The Cytokine Network: Contributions of Proinflammatory Cytokines and Chemokines

1993 ◽  
pp. 297-304
Author(s):  
J. J. Oppenheim ◽  
J.-M. Wang ◽  
A. W. Lloyd ◽  
D. D. Taub ◽  
D. J. Kelvin ◽  
...  
2021 ◽  
Vol 26 (1) ◽  
pp. 58-63
Author(s):  
N. L. Erokina ◽  
A. V. Lepilin ◽  
A. Yu. Mironov ◽  
N. B. Zakharova ◽  
S. B. Fishtchev

Relevance. Reparative processes in the extraction socket include hemostasis, inflammation, proliferation and tissue remodelling. These processes are caused by mediators which determine interactions in the immunoregulatory, cytokine network. After the tooth extraction, pro- and anti-inflammatory mediators are unbalanced. The number of macrophages, lymphocytes, neutrophils releasing lysosomal enzymes increases in the surrounding tissues, and it leads to cleaning of the extraction socket from the damaged tissues and microorganisms. The growth factors are of great importance for reparative processes. The level of cytokines, chemokines and growth factors in biological fluids is the assessment criterium of various physiological and pathological processes and effectiveness of the treatment procedures. Purpose – to assess the activity of the wound healing processes by studying the level of cytokines/ chemokines and growth factors in the extraction socket. Materials and methods. The data received on examination of 40 patients was used in the study. 20 of the patients had their teeth extracted for chronic periodontitis and the socket healing was studied by clinical and laboratory findings (seven mediators of immunoregulatory processes were studied). The comparison group consisted of 20 subjects without periodontal pathology. Results. Clinical data, typical for the normal socket healing, are characterized by the certain content of immunoregulatory mediators (IL1β and IL6 – proinflammatory cytokines, IL8 and MCP1 – chemokines, RAIL1 – anti-inflammatory cytokine, VEGF and TGFβ1- growth factors). The content of proinflammatory cytokines and chemokines was detected to increase in the socket on the first day after the extraction, which indicates the activity of the local inflammatory process. The level of RAIL 1 and VEGF and TGFβ1 growth factors increases in the extraction socket five days later. Conclusion. The post-surgical activity of the inflammatory and regenerative processes in the tissues is revealed by the level of cytokines/ chemokines on the first day after surgery and the level of growth factors and RAIL1 in the socket discharge on the fifth day after surgery.


2021 ◽  
Vol 22 (13) ◽  
pp. 6921
Author(s):  
Norihisa Nishimura ◽  
Kosuke Kaji ◽  
Koh Kitagawa ◽  
Yasuhiko Sawada ◽  
Masanori Furukawa ◽  
...  

Recent studies have suggested that an alteration in the gut microbiota and their products, particularly endotoxins derived from Gram-negative bacteria, may play a major role in the pathogenesis of liver diseases. Gut dysbiosis caused by a high-fat diet and alcohol consumption induces increased intestinal permeability, which means higher translocation of bacteria and their products and components, including endotoxins, the so-called “leaky gut”. Clinical studies have found that plasma endotoxin levels are elevated in patients with chronic liver diseases, including alcoholic liver disease and nonalcoholic liver disease. A decrease in commensal nonpathogenic bacteria including Ruminococaceae and Lactobacillus and an overgrowth of pathogenic bacteria such as Bacteroidaceae and Enterobacteriaceae are observed in cirrhotic patients. The decreased diversity of the gut microbiota in cirrhotic patients before liver transplantation is also related to a higher incidence of post-transplant infections and cognitive impairment. The exposure to endotoxins activates macrophages via Toll-like receptor 4 (TLR4), leading to a greater production of proinflammatory cytokines and chemokines including tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8, which play key roles in the progression of liver diseases. TLR4 is a major receptor activated by the binding of endotoxins in macrophages, and its downstream signal induces proinflammatory cytokines. The expression of TLR4 is also observed in nonimmune cells in the liver, such as hepatic stellate cells, which play a crucial role in the progression of liver fibrosis that develops into hepatocarcinogenesis, suggesting the importance of the interaction between endotoxemia and TLR4 signaling as a target for preventing liver disease progression. In this review, we summarize the findings for the role of gut-derived endotoxemia underlying the progression of liver pathogenesis.


2000 ◽  
Vol 279 (3) ◽  
pp. R786-R792 ◽  
Author(s):  
Takeshi Kubota ◽  
Jidong Fang ◽  
Tetsuya Kushikata ◽  
James M. Krueger

Proinflammatory cytokines, including interleukin-1β and tumor necrosis factor-α are involved in physiological sleep regulation. Interleukin (IL)-13 and transforming growth factor (TGF)-β1 are anti-inflammatory cytokines that inhibit proinflammatory cytokines by several mechanisms. Therefore, we hypothesized that IL-13 and TGF-β1 could attenuate sleep in rabbits. Three doses of IL-13 (8, 40, and 200 ng) and TGF-β1 (40, 100, and 200 ng) were injected intracerebroventricularly 3 h after the beginning of the light period. In addition, one dose of IL-13 (200 ng) and one dose of TGF-β1 (200 ng) were injected at dark onset. The two higher doses of IL-13 and the highest dose of TGF-β1 significantly inhibited spontanenous non-rapid eye movement sleep (NREMS) when they were given in the light period. IL-13 also inhibited NREMS after dark onset administration; however, the inhibitory effect was less potent than that observed after light period administration. The 40-ng dose of IL-13 inhibited REMS duration during the dark period. TGF-β1 administered at dark onset had no effect on sleep. These data provide additional evidence for the hypothesis that a brain cytokine network is involved in regulation of physiological sleep.


