scholarly journals Comparative Study on Pulmonary Toxicity in Mice Induced by Exposure to Unflavoured and Apple- and Strawberry-Flavoured Tobacco Waterpipe Smoke

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Badreldin H. Ali
Keyword(s):  
Pulmonary Toxicity ◽  
Nuclear Factor Kappa B ◽  
Caspase 3 ◽  
Inflammatory Cells ◽  
Airway Hyperreactivity ◽  
Histological Evaluation ◽  
Air Exposure ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

The use of flavoured tobacco products in waterpipe smoking (WPS) has increased its attractiveness and consumption. Nonetheless, the influence of flavourings on pulmonary toxicity caused by WPS remains unclear. Here, the pulmonary toxicity induced by plain (P)-WPS, apple-flavoured (AF)-WPS, and strawberry-flavoured (SF)-WPS (30 minutes/day, 5 days/week for 1 month) was investigated in mice. Control mice were exposed to air. Exposure to P-WPS or AF-WPS or SF-WPS induced a dose-dependent increase of airway hyperreactivity to methacholine. The histological evaluation of the lungs in all the WPS groups revealed the presence focal areas of dilated alveolar spaces and foci of widening of interalveolar spaces with inflammatory cells. In the lung, the activity of neutrophil elastase and myeloperoxidase and the concentrations of tumor necrosis factor-α and glutathione were increased by the exposure to P-WPS, AF-WPS, or SF-WPS. However, the levels of interleukin-6 and catalase were only increased in the AF-WPS and SF-WPS groups, while nitric oxide activity was only increased in the SF-WPS group. DNA injury was increased in all the WPS groups, but the concentration of cleaved caspase-3 was only elevated in the SF-WPS group. The exposure to either P-WPS or AF-WPS or SF-WPS increased the expression of nuclear factor kappa-B (NF-κB) in the lung. In conclusion, the exposure to P-WPS or AF-WPS or SF-WPS induces alterations in lung function and morphology and causes oxidative stress and inflammation via mechanisms that include activation of NF-κB. Overall, the toxicity of flavoured tobacco WPS, in particular SF-WPS, was found to be greater than that of unflavoured WPS.

scholarly journals Elevated Plasma Level of Interferon-λ1 in Chronic Spontaneous Urticaria: Upregulated Expression in CD8+and Epithelial Cells and Induction of Inflammatory Cell Accumulation

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
S. F. Wang ◽  
X. Q. Gao ◽  
Y. N. Xu ◽  
D. N. Li ◽  
H. Y. Wang ◽  
...  
Keyword(s):  
Mast Cells ◽  
Inflammatory Cell ◽  
Inflammatory Cells ◽  
Chronic Spontaneous Urticaria ◽  
Intercellular Adhesion Molecule ◽  
Double Labeling ◽  
Cell Accumulation ◽  
Healthy Control ◽  
Dose Dependent Increase ◽  
Dose Dependent

Interferon- (IFN-)λ1 is regarded as a potent bio-active molecule in innate immunity. However, little is known about its role in chronic spontaneous urticaria (CSU). We therefore investigated expression of IFN-λ1 in CSU, its cellular location, and its influence on inflammatory cell accumulation by using flow cytometry analysis, skin tissue dispersion, immunohistochemical stain, and a mouse peritoneal inflammation model. The results showed that level of IFN-λ1 was 2.0-fold higher in plasma of the patients with CSU than the level in healthy control (HC) subjects. Among leukocytes examined, only CD8+T cells expressed more IFN-λ1 in CSU blood. Double labeling immunohistochemical staining revealed that IFN-λ1+inflammatory cells such as mast cells, eosinophils, B cells, neutrophils, and macrophages were mainly located in dermis, whereas epidermis tissue highly expressed IFN-λ1. IFN-λ1 induced a dose-dependent increase in number of eosinophils, lymphocytes, mast cells, macrophages, and neutrophils in the peritoneum of mice at 6 h following injection, which was inhibited by pretreatment of the animals with anti-intercellular adhesion molecule- (ICAM-) 1 and/or anti-L-selectin antibodies. In conclusion, IFN-λ1 is likely to play a role in the pathogenesis of CSU. Blocking IFN-λ1 production may help to reduce the accumulation of inflammatory cells in the involved CSU skin.

