditions, including autoimmune and metabolic diseases, such as diabetes, metabolic syndrome and atherosclerosis, which until recently were not even considered inflammatory diseases. This review will discuss the role of innate immunity in the development of type 1 and type 2 diabetes, focusing on the role of specific innate immunity receptors and insulin resistance involved in these diseases pathogenesis.

scholarly journals Constructing im/migrants and ethnic minority groups as ‘carriers of disease’: Power effects of categorization practices in tuberculosis health reporting in the UK and Germany

Ethnicities ◽  
2019 ◽  
Vol 19 (3) ◽  
pp. 518-534
Author(s):  
Hella von Unger ◽  
Penelope Scott ◽  
Dennis Odukoya
Keyword(s):  
Ethnic Minority ◽  
Minority Groups ◽  
Epidemiological Data ◽  
Vulnerable Groups ◽  
Potential Contribution ◽  
Health Reporting ◽  
Ethnic Minority Groups ◽  
Core Feature ◽  
The Uk

Migration- and ethnicity-related categories are a core feature of public health systems internationally, particularly in health reporting on communicable infectious diseases. The specific categories and classifications used differ from country to country and are subject to controversy and change. The article compares categorization practices in health reporting in the UK and Germany with regard to tuberculosis. Tuberculosis has been framed as a ‘migrants’ disease’ in recent decades and new categories were introduced to collect and report epidemiological data. We reconstruct the genesis, change and power effects of categories related to im/migrants and ethnic minority groups. In both countries, migration-related categorizations entail constructions of im/migrants as ‘carriers of disease’. However, the categories also connect with discourses on human rights, prevention, treatment and care for migrants as vulnerable groups. While this ambivalent role of migration-related categories is not unique to health statistics, the potential contribution to processes of ‘othering’ and politics of exclusion seem particularly imminent in the context of communicable diseases such as tuberculosis. Ethnicity categories used in the UK, but not in Germany, also contribute to othering through racialization and culturalization, yet at the same time provide opportunities for community participation in the discourse.

scholarly journals MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Hans Carl Hasselbalch ◽  
Mads Emil Bjørn
Keyword(s):  
Chronic Inflammation ◽  
Residual Disease ◽  
Inflammatory Diseases ◽  
Myeloproliferative Neoplasms ◽  
Clonal Evolution ◽  
Increased Risk ◽  
Comorbidity Burden ◽  
To Come ◽  
New Treatment

In recent years the evidence is increasing that chronic inflammation may be an important driving force for clonal evolution and disease progression in the Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). Abnormal expression and activity of a number of proinflammatory cytokines are associated with MPNs, in particular MF, in which immune dysregulation is pronounced as evidenced by dysregulation of several immune and inflammation genes. In addition, chronic inflammation has been suggested to contribute to the development of premature atherosclerosis and may drive the development of other cancers in MPNs, both nonhematologic and hematologic. The MPN population has a substantial inflammation-mediated comorbidity burden. This review describes the evidence for considering the MPNs as inflammatory diseases,A Human Inflammation Model of Cancer Development, and the role of cytokines in disease initiation and progression. The consequences of this model are discussed, including the increased risk of second cancers and other inflammation-mediated diseases, emphasizing the urgent need for rethinking our therapeutic approach. Early intervention with interferon-alpha2, which as monotherapy has been shown to be able to induce minimal residual disease, in combination with potent anti-inflammatory agents such as JAK-inhibitors is foreseen as the most promising new treatment modality in the years to come.

scholarly journals Homeobox genes and Hepatocellular Carcinoma

2019 ◽  
Author(s):  
Kwei-Yan Liu ◽  
Li-Ting Wang ◽  
Shih-Hsien Hsu ◽  
Shen-Nien Wang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hox Genes ◽  
Viral Infections ◽  
Human Cancer ◽  
Control Cell ◽  
Environmental Toxins ◽  
Regulatory Mechanisms ◽  
Transcription Factor Family ◽  
Potential Use

Hepatocellular carcinoma (HCC) is the fifth most common type of cancer, and is the third leading cause of cancer-related deaths each year. It involves a multi-step progression and is strongly associated with chronic inflammation induced by the intake of environmental toxins and/or viral infections (i.e., hepatitis B and C viruses). Although several genetic dysregulations are considered to be involved in disease progression, the detailed regulatory mechanisms are not well defined. Homeobox (Hox) genes that encode transcription factors with homeodomains control cell growth, differentiation, and morphogenesis in embryonic development. Recently, more aberrant expressions of Hox genes were found in a wide variety of human cancer, including HCC. In this review, we summarize the currently available evidence related to the role of Hox genes in the development of HCC. The objective is to determine the roles of this conserved transcription factor family and its potential use as a therapeutic target in future investigations.

