Effects of Sulfur Mustard on Cytokines Released from Cultured Human Epidermal Keratinocytes

1998 ◽  
Vol 17 (3) ◽  
pp. 223-229 ◽  
Author(s):  
Elien M. Kurt ◽  
Robert J. Schafer ◽  
Carmen M. Arroyo
Keyword(s):  
Sulfur Mustard ◽  
Cell Types ◽  
Epidermal Keratinocytes ◽  
Cytokine Release ◽  
Experimental Conditions ◽  
Human Epidermal Keratinocytes ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Factor Alpha

The release of the cytokines interleukin (IL)-1α, IL-1β, IL-6, IL-8, and tumor necrosis factor alpha (TNF-α was measured from epiderm alkeratinocytes in an attempt to characterize the immunologic response in keratinocytes following exposure to bis (2-chloroethyl)sulfide (sulfur mustard, HD). Enzyme-linked immunosorbentassay (ELISA) was used to measure cytokine levels in adult and neonatal culture human epidermal keratinocytes (HEK) 3 h after exposure to 0.50 and 1.0 m M HD. A two-way analysis of variance was carried out for cell type and HD concentration. That analysis showed significant differences between cell types for IL-1α and IL-1β(p =.001 and p =.015, respectively). In both of these cytokines, release in neonatal HEK decreased less than in adult HEK. A significant effectof HD concentration was shown only for IL-1β (P <.001), with cytokine release decreasing with increasing HD dose. In addition, a significant cell donor type by HD concentration interaction effect was found for IL-1β under the experimental conditions described in materials and methods. With increasing HD concentration, the relative decrease in cytokine release was much greater for adult than for neonatal HEK.

scholarly journals Interleukin-8 and Tumor Necrosis Factor Alpha Production in Human Epidermal Keratinocytes Induced by Trichophyton mentagrophytes

2002 ◽  
Vol 9 (4) ◽  
pp. 935-937 ◽  
Author(s):  
Yuka Nakamura ◽  
Rui Kano ◽  
Atsuhiko Hasegawa ◽  
Shinichi Watanabe
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Trichophyton Mentagrophytes ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Production of interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-α) was confirmed by enzyme-linked immunosorbent assay in a medium where human epidermal keratinocytes were cocultured with Trichophyton mentagrophytes for 1 to 12 h. IL-8 and TNF-α mRNAs were also detected in the keratinocytes cocultured with T. mentagrophytes.

scholarly journals Tetracyclines Modulate Protease-Activated Receptor 2-Mediated Proinflammatory Reactions in Epidermal Keratinocytes

2009 ◽  
Vol 53 (5) ◽  
pp. 1760-1765 ◽  
Author(s):  
Chika Ishikawa ◽  
Tatsuya Tsuda ◽  
Hiroe Konishi ◽  
Noboru Nakagawa ◽  
Kiyofumi Yamanishi
Keyword(s):  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Proinflammatory Responses ◽  
Normal Human ◽  
Factor Alpha ◽  
Anti Inflammatory ◽  
Protease Activated Receptor 2 ◽  
Interfering Rna

ABSTRACT In addition to their antibiotic effects, tetracyclines have anti-inflammatory action that is often beneficial in the control of inflammatory skin disorders. In this study, we examined the effects of tetracycline (TET) and two of its derivatives, doxycycline (DOX) and minocycline (MIN), on the production of interleukin-8 (IL-8) elicited by the activation of protease-activated receptor 2 (PAR2) in normal human epidermal keratinocytes (NHEK). In NHEK, the production of IL-8 stimulated by an agonist peptide of PAR2, SLIGKIV-NH2, at 100 μM was significantly reduced by TET, DOX, or MIN at 5 and 10 μM, concentrations that are noncytotoxic. The tumor necrosis factor alpha (TNF-α)-induced production of IL-8 was synergistically augmented by SLIGKIV-NH2, and that synergistic increase in the production of IL-8 was suppressed by 100 nM PAR2-specific small interfering RNA. It was also suppressed by TET, DOX, or MIN but not by the 14-membered-ring macrolide antibiotics erythromycin, roxithromycin, and clarithromycin, which also have anti-inflammatory activities, at 10 μM. These results suggest that tetracyclines attenuate the PAR2-IL-8 axis in keratinocytes and thereby effectively modulate proinflammatory responses in the skin.