2000 ◽  
Vol 113 (20) ◽  
pp. 3549-3550
Author(s):  
M.J. Townsend ◽  
A.N. McKenzie

The Cytokine Network edited by Fran Balkwill Frontiers in Molecular Biology Series (seried editors B. D. Hames and D. M. Glover) Oxford University Press (2000) pp. 199. ISBN 019–963-702-4. 29.95 Cytokines are small- to medium-sized proteins and glycoproteins that mediate highly potent biological effects on many cell types. They have critical roles in haematopoiesis, inflammatory responses and the development and maintenance of immune responses. Importantly, cytokines act in networks or cascades. Typical properties of cytokines in these networks are pleiotropy, redundancy, synergistic activity and antagonistic effects upon each other. Knowledge of how these networks are comprised and operate is important in understanding how cytokines mediate their diverse effects on biological systems. In The Cytokine Network, Fran Balkwill brings together some distinguished investigators to produce a survey, in eight independently written and concise chapters, of the complex cytokine and chemokine (chemotactic cytokine) networks present in mouse and man. The ever-increasing complexity of cytokine networks is introduced in the initial chapter with a summary of the bioinformatics approach for the high throughput discovery of novel cytokines and chemokines. The burgeoning number of newly identified chemokines, chemokine receptors and TNF family members reminds us that our understanding of the cytokine network is extremely dynamic and that our interpretation of some pathways will change with the characterisation of new factors. The following chapters address the interactions of the cytokines, both with reference to their signalling pathways (well summarised in chapter 2) and their biological roles. The point is made that cytokines should be studied as a network rather than individually and that in vivo models, including the generation of transgenic and gene knock-out mice, are powerful tools for doing so. Rheumatoid arthritis is presented as a well-studied example of how inappropriate regulation of pro- and anti-inflammatory cytokines mediates autoimmune disease, and examples of immunoregulatory cytokines that have both overlapping and independent regulatory effects on inflammation are demonstrated within this context. The important Th1/Th2 paradigm receives a dedicated chapter. T helper type 1 and T helper type 2 cells produce distinct and restricted patterns of cytokines that cross regulate each other and thus mediate different types of immune response. The development of these subsets of T helper cells from a common precursor, as part of a developing immune response, has important effects on the cytokine network. The mechanisms of Th1/Th2 development together with modulating factors and associated intracellular signalling are well described. The chapter summarises well the role of Th1/Th2 development in human diseases with reference to transplantation immunology, neonatal development, autoimmune diseases, and atopic diseases. A very interesting review of the relationships between cytokines and viruses is given. Cytokines are critically involved in mediating antiviral immune responses. However, homologues of cytokines, chemokines and their receptors, after being ‘hijacked’ from the host genome and undergoing evolution along with the viral genes, are utilised by viruses themselves to promote their replication and to suppress immune responses against them. The chapter describes several noteworthy examples of these virally encoded cytokines and receptors together with their roles in vivo. This is a well-written book that provides a good introduction to understanding how cytokines and chemokines interact as a network in the immune system. The volume links together diverse subjects that include cytokine signalling, genomic polymorphism, disease processes and immunotherapies. The book does not aim to describe comprehensively the biology of all the currently known cytokines and chemokines and therefore alternative texts should be considered for this. (ABSTRACT TRUNCATED)


2017 ◽  
Vol 130 (17) ◽  
pp. 2033-2040 ◽  
Author(s):  
Ting Yang ◽  
Yan Li ◽  
Zhe Lyu ◽  
Kewu Huang ◽  
Chris J Corrigan ◽  
...  

2002 ◽  
Vol 62 ◽  
pp. S12-S22 ◽  
Author(s):  
Marta Ruiz-Ortega ◽  
Mónica Ruperez ◽  
Oscar Lorenzo ◽  
Vanesa Esteban ◽  
Julia Blanco ◽  
...  

Author(s):  
Zahra Mousavi ◽  
Zinat Yazdani ◽  
Alireza Moradabadi ◽  
Fatemeh Hoseinpourkasgari ◽  
Gholamhossein Hassanshahi

Abstract The word of hemoglobinopathy is described for an array of disorders that affecting hemoglobin (Hb) functions. Hb is a molecule with 68 kDa molecular weight, serving as oxygen carrying metalloprotein. Hemoglobinopathy includes a wide range of Hb structural deficits varying from thalassemia to sickle cell disease. Cyto-chemokine network members are pivotally involved in the pathogenesis of hemoglobinopathies, however, the exact role of these mediators in the development of these disorders yet to be well addressed. Cytokines and chemokines are generated by inflamed endothelial cells that promote the expression of their respected receptors and further activate NF-κβ, recruit red blood cells (RBCs) and white blood cells (WBCs) toward the inflamed endothelium. Therefore, due to critical roles played by the cyto-chemokine network in several aspects of hemoglobinopathies pathophysiology including apoptosis of endothelial cells, RBC, WBC and etc.…, in the present review, we focused on the critical parts played by this network in the pathogenesis of hemoglobinopathies.


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