scholarly journals Anti-Atopic Dermatitis Effect of Seaweed Fulvescens Extract via Inhibiting the STAT1 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Tae-Young Gil ◽  
Yun-Mi Kang ◽  
Ye-Jin Eom ◽  
Chul-Hee Hong ◽  
Hyo-Jin An
Keyword(s):  
Atopic Dermatitis ◽  
Proinflammatory Cytokines ◽  
Inflammatory Cells ◽  
Control Group ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Hacat Keratinocytes ◽  
Cellular Inflammation ◽  
Dose Dependent ◽  
Necrosis Factor

Seaweed fulvescens (SF) is a green alga rich in chlorophyll with unique flavor and taste. It is also called Maesaengi which has antioxidant and other physiological activities. In the present study, we evaluated the therapeutic effects of SF in a mouse model of Dermatophagoides farinae body-induced atopic dermatitis (AD) and in tumor necrosis factor-α and interferon-γ-stimulated HaCaT keratinocytes. SF treatment (200 mg/mouse) inhibited the development of AD symptoms, compared to that in the control group, as evidenced from the improved dorsal skin lesion, reduced thickness and infiltration of inflammatory cells and smaller lymph nodes, and reduced levels of proinflammatory cytokines. In HaCaT keratinocytes, SF (10, 25, and 50 μg/mL) suppressed the production of proinflammatory cytokines in a dose-dependent manner. In addition, SF reduced the phosphorylation of signal transducer and activator of transcription 1, which is one of the major signaling molecules involved in cellular inflammation. These results suggested that SF could be a potential therapeutic alternative for the treatment of AD.

Effect of Tumor Necrosis Factor-α on in vitro Prostaglandin Production in Buffalo Corpus Luteum

2021 ◽  
Author(s):  
M.K. Tripathi ◽  
S. Mondal ◽  
I.J. Reddy ◽  
A. Mor
Keyword(s):  
Mrna Expression ◽  
Corpus Luteum ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Important Regulator ◽  
Factor Α ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

Background: Corpus luteum plays key role in embryonic survival. Prostaglandins are the important regulator controlling the life span of corpus luteum. The present study investigated the effect of various doses of TNFα on in vitro PGF2α and PGE2 production and expression profiling of PGFS and PGES mRNA in buffalo Corpus Luteum (CL).Methods: Buffalo ovaries with mid-luteal phase CL were collected from the abattoir and CL were enucleated from surrounding tissues. Corpus luteum were finely chopped, rinsed with HBSS (Hanks Balanced Salt Solution) medium; supplemented with gentamycin and 0.1% BSA and incubated at 37°C for 1 hr in HBSS containing 0.1% collagenase. The cell suspension following filtration was washed by HBBS supplemented with gentamycin and 0.1% BSA (bovine serum albumin) and was treated with increasing doses of TNFα (0.1, 0.5 and 1.0 nM) and cultured at 38.5°C, 5% CO2 level for 24 hr. Result: There was dose dependent increase in concentrations of PGF2α and PGE2 with increasing doses of TNFα. The PGFS (prostaglandin F synthase) mRNA expression increased with increasing doses of TNFα. However, there was decrease in PGES (prostaglandin E synthase) mRNA expression at 0.1 nM and 0.5 nM TNFα but PGES mRNA expression increased at 1.0 nM TNFα as compared to control. It can be concluded that TNFα may alter PGES and PGFS mRNA expression and prostaglandin secretion in buffalo CL. 

Formononetin protects against concanavalin-A-induced autoimmune hepatitis in mice through its anti-apoptotic and anti-inflammatory properties

2021 ◽  
Vol 99 (2) ◽  
pp. 231-240
Author(s):  
Guangwei Liu ◽  
Wenxia Zhao ◽  
Jiameng Bai ◽  
Jianjiao Cui ◽  
Haowei Liang ◽  
...  
Keyword(s):  
Autoimmune Hepatitis ◽  
Concanavalin A ◽  
Nuclear Factor Kappa B ◽  
Caspase 3 ◽  
Receptor Protein ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Apoptotic Protein ◽  
Natural Herb ◽  
Dose Dependent

Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease that seriously threatens the health of humans globally. Formononetin (FMN) is a natural herb extract with multiple biological functions. In this study, an experimental model of AIH was established in mice through the use of concanavalin A (ConA). To investigate the effects of FMN on ConA-induced hepatitis, the mice were pretreated with 50 or 100 mg/kg body mass of FMN. The results show that FMN alleviated ConA-induced liver injury of mice in a dose-dependent manner. Moreover, pretreatment with FMN inhibited the apoptosis of hepatocytes in the ConA-treated mice through downregulating the expression of pro-apoptotic proteins (Bax, cleaved caspase 9, and cleaved caspase 3) and upregulating the expression of anti-apoptotic protein (Bcl-2). It was also found that the levels of proinflammatory cytokines were greatly reduced in the serum and liver tissues of mice pretreated with FMN. Further studies showed that FMN reduced the level of phosphorylated nuclear factor kappa B (p-NF-κB) p65 and enhanced the level of IκBα (inhibitor of NF-κB), suggesting that FMN inhibits the activation of the NF-κB signaling pathway. In addition, FMN inhibited activation of the NOD-like receptor protein 3 (NLRP3) inflammasome. Therefore, FMN could be a promising agent for the treatment of AIH.