The role of interleukins in the ovary

1996 ◽  
Vol 5 (1) ◽  
pp. 51-63 ◽  
Author(s):  
C Simón ◽  
A Tsafriri ◽  
A Pellicer ◽  
ML Polan
Keyword(s):  
Cell Types ◽  
Necrosis Factor Alpha ◽  
Communication Signals ◽  
Ability To Act ◽  
Tnf Α ◽  
History Of ◽  
Specific Antigens ◽  
Factor Alpha ◽  
Different Populations

A brief look at the history of cytokine research shows that the term ‘lymphokine’ was first described in 1969 as the product of sensitized lymphocytes exposed to specific antigens. To eliminate the incorrect notion that such proteins can be produced only by lymphocytes, Cohenet al.(1974) proposed the term ‘cytokines’ to indicate their production also by nonlymphoid cells.2After a long-persisting reluctance, it seems that ‘cytokine’ is becoming the prevalent term for these proteins. Meanwhile, a group of participants at the Second International Lymphokine Workshop held in 1979 proposed the term ‘interleukin’ in order to develop, ‘a system of nomenclature based on the protein's ability to act as communication signals between different populations of leukocytes’.3They introduced the names IL-I and IL-2 for two important cytokines. Since then the number of described interleukins reached 16 and this number may increase. Furthermore, notwithstanding this previous notion, interleukins are now known to be produced in a variety of tissues other than leucocytes and affect the functions of many and diverse somatic cell types (e.g. IL-1 or IL-6). Therefore, while many cytokines are now termed as interleukins, others continue to be known by their old names [e.g. tumour necrosis factor-alpha (TNF-α)], suggesting that they had been recognized earlier, but all of them are included under the generic name of cytokines.

scholarly journals Interaction of Neisseria meningitidis with Human Dendritic Cells

2001 ◽  
Vol 69 (11) ◽  
pp. 6912-6922 ◽  
Author(s):  
Annette Kolb-Mäurer ◽  
Alexandra Unkmeir ◽  
Ulrike Kämmerer ◽  
Claudia Hübner ◽  
Thomas Leimbach ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Neisseria Meningitidis ◽  
Proinflammatory Cytokines ◽  
Interleukin 1 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Factor Alpha ◽  
Human Dendritic Cells ◽  
Necrosis Factor

ABSTRACT Infection with Neisseria meningitidis serogroup B is responsible for fatal septicemia and meningococcal meningitis. The severity of disease directly correlates with the production of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), IL-6, and IL-8. However, the source of these cytokines has not been clearly defined yet. Since bacterial infection involves the activation of dendritic cells (DCs), we analyzed the interaction of N. meningitidis with monocyte-derived DCs. Using N. meningitidis serogroup B wild-type and unencapsulated bacteria, we found that capsule expression significantly impaired neisserial adherence to DCs. In addition, phagocytic killing of the bacteria in the phagosome is reduced by at least 10- to 100-fold. However, all strains induced strong secretion of proinflammatory cytokines TNF-α, IL-6, and IL-8 by DCs (at least 1,000-fold at 20 h postinfection [p.i.]), with significantly increased cytokine levels being measurable by as early as 6 h p.i. Levels of IL-1β, in contrast, were increased only 200- to 400-fold at 20 h p.i. with barely measurable induction at 6 h p.i. Moreover, comparable amounts of cytokines were induced by bacterium-free supernatants of Neisseria cultures containing neisserial lipooligosaccharide as the main factor. Our data suggest that activated DCs may be a significant source of high levels of proinflammatory cytokines in neisserial infection and thereby may contribute to the pathology of meningococcal disease.

scholarly journals DYNAMICS OF CYTOKINS AND THEIR INTERRELATION IN LIVER CIRRHOSIS

2015 ◽  
Vol 7 (1) ◽  
pp. 110-114
Author(s):  
B B Fishman ◽  
M A Toneeva ◽  
V E Kulikov ◽  
V A Kornilova ◽  
E R Antonova
Keyword(s):  
Liver Cirrhosis ◽  
Reference Values ◽  
Average Concentration ◽  
Necrosis Factor Alpha ◽  
Class A ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Class B ◽  
Factor Alpha ◽  
Necrosis Factor