scholarly journals Elevated Levels of IL-33, IL-17 and IL-25 Indicate the Progression from Chronicity to Hepatocellular Carcinoma in Hepatitis C Virus Patients

Pathogens ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 57
Author(s):  
Momen Askoura ◽  
Hisham A. Abbas ◽  
Hadeel AlSadoun ◽  
Wesam H. Abdulaal ◽  
Amr S. Abu Lila ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis C Virus ◽  
Viral Load ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Serum Level ◽  
Viral Infections ◽  
Serum Levels ◽  
Chronic Patients

Hepatitis C virus (HCV) is one of the most epidemic viral infections in the world. Three-quarters of individuals infected with HCV become chronic. As a consequence of persistent inflammation, a considerable percentage of chronic patients progress to liver fibrosis, cirrhosis, and finally hepatocellular carcinoma. Cytokines, which are particularly produced from T-helper cells, play a crucial role in immune protection against HCV and the progression of the disease as well. In this study, the role of interleukins IL-33, IL-17, and IL-25 in HCV patients and progression of disease from chronicity to hepatocellular carcinoma will be characterized in order to use them as biomarkers of disease progression. The serum levels of the tested interleukins were measured in patients suffering from chronic hepatitis C (CHC), hepatocellular carcinoma (HCC), and healthy controls (C), and their levels were correlated to the degree of liver fibrosis, liver fibrosis markers and viral load. In contrast to the IL-25 serum level, which increased in patients suffering from HCC only, the serum levels of both IL-33 and IL-17 increased significantly in those patients suffering from CHC and HCC. In addition, IL-33 serum level was found to increase by liver fibrosis progression and viral load, in contrast to both IL-17 and IL-25. Current results indicate a significant role of IL-33 in liver inflammation and fibrosis progress in CHC, whereas IL-17 and IL-25 may be used as biomarkers for the development of hepatocellular carcinoma.

scholarly journals Role of Immune Cells in Patients with Hepatitis B Virus-Related Hepatocellular Carcinoma

2021 ◽  
Vol 22 (15) ◽  
pp. 8011
Author(s):  
Hyo-Jung Cho ◽  
Jae-Youn Cheong
Keyword(s):  
Hepatocellular Carcinoma ◽  
T Cells ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Inflammation ◽  
Cd8 T Cells ◽  
Immune Cells ◽  
Adaptive Immune ◽  
B Virus

Hepatocellular carcinoma (HCC) develops almost entirely in the presence of chronic inflammation. Chronic hepatitis B virus (HBV) infection with recurrent immune-mediated liver damage ultimately leads to cirrhosis and HCC. It is widely accepted that HBV infection induces the dysfunction of the innate and adaptive immune responses that engage various immune cells. Natural killer (NK) cells are associated with early antiviral and antitumor properties. On the other hand, inflammatory cells release various cytokines and chemokines that may promote HCC tumorigenesis. Moreover, immunosuppressive cells such as regulatory T cells (Treg) and myeloid-derived suppressive cells play a critical role in hepatocarcinogenesis. HBV-specific CD8+ T cells have been identified as pivotal players in antiviral responses, whilst extremely activated CD8+ T cells induce enormous inflammatory responses, and chronic inflammation can facilitate hepatocarcinogenesis. Controlling and maintaining the balance in the immune system is an important aspect in the management of HBV-related HCC. We conducted a review of the current knowledge on the immunopathogenesis of HBV-induced inflammation and the role of such immune activation in the tumorigenesis of HCC based on the recent studies on innate and adaptive immune cell dysfunction in HBV-related HCC.

Calcium Signaling in T Cells and Chronic Inflammatory Disorders of the Oral Cavity

2021 ◽  
pp. 002203452199065
Author(s):  
S. Hasiakos ◽  
Y. Gwack ◽  
M. Kang ◽  
I. Nishimura
Keyword(s):  
T Cells ◽  
T Cell ◽  
Oral Cavity ◽  
Calcium Signaling ◽  
Signaling Pathways ◽  
Chronic Inflammation ◽  
Th17 Cells ◽  
Inflammatory Diseases ◽  
Chronic Inflammatory Diseases

