scholarly journals Antimonial Therapy Induces Circulating Proinflammatory Cytokines in Patients with Cutaneous Leishmaniasis

2002 ◽  
Vol 70 (12) ◽  
pp. 6589-6591 ◽  
Author(s):  
Abdurrahim Kocyigit ◽  
Selahaddin Gur ◽  
Mehmet S. Gurel ◽  
Vedat Bulut ◽  
Mustafa Ulukanligil
Keyword(s):  
Cutaneous Leishmaniasis ◽  
Host Defense ◽  
Proinflammatory Cytokines ◽  
Healthy Subjects ◽  
Necrosis Factor Alpha ◽  
Defense Strategies ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Host Defense System ◽  
Factor Alpha

ABSTRACT The objective of this study was to evaluate the association between antimonial therapy and circulating levels of proinflammatory cytokines in patients with cutaneous leishmaniasis (CL). Patients were treated with conventional chemotherapy by using pentavalent antimonium salts (Glucantime) for 3 weeks. Circulating plasma levels of the proinflammatory cytokines interleukin-1β (IL-1β), IL-6, IL-8, and tumor necrosis factor alpha (TNF-α) were determined for CL patients and healthy subjects before and 3 weeks after the treatment was started. Plasma IL-1β, IL-6, IL-8, and TNF-α levels were significantly higher for pretreatment CL patients than for healthy subjects. Proinflammatory cytokines significantly increased after 21 days postinfection compared to levels for the pretreatment patients. These increments were approximately 3-fold for IL-1β and TNF-α levels, 10-fold for IL-6 levels, and 20-fold for IL-8 levels in patients with CL. Taken together these results indicate that circulating proinflammatory cytokine levels were increased in patients with CL as a consequence of host defense strategies, and antimonial therapy may induce these cytokines by affecting the macrophage or other components of the host defense system.

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 Enzyme Degradation and Proinflammatory Activity in Arthritogenic and Nonarthritogenic Eubacterium aerofaciens Cell Walls

2001 ◽  
Vol 69 (12) ◽  
pp. 7277-7284 ◽  
Author(s):  
Xiang Zhang ◽  
Marja Rimpiläinen ◽  
Egle Šimelyte ◽  
Paavo Toivanen
Keyword(s):  
Proinflammatory Cytokines ◽  
Chronic Arthritis ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Enzyme Degradation ◽  
Tnf Α ◽  
Stimulatory Capacity ◽  
Normal Human ◽  
Proinflammatory Activity ◽  
Factor Alpha

ABSTRACT Two almost-identical strains of Eubacterium aerofaciens isolated from the normal human gut flora were used. The cell wall (CW) of one strain with a peptidoglycan (PG) type A4α induces chronic arthritis in the rat after a single intraperitoneal injection, whereas CW of the other with PG type A4β induces only a transient acute arthritis. The CW of the arthritogenic E. aerofaciens was a twofold-more-potent stimulator of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and monocyte chemoattractant protein 1 (MCP-1) than the nonarthritogenic CW. After degradation with mutanolysin, the capacity of the arthritogenic PG to stimulate production of TNF-α and MCP-1 was significantly increased, whereas that of the nonarthritogenic PG was significantly decreased. In other words, after enzyme degradation the arthritogenic PG had a four- to fivefold-stronger stimulatory capacity than that of the enzyme-treated nonarthritogenic PG. These findings indicate that the arthritogenicity of CW or a PG is not dependent on the enzyme resistance alone but also on how the PG fragments released by enzyme degradation stimulate the production of proinflammatory cytokines.

scholarly journals Salivary Cytokines and Airways Disease Severity in Patients with Cystic Fibrosis

Diagnostics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 222 ◽  
Author(s):  
Alice Castaldo ◽  
Paola Iacotucci ◽  
Vincenzo Carnovale ◽  
Roberta Cimino ◽  
Renato Liguori ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Lung Disease ◽  
Healthy Subjects ◽  
Inferior Turbinate ◽  
Lavage Fluid ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Inferior Turbinate Hypertrophy ◽  
Sinonasal Disease

About 50% of patients with cystic fibrosis (CF) have sinonasal complications, which include inferior turbinate hypertrophy (NTH) and/or nasal polyposis (NP), and different degrees of lung disease, which represents the main cause of mortality. Monitoring of sinonasal disease requires complex instrumental procedures, while monitoring of lung inflammation requires invasive collection of bronchoalveolar lavage fluid. The aim of this study was to investigate the associations between salivary cytokines levels and CF-related airway diseases. Salivary biochemical parameters and cytokines, i.e., interleukin-6 (IL-6), IL-8, and tumor necrosis factor alpha (TNF-α), were analyzed in resting saliva from healthy subjects and patients with CF. Patients with CF showed significantly higher levels of salivary chloride, IL-6, IL-8, and TNF-α and lower calcium levels than healthy subjects. Among patients with CF, IL-6 and IL-8 were significantly higher in patients with NTH, while TNF-α was significantly lower in patients with NP. A decreasing trend of TNF-α in patients with severe lung disease was also observed. On the other hand, we did not find significant correlation between cytokine levels and Pseudomonas aeruginosa or Stenotrophomonas maltophilia colonization. These preliminary results suggest that salivary IL-6 and IL-8 levels increase during the acute phase of sinonasal disease (i.e., NTH), while the end stages of pulmonary disease and sinonasal disease (i.e., NP) show decreased TNF-α levels.

scholarly journals Febrile Core Temperature Is Essential for Optimal Host Defense in Bacterial Peritonitis