The research objectives are to determine serum interleukins (IL-2, IL-6) and tumor necrosis factor alpha (TNF - α) and evaluate their interrelation in liver cirrhosis (class A, B, C according to Chad - Pugh). 117 patients were examined and their cytokines levels were determined using enzyme-linked immunosorbent assay.Elevation of cytokine levels IL-2, I-6 and TNF-α within reference values was found in liver cirrhosis cases, expect for level IL-6 in liver cirrhosis cases of class C. In these cases IL-6 level exceeds reference values and is within the limit of 9,94 - 25,21 pg / ml with average concentration of 14,89±4,96 pg / ml. Correlation is found between TNF- α and IL-6 (r = - 0,499) in liver cirrhosis of class A and correlation between TNF- α and IL-2 (r = 0,421) is found in liver cirrhosis of class B.

scholarly journals Borrelia burgdorferiSpirochetes Induce Mast Cell Activation and Cytokine Release

1999 ◽  
Vol 67 (3) ◽  
pp. 1107-1115 ◽  
Author(s):  
Jeffrey Talkington ◽  
Steven P. Nickell
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Activation ◽  
Cell Types ◽  
Host Cells ◽  
Mast Cell Activation ◽  
Cytokine Release ◽  
Necrosis Factor Alpha ◽  
Tnf Α

ABSTRACT The Lyme disease spirochete, Borrelia burgdorferi, is introduced into human hosts via tick bites. Among the cell types present in the skin which may initially contact spirochetes are mast cells. Since spirochetes are known to activate a variety of cell types in vitro, we tested whether B. burgdorferi spirochetes could activate mast cells. We report here that freshly isolated rat peritoneal mast cells or mouse MC/9 mast cells cultured in vitro with live or freeze-thawed B. burgdorferi spirochetes undergo low but detectable degranulation, as measured by [5-3H] hydroxytryptamine release, and they synthesize and secrete the proinflammatory cytokine tumor necrosis factor alpha (TNF-α). In contrast to findings in previous studies, where B. burgdorferi-associated activity was shown to be dependent upon protein lipidation, mast cell TNF-α release was not induced by either lipidated or unlipidated recombinant OspA. This activity was additionally shown to be protease sensitive and surface expressed. Finally, comparisons of TNF-α-inducing activity in known low-, intermediate-, and high-passage B. burgdorferi B31 isolates demonstrated passage-dependent loss of activity, indicating that the activity is probably plasmid encoded. These findings document the presence in low-passage B. burgdorferi spirochetes of a novel lipidation-independent activity capable of inducing cytokine release from host cells.

scholarly journals A Low Concentration of Ethanol Reduces the Chemiluminescence of Human Granulocytes and Monocytes but Not the Tumor Necrosis Factor Alpha Production by Monocytes after Endotoxin Stimulation

1998 ◽  
Vol 66 (6) ◽  
pp. 2809-2813 ◽  
Author(s):  
Alexandr Parlesak ◽  
Jens P. Diedrich ◽  
Christian Schäfer ◽  
Christiane Bode
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Cell Types ◽  
Polymorphonuclear Neutrophils ◽  
Alcohol Abusers ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The ability of polymorphonuclear neutrophils (PMNs) and monocytes (Mφ) to produce reactive oxygen species (ROS) has been related closely to their potential in the killing of microorganisms. Ethanol has been shown to impair the generation of ROS in these phagocytes after stimulation with some immunogens and to increase the susceptibility of alcohol abusers to infectious diseases. As endotoxemia is common in alcohol abusers, we investigated the effect of ethanol (21.7 mmol/liter) on the luminol-amplified chemiluminescence of PMNs and Mφ after endotoxin stimulation and the release of tumor necrosis factor alpha (TNF-α) from Mφ. Further, the efficiency of ethanol to inactivate chemically generated ROS was tested. Significant stimulation of ROS release occurred at endotoxin concentrations of 1 ng/ml or higher in both PMNs and Mφ. Ethanol significantly suppressed the formation of ROS in both cell types, the decrease being more pronounced in Mφ (−73.8%) than in PMNs (−45.7%). The correlations between endotoxin concentration and the amount of released ROS showed a dose-dependent, sigmoidal course. Concentrations of endotoxin necessary for half-maximum stimulation were nearly identical (6 to 8 ng/ml) in both PMNs and Mφ, independent of the presence of ethanol. In contrast to ROS formation, ethanol had no effect on the amount of TNF-α produced by endotoxin-stimulated Mφ. Ethanol was shown to be unable to decrease the levels of chemically generated ROS under physiological conditions. Therefore, ethanol cannot be assumed to be an “antioxidative” compound but rather seems to modify processes of endotoxin recognition, intracellular signal transduction, or metabolism.