Inhibition of Apoptosis in Periodontitis

2009 ◽  
Vol 89 (1) ◽  
pp. 29-33 ◽  
Author(s):  
H. Lucas ◽  
P.M. Bartold ◽  
A.A.S.S.K. Dharmapatni ◽  
C.A. Holding ◽  
D.R. Haynes
Keyword(s):  
Caspase 3 ◽  
Inflammatory Cells ◽  
Gingival Tissue ◽  
Healthy Individuals ◽  
Tissue Samples ◽  
Periodontal Tissues ◽  
Decoy Receptors ◽  
Trail Receptors ◽  
Elevated Expression ◽  
Necrosis Factor

This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues ( p < 0.005). Statistically ( p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors.

scholarly journals NFκB and Caspase-3 Activity in Apoptotic Hepatocytes of Galactosamine-sensitized Mice Treated with TNFα

2002 ◽  
Vol 50 (12) ◽  
pp. 1599-1609 ◽  
Author(s):  
Dan Tapalaga ◽  
Gisa Tiegs ◽  
Sabine Angermüller
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Nuclear Factor Kappa B ◽  
Caspase 3 ◽  
Nuclear Fraction ◽  
Nuclear Factor ◽  
Factor Α ◽  
Transcription Factor Nfκb ◽  
Necrosis Factor ◽  
Control Samples

Tumor necrosis factor-α (TNFα) induces apoptosis in hepatocytes only under transcriptional arrest induced by galactosamine (GalN). In this study we demonstrated the shuttle of the transcription factor NFκB (nuclear factor-kappa B) in the liver tissue of mice within 30 min-4.5 hr hours after GalN/TNFα treatment. NFκB translocation from cytoplasm to the nucleus is initiated by its separation from the inhibitory IκB proteins which include lIκBα, IκBβ, and IκB∊. Thirty minutes after GalN/TNFα administration, NFκBp65 in hepatocellular nuclei becomes increasingly detectable and reaches its highest level after 2.5 hr. Then export back into cytoplasm begins but, surprisingly, approximately 30% of NFκB remains in the nuclear fraction and appears as an immunoprecipitate in the nuclei of apoptotic hepatocytes. Non-apoptotic hepatocytes do not show any reaction product in the nuclei 4.5 hr after treatment. Correspondingly, the amount of dissociated IκBβ decreases in the cytoplasm up to 2.5 hr and increases again afterwards, although it does not reach the level of the control samples. No evidence of IκBβ in the nuclei was found either immunocytochemically or biochemically. Caspase-3 activity, which is responsible for apoptosis, increases significantly after 3.5 hr. At that time, apoptotic hepatocytes can occasionally be observed and, 4.5 hr after GalN/TNFα treatment, constitute approximately 30% of the hepatocytes.

scholarly journals Stimulation of sulphated glycosaminoglycan and decorin production in adult dermal fibroblasts by recombinant human interleukin-4

1995 ◽  
Vol 307 (3) ◽  
pp. 673-678 ◽  
Author(s):  
Y Wegrowski ◽  
V Paltot ◽  
P Gillery ◽  
B Kalis ◽  
A Randoux ◽  
...  
Keyword(s):  
Culture Medium ◽  
Core Protein ◽  
Human Fibroblasts ◽  
Inflammatory Cells ◽  
Dermal Fibroblasts ◽  
Interleukin 4 ◽  
Proteoglycan Synthesis ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Sulphated Glycosaminoglycan

