Intracytoplasmic Detection of Proinflammatory Cytokines and Chemokines in Monocytes by Flow Cytometry

2003 ◽  
pp. 29-39 ◽  
Author(s):  
Christian Schultz
Keyword(s):  
Flow Cytometry ◽  
Proinflammatory Cytokines ◽  
Cytokines And Chemokines

scholarly journals Intestinal Permeability Is a Mechanical Rheostat in the Pathogenesis of Liver Cirrhosis

2021 ◽  
Vol 22 (13) ◽  
pp. 6921
Author(s):  
Norihisa Nishimura ◽  
Kosuke Kaji ◽  
Koh Kitagawa ◽  
Yasuhiko Sawada ◽  
Masanori Furukawa ◽  
...  
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Intestinal Permeability ◽  
Proinflammatory Cytokines ◽  
Liver Diseases ◽  
Pathogenic Bacteria ◽  
Necrosis Factor Alpha ◽  
Cytokines And Chemokines ◽  
Liver Disease Progression ◽  
Cirrhotic Patients

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.

The effect of a leukodepletion model on the activation stage of platelets

Open Medicine ◽  
2011 ◽  
Vol 6 (2) ◽  
pp. 181-184
Author(s):  
Miodrag Vucic ◽  
Ivan Tijanic ◽  
Nenad Govedarevic ◽  
Lana Macukanovic ◽  
Zoran Pavlovic
Keyword(s):  
Flow Cytometry ◽  
Proinflammatory Cytokines ◽  
Mononuclear Cells ◽  
Buffy Coat ◽  
The Other ◽  
Therapeutic Doses ◽  
Cell Counter ◽  
Automatic Cell Counter

AbstractThe preparation of thrombocyte concentrates with filtration before storage (in-line) makes it possible to avoid the presence of mononuclear cells in the concentrate and proinflammatory cytokines. Therefore, this filtration may result with decreased activation of trombocyte receptors in vitro, which may improve therapeutic efficiancy. Methods. We compared two groups, each with 30 therapeutic doses of concentrated thrombocytes. We prepared the first group using the classic model from the buffy coat and the other with concentrated thrombocyte samples filtrated during sampling, so-called in-line, with the WBC filter Imuflex (Terumo). Mononuclear cells (MNC), thrombocyte, and erythrocyte counts in the units of concentrated thrombocytes were obtained on an automatic cell counter, and we used flow cytometry to measure the expression of surface thrombocyte receptors. The results demonstrated that the trombocytes prepared with pre-storage filtration contained a very low level of mononuclear cells and markedly reduced trombocyte receptors. Conclusion. The number of MNC and expression of surface thrombocyte receptors were markedly lower in the concentrated thrombocyte units prepared with in-line filtration. The thrombocytes prepared in this way contain fewer mononuclear cells, are of higher quality, are more functional, and may produce a better therapeutic effect in vivo.

scholarly journals Characteristics of Proinflammatory Cytokines and Chemokines in Airways of Asthmatics

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

scholarly journals Angiotensin II regulates the synthesis of proinflammatory cytokines and chemokines in the kidney

2002 ◽  
Vol 62 ◽  
pp. S12-S22 ◽  
Author(s):  
Marta Ruiz-Ortega ◽  
Mónica Ruperez ◽  
Oscar Lorenzo ◽  
Vanesa Esteban ◽  
Julia Blanco ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Proinflammatory Cytokines ◽  
Cytokines And Chemokines

scholarly journals Campylobacter jejuni-Induced Cytokine Responses in Avian Cells

2005 ◽  
Vol 73 (4) ◽  
pp. 2094-2100 ◽  
Author(s):  
Chris K. Smith ◽  
Pete Kaiser ◽  
Lisa Rothwell ◽  
Tom Humphrey ◽  
Paul A. Barrow ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Proinflammatory Cytokines ◽  
Disease Process ◽  
Avian Host ◽  
Macrophage Cell ◽  
Proinflammatory Response ◽  
Cytokines And Chemokines ◽  
Cytokine Responses ◽  
Chick Kidney

ABSTRACT Campylobacter jejuni is a major cause of human inflammatory enteritis. During the course of human disease numerous proinflammatory cytokines are produced. Little is known, however, about the cytokine responses produced during the interaction of this bacterium with the avian host. Campylobacter has been considered a commensal of the avian host. Any differences in innate responses to this pathogen between the human and avian hosts should lead to a greater understanding of the disease process in humans. We have demonstrated expression of proinflammatory cytokines and chemokines in response to Campylobacter infection in avian primary chick kidney cells and the avian macrophage cell line HD11. The data indicate that Campylobacter can stimulate the avian host in a proinflammatory manner. The data strongly suggest that the lack of pathology in vivo is not due to an inability of Campylobacter to stimulate a proinflammatory response from avian cells.

scholarly journals Pseudomonas aeruginosa Exoenzyme S Induces Transcriptional Expression of Proinflammatory Cytokines and Chemokines

2000 ◽  
Vol 68 (8) ◽  
pp. 4811-4814 ◽  
Author(s):  
Slava Epelman ◽  
Tony F. Bruno ◽  
Graham G. Neely ◽  
Donald E. Woods ◽  
Christopher H. Mody
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Proinflammatory Cytokines ◽  
Pulmonary Inflammation ◽  
Lung Damage ◽  
Gene Probe ◽  
Necrosis Factor Alpha ◽  
Exoenzyme S ◽  
Cytokines And Chemokines ◽  
Immunoregulatory Cytokines

ABSTRACT Pseudomonas aeruginosa infection of cystic fibrosis patients causes lung damage that is substantially orchestrated by cytokines. In this study, multi-gene probe analysis was used to characterize the ability of the P. aeruginosamitogen, exoenzyme S, to induce proinflammatory and immunoregulatory cytokines and chemokines. Exoenzyme S strongly induced transcription of proinflammatory cytokines and chemokines (tumor necrosis factor alpha, interleukin-1α [IL-1α], IL-1β, IL-6, IL-8, MIP-1α, MIP-1β, MCP-1, RANTES, and I-309), modest transcription of immunoregulatory cytokines (IL-10 and IL-12p40), and weak transcription of Th1 cytokines (IL-2 and gamma interferon). The response occurred early and subsided without evolving over time. These data suggest that cells responding to exoenzyme S would rapidly express proinflammatory cytokines and chemokines that may contribute to pulmonary inflammation in cystic fibrosis.

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