Acute immune responses to microbial insults in the oral cavity often progress to chronic inflammatory diseases such as periodontitis and apical periodontitis. Chronic oral inflammation causes destruction of the periodontium, potentially leading to loss of the dentition. Previous investigations have demonstrated that the composition of oral immune cells, rather than the overall extent of cellular infiltration, determines the pathological development of chronic inflammation. The role of T lymphocyte populations, including Th1, Th2, Th17, and Treg cells, has been extensively described. Studies now propose pathogenic Th17 cells as a distinct subset, uniquely classifiable from traditional Th17 populations. In situ differentiation of pathogenic Th17 cells has been verified as a source of destructive inflammation, which critically drives pathogenesis in chronic inflammatory diseases such as diabetes, rheumatoid arthritis, and inflammatory bowel disease. Pathogenic Th17 cells resemble a Th1 penotype and produce not only interleukin 17 (IL-17) but also γ-interferon (IFN-γ) and granulocyte-macrophage colony-stimulating factor (GM-CSF). The proinflammatory cytokine-specific mechanisms known to induce IL-17 expression in Th17 cells are well characterized; however, differentiation mechanisms that lead to pathogenic Th17 cells are less understood. Recently, Ca2+ signaling through Ca2+ release-activated Ca2+ channels (CRAC) in T cells has been uncovered as a major signaling axis involved in the regulation of T-cell-mediated chronic inflammation. In particular, pathogenic Th17 cell–mediated immunological diseases appear to be effectively targeted via such Ca2+ signaling pathways. Pathogenic plasticity of Th17 cells has been extensively illustrated in autoimmune and chronic inflammatory diseases. Although their specific causal relationship to oral infection-induced chronic inflammatory diseases is not fully established, pathogenic Th17 cells may be involved in the underlining mechanism. This review highlights the current understanding of T-cell phenotype regulation, calcium signaling pathways in this event, and the potential role of pathogenic Th17 cells in chronic inflammatory disorders of the oral cavity.

Chitinases: Therapeutic Scaffolds for Allergy and Inflammation

2020 ◽  
Vol 14 (1) ◽  
pp. 46-57
Author(s):  
Kirtika Madan ◽  
Mansi Madan ◽  
Swapnil Sharma ◽  
Sarvesh Paliwal
Keyword(s):  
Metabolic Diseases ◽  
Inflammatory Diseases ◽  
Polycystic Ovary ◽  
Present Review ◽  
Drug Molecules ◽  
Area Of Interest ◽  
Clinical Investigations ◽  
Chitinase Inhibitors ◽  
Key Terms

Background: Chitinases are the evolutionary conserved glycosidic enzymes that are characterized by their ability to cleave the naturally abundant polysaccharide chitin. The potential role of chitinases has been identified in the manifestation of various allergies and inflammatory diseases. In recent years, chitinases inhibitors are emerging as an alluring area of interest for the researchers and scientists and there is a dire need for the development of potential and safe chitinase antagonists for the prophylaxis and treatment of several diseases. Objective: The present review expedites the role of chitinases and their inhibitors in inflammation and related disorders. Methods: At first, an exhaustive survey of literature and various patents available related to chitinases were carried out. Useful information on chitinases and their inhibitor was gathered from the authentic scientific databases namely SCOPUS, EMBASE, PUBMED, GOOGLE SCHOLAR, MEDLINE, EMBASE, EBSCO, WEB OF SCIENCE, etc. This information was further analyzed and compiled up to prepare the framework of the review article. The search strategy was conducted by using queries with key terms “ chitin”, “chitinase”, “chitotrisidase”, “acidic mammalian chitinase”, “chitinase inhibitors”, “asthma” and “chitinases associated inflammatory disorders”, etc. The patents were searched using the key terms “chitinases and uses thereof”, “chitinase inhibitors”, “chitin-chitinase associated pathological disorders” etc. from www.google.com/patents, www.freepatentsonline.com, and www.scopus.com. Results: The present review provides a vision for apprehending human chitinases and their participation in several diseases. The patents available also signify the extended role and effectiveness of chitinase inhibitors in the prevention and treatment of various diseases viz. asthma, acute and chronic inflammatory diseases, autoimmune diseases, dental diseases, neurologic diseases, metabolic diseases, liver diseases, polycystic ovary syndrome, endometriosis, and cancer. In this regard, extensive pre-clinical and clinical investigations are required to develop some novel, potent and selective drug molecules for the treatment of various inflammatory diseases, allergies and cancers in the foreseeable future. Conclusion: In conclusion, chitinases can be used as potential biomarkers in prognosis and diagnosis of several inflammatory diseases and allergies and the design of novel chitinase inhibitors may act as key and rational scaffolds in designing some novel therapeutic agents in the treatment of variety of inflammatory diseases.

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