Interleukin-4 (IL-4) is a pleiotropic cytokine expressed by inflammatory cells. Previous work from our laboratory has shown that it stimulates collagen synthesis in fibroblasts. Here we report the effects of recombinant human IL-4 on glycosaminoglycan (GAG) and proteoglycan synthesis in normal dermal fibroblasts from adult donors. IL-4 (10 and 100 units/ml) induced a dose-dependent increase of [3H]glucosamine and [35S]sulphate incorporation into total GAGs. The analysis of the different GAG fractions indicated the enhanced synthesis of dermatan/chondroitin sulphates. IL-4 had no effect on hyaluronan synthesis. The increase of sulphated GAG synthesis was correlated with an increase of proteoglycans in the culture medium. Decorin was identified as the major chondroitin/dermatan sulphate-containing proteoglycan in the culture medium of fibroblasts. Its synthesis was strongly stimulated by IL-4. Both the core-protein synthesis and mRNA expression were enhanced, indicating that the cytokine acted, at least in part, at the pre-translational level. These results indicate that IL-4 is able to modulate not only collagen, but also proteoglycan, production by human fibroblasts. Their implications in physiopathological processes such as wound healing or fibrosis is suggested.

Stimulation of NGF expression and secretion in 3T3-L1 adipocytes by prostaglandins PGD2, PGJ2, and Δ12-PGJ2

2005 ◽  
Vol 289 (1) ◽  
pp. E62-E67 ◽  
Author(s):  
Mònica Bulló ◽  
Muhammad R. Peeraully ◽  
Paul Trayhurn
Keyword(s):  
Mrna Level ◽  
Peroxisome Proliferator ◽  
Related Factors ◽  
Peroxisome Proliferator Activated Receptor ◽  
White Adipocytes ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

Nerve growth factor (NGF) has recently been shown to be secreted from white adipocytes, its production being strongly stimulated by the proinflammatory cytokine tumor necrosis factor-α. In this study, we have examined whether a series of prostaglandins and other inflammation-related factors also stimulate NGF expression and secretion by adipocytes, using 3T3-L1 cells. Although interleukin (IL)-1β, IL-10, and IL-18 each induced a small decrease in NGF mRNA level in 3T3-L1 adipocytes, there was no significant effect of these cytokines on NGF secretion. A small reduction in NGF expression and/or secretion was also observed with adiponectin and prostaglandins PGE2, PGF2α, and PGI2. In marked contrast, prostaglandin PGD2induced a major, dose-dependent increase (up to 20- to 40-fold) in NGF expression and secretion. The PGD2metabolites, PGJ2and Δ12-PGJ2, also induced major increases (up to 30-fold) in NGF production. A further metabolite of PGJ2, 15-deoxy-Δ12,14-PGJ2, a peroxisome proliferator-activated receptor-γ agonist, led paradoxically to a small increase in NGF mRNA level but a fall in NGF secretion. Both PGD2and PGJ2induced significant increases in NGF gene expression by 4 h after their addition. It is concluded that PGD2and the J series prostaglandins, PGJ2and Δ12-PGJ2, can play a significant role in the regulation of NGF production by white adipocytes. These results provide support for the view that NGF is an important inflammatory response protein, as well as a target-derived neurotrophin, in white adipose tissue.

Phosphate-induced chondrocyte apoptosis is linked to nitric oxide generation

2001 ◽  
Vol 281 (3) ◽  
pp. C833-C839 ◽  
Author(s):  
Cristina C. Teixeira ◽  
Kyle Mansfield ◽  
Caryn Hertkorn ◽  
Harry Ischiropoulos ◽  
Irving M. Shapiro
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Inorganic Phosphate ◽  
Caspase 3 ◽  
No Synthase ◽  
Chondrocyte Apoptosis ◽  
Threefold Increase ◽  
Induced Apoptosis ◽  
Dose Dependent Increase ◽  
Dose Dependent

An elevation in inorganic phosphate (Pi) concentration activates epiphyseal chondrocyte apoptosis. To determine the mechanism of apoptosis, tibial chondrocytes were treated with Pi, and nitrate/nitrite (NO[Formula: see text]/NO[Formula: see text]) levels were determined. Piinduced a threefold increase in the NO[Formula: see text]/NO[Formula: see text] concentration; inhibitors of nitric oxide (NO) synthase activity and Pitransport significantly reduced NO[Formula: see text]/NO[Formula: see text]levels and prevented cell death. Furthermore, a dose-dependent increase in cell death was observed after exposure of chondrocytes to S-nitrosoglutathione. Piincreased caspase 3 activity 2.7-fold. Both caspase 1 and caspase 3 inhibitors protected chondrocytes from Pi-induced apoptosis. Picaused a significant decrease in the mitochondrial membrane potential, while NO synthase inhibitors maintained mitochondrial function. While Picaused thiol depletion, inhibition of Piuptake or NO generation served to maintain glutathione levels. The results suggest that NO serves to mediate key metabolic events linked to Pi-dependent chondrocyte apoptosis.

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