Triterpenoid CDDO-IM protects against lipopolysaccharide-induced inflammatory response and cytotoxicity in macrophages: The involvement of the NF-κB signaling pathway

2022 ◽  
pp. 153537022110669
Author(s):  
Hassan Ahmed ◽  
Urooj Amin ◽  
Xiaolun Sun ◽  
Demetrius R Pitts ◽  
Yunbo Li ◽  
...  
Keyword(s):  
Septic Shock ◽  
Inflammatory Cytokine ◽  
Interleukin 1 ◽  
Severe Form ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Factor Alpha ◽  
Gene Expression Levels

Lipopolysaccharide (LPS), also known as endotoxin, can trigger septic shock, a severe form of inflammation-mediated sepsis with a very high mortality rate. However, the precise mechanisms underlying this endotoxin remain to be defined and detoxification of LPS is yet to be established. Macrophages, a type of immune cells, initiate a key response responsible for the cascade of events leading to the surge in inflammatory cytokines and immunopathology of septic shock. This study was undertaken to determine whether the LPS-induced inflammation in macrophage cells could be ameliorated via CDDO-IM (2-cyano-3,12 dioxooleana-1,9 dien-28-oyl imidazoline), a novel triterpenoid compound. Data from this study show that gene expression levels of inflammatory cytokine genes such as interleukin-1 beta (IL-1β), interleukin-8 (IL-8), tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) were considerably increased by treatment with LPS in macrophages differentiated from ML-1 monocytes. Interestingly, LPS-induced increase in expression of pro-inflammatory cytokine levels is reduced by CDDO-IM. In addition, endogenous upregulation of a series of antioxidant molecules by CDDO-IM provided protection against LPS-induced cytotoxicity in macrophages. LPS-mediated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) transcriptional activity was also noted to decrease upon treatment with CDDO-IM in macrophages suggesting the involvement of the NF-κB signaling. This study would contribute to improve our understanding of the detoxification of endotoxin LPS by the triterpenoid CDDO-IM.

Modulation of sulfur mustard induced cell death in human epidermal keratinocytes using IL-10 and TNF-α

2005 ◽  
Vol 19 (4) ◽  
pp. 213-225 ◽  
Author(s):  
Aziz Qabar ◽  
Marian Nelson ◽  
Juanita Guzman ◽  
Charlene Corun ◽  
Bor-Jang Hwang ◽  
...  
Keyword(s):  
Cell Death ◽  
Sulfur Mustard ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Tnf Α

scholarly journals Ultra-purified alginate gel implantation decreases inflammatory cytokine levels, prevents intervertebral disc degeneration, and reduces acute pain after discectomy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Katsuro Ura ◽  
Katsuhisa Yamada ◽  
Takeru Tsujimoto ◽  
Daisuke Ukeba ◽  
Norimasa Iwasaki ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Sensory Nerve ◽  
Key Factors ◽  
Lumbar Intervertebral Disc ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Low Toxicity ◽  
Factor Alpha ◽  
Ivd Degeneration

AbstractLumbar intervertebral disc (IVD) herniation causes severe low back pain (LBP), which results in substantial financial and emotional strains. Despite the effectiveness of discectomy, there is no existing treatment for post-operative LBP induced by progressive IVD degeneration. Two key factors of LBP are intradiscal inflammation, indicated by tumour necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), and sensory nerve ingrowth into the inner layer of the annulus fibrosus, triggered by nerve growth factor/high-affinity tyrosine kinase A (TrkA) signalling. In an animal models of discectomy, the bioresorbable ultra-purified alginate (UPAL) gel with an extremely low-toxicity has been effective in acellular tissue repair. We aimed to investigate whether UPAL gel can alleviate LBP using a rat nucleus pulposus (NP) punch model and a rabbit NP aspirate model. In both models, we assessed TNF-α and IL-6 production and TrkA expression within the IVD by immunohistochemistry. Further, histological analysis and behavioural nociception assay were conducted in the rat model. UPAL gel implantation suppressed TNF-α and IL-6 production, downregulated TrkA expression, inhibited IVD degeneration, and reduced nociceptive behaviour. Our results suggest the potential of UPAL gel implantation as an innovative treatment for IVD herniation by reducing LBP and preventing IVD degeneration after discectomy.

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