2000 ◽  
Vol 68 (3) ◽  
pp. 1265-1270 ◽  
Author(s):  
Qinqqi Jiang ◽  
Alan S. Cross ◽  
Ishwar S. Singh ◽  
T. Timothy Chen ◽  
Rose M. Viscardi ◽  
...  
Keyword(s):  
Core Temperature ◽  
Host Defense ◽  
Bacterial Infections ◽  
Bacterial Load ◽  
Cytokine Expression ◽  
Microbial Pathogens ◽  
Necrosis Factor Alpha ◽  
Bacterial Peritonitis ◽  
Tnf Α ◽  
Factor Alpha

ABSTRACT Fever, a nonspecific acute-phase response, has been associated with improved survival and shortened disease duration in infections, but the mechanisms of these beneficial responses are poorly understood. We previously reported that increasing core temperature of bacterial endotoxin (LPS)-challenged mice to the normal febrile range modified expression of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), and IL-6, three cytokines critical to mounting an initial defense against microbial pathogens, but survival was not improved in the warmer animals. We speculated that our inability to show a survival benefit of optimized cytokine expression in the warmer animals reflected our use of LPS, a nonreplicating agonist, rather than an infection with viable pathogens. The objective of this study was to determine if increasing murine core temperature altered cytokine expression and improved survival in an experimental bacterial peritonitis model. We showed that housing mice at 35.5°C rather than 23°C increased core temperature from 36.5 to 37.5°C to 39.2 to 39.7°C, suppressed plasma TNF-α expression for the initial 48 h, delayed gamma interferon expression, improved survival, and reduced the bacterial load in mice infected with Klebsiella pneumoniae peritonitis. We showed that the reduced bacterial load was not caused by a direct effect on bacterial proliferation and probably reflected enhanced host defense. These data suggest that the increase in core temperature that occurs during bacterial infections is essential for optimal antimicrobial host defense.

scholarly journals NK Cells Mediate Increase of Phagocytic Activity but Not of Proinflammatory Cytokine (Interleukin-6 [IL-6], Tumor Necrosis Factor Alpha, and IL-12) Production Elicited in Splenic Macrophages by Tilorone Treatment of Mice during Acute Systemic Candidiasis

2002 ◽  
Vol 9 (6) ◽  
pp. 1282-1294 ◽  
Author(s):  
José Juan Gaforio ◽  
Elena Ortega ◽  
Ignacio Algarra ◽  
María José Serrano ◽  
Gerardo Alvarez de Cienfuegos
Keyword(s):  
Nk Cells ◽  
Mhc Class Ii ◽  
Proinflammatory Cytokines ◽  
Tumor Necrosis ◽  
Systemic Candidiasis ◽  
Necrosis Factor Alpha ◽  
Splenic Macrophages ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The participation of NK cells in the activation of splenic macrophages or in resistance to systemic candidiasis is still a matter of debate. We had previously reported that there is a correlation between natural killer cell activation and resistance to systemic candidiasis. In those experiments we had used tilorone to boost NK cell activity in mice. Here we show a mechanism elicited by tilorone in splenic macrophages which could explain their effect on mouse survival during acute disseminated Candida albicans infection. The results demonstrate that tilorone treatment elicits, by a direct effect, the production of proinflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor alpha [TNF-α], and IL-12) by splenic macrophages. In addition, it increases the capacity of splenic macrophages to phagocytize C. albicans through activation of NK cells. We also demonstrate that the presence of NK cells is essential for maintaining a basal level of phagocytic activity, which characterizes splenic macrophages of naïve control mice. The results demonstrate that it is possible to identify two phenotypically and functionally peculiar cell populations among splenic macrophages: (i) cells of the “stimulator/secretor phenotype,” which show high levels of major histocompatibility complex (MHC) class II surface expression, are poorly phagocytic, and synthesize the proinflammatory cytokines IL-6, TNF-α, and IL-12, and (ii) cells of the “phagocytic phenotype,” which express low levels of MHC class II molecules, are highly phagocytic, and do not secrete proinflammatory cytokines.

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 Tumor Necrosis Factor Alpha Transcription in Macrophages Is Attenuated by an Autocrine Factor That Preferentially Induces NF-κB p50

1998 ◽  
Vol 18 (10) ◽  
pp. 5678-5689 ◽  
Author(s):  
Mark Baer ◽  
Allan Dillner ◽  
Richard C. Schwartz ◽  
Constance Sedon ◽  
Sergei Nedospasov ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Proinflammatory Cytokines ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Tumor Cell Line ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Macrophages are a major source of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α), which are expressed during conditions of inflammation, infection, or injury. We identified an activity secreted by a macrophage tumor cell line that negatively regulates bacterial lipopolysaccharide (LPS)-induced expression of TNF-α. This activity, termed TNF-α-inhibiting factor (TIF), suppressed the induction of TNF-α expression in macrophages, whereas induction of three other proinflammatory cytokines (interleukin-1β [IL-1β], IL-6, and monocyte chemoattractant protein 1) was accelerated or enhanced. A similar or identical inhibitory activity was secreted by IC-21 macrophages following LPS stimulation. Inhibition of TNF-α expression by macrophage conditioned medium was associated with selective induction of the NF-κB p50 subunit. Hyperinduction of p50 occurred with delayed kinetics in LPS-stimulated macrophages but not in fibroblasts. Overexpression of p50 blocked LPS-induced transcription from a TNF-α promoter reporter construct, showing that this transcription factor is an inhibitor of the TNF-α gene. Repression of the TNF-α promoter by TIF required a distal region that includes three NF-κB binding sites with preferential affinity for p50 homodimers. Thus, the selective repression of the TNF-α promoter by TIF may be explained by the specific binding of inhibitory p50 homodimers. We propose that TIF serves as a negative autocrine signal to attenuate TNF-α expression in activated macrophages. TIF is distinct from the known TNF-α-inhibiting factors IL-4, IL-10, and transforming growth factor β and may represent a novel cytokine.

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.

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.

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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