scholarly journals Chronic cigarette smoking enhances spontaneous release of tumour necrosis factor-α from alveolar macrophages of rats

1993 ◽  
Vol 2 (6) ◽  
pp. 423-428 ◽  
Author(s):  
G. P. Pessina ◽  
L. Paulesu ◽  
F. Corradeschi ◽  
E. Luzzi ◽  
M. Tanzini ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Alveolar Macrophages ◽  
Superoxide Anion ◽  
Biological Effects ◽  
Peritoneal Macrophages ◽  
Control Group ◽  
Polymorphonuclear Cells ◽  
Tnf Α ◽  
Activated State ◽  
Bronchoalveolar Fluid

Some biological effects of chronic cigarette smoking (two cigarettes for 2 h, daily for 4 months) in rats were evaluated. During the smoking period, body weight of smoker rats was always significantly lower than that of control rats. Immediately after the last smoking session the carboxyhaemoglobin concentration in the blood was about 8.5% and the polymorphonuclear cells in the bronchoalveolar fluid increased significantly. At the same time, enzymatic analyses on the supernatants of bronchoalveolar fluid revealed a significant increase of β-glucuronidase in the smoker group. Alveolar macrophages, collected 0, 8 and 24 h after the last smoking session, significantly increased the generation of superoxide anion and, after incubation for 24 h at 37°C in a humidified atmosphere, released significantly high amounts of TNF-α. When challenged with lipopolysaccharide, alveolar macrophages of smoker rats released much more TNF-α but, in such a case, TNF-α release was about one half of that observed in the control group. Peritoneal macrophages of both control and smoker rats were unable either to generate high levels of superoxide anion or to release significant amounts of TNF-α. The results clearly demonstrated the activated state of alveolar macrophages and the resting state of peritoneal macrophages.

scholarly journals UVB Dose Optimization for Phototherapy in Vitamin D Deficiency : Profile Analysis of Vitamin D, TNF-α, Vascular Endothelial Growth Factor (VEGF) and Platelet Derived Growth Factor (PDGF) in Wistar Rats

2020 ◽  
Vol 19 (4) ◽  
pp. 749-754
Author(s):  
Cynthia Arsita ◽  
Taufiqurrachman Nasihun ◽  
Atina Hussaana
Keyword(s):  
Vitamin D ◽  
Growth Factor ◽  
Wistar Rats ◽  
Biological Effects ◽  
Medical Science ◽  
The Other ◽  
Control Group ◽  
Uvb Radiation ◽  
Tnf Α ◽  
Post Radiation

Background : UVB radiation responsible for the most important biological effects including Vitamin D3 synthesis and inflammation. UVB radiation are absorbed by 7-dehydrocholesterol in the plasma membrane of epidermal cells resulting in production of cis-previtamin D3. In the other hand, an exposure to UVB leads to cutaneous tissue inflammation modulates by TNF-α which also increases platelet activating factor. VEGF and PDGF induced by TNF-α during wound healing, characterized with angiogenesis and reephitalization. Furthermore, vitamin D plays a role in inflammation inhibition and upregulates growth factors. However, the study of the mechanism has not yet been thoroughly investigated. Methods: This study uses post test only group design, subjected wistar rats divided into four groups. Control group, non irradiated with UVB, and the other three groups, treated with graded UVB dose started with 1 MED (50 mJ/cm2), 2 MED (100mJ/cm2) and 3 MED (150 mJ/cm2) and investigated at 6, 12, 24 and 48 hours post UVB irradiation. Result : The serum level of vitamin D, VEGF and PDGF were increasing due to UVB dose addition. The highest level was reached at 6 hours post radiation using 3 MED, which gradually decrease up to 48 hours (p =0,000). The rise of vitamin D after UVB radiation, inhibit TNF-α induction in every dose accordant UVB dose addition and the lowest level is using 3 MED at 12 hours post radiation (p =0,000). TNF-α reach its highest level at 24 hours post radiation using 1 MED, it is related with the acute phase of inflammation. Conclusion : This study reveal that higher UVB irradiance increases vitamin D and inhibit TNF-α which also promotes VEGF and PDGF. Bangladesh Journal of Medical Science Vol.19(4) 2020 p.749-754

scholarly journals The Effects of Particulate Matter on C57BL/6 Peritoneal and Alveolar Macrophages

2020 ◽  
Author(s):  
Hoda Rahmani ◽  
Somaye Sadeghi ◽  
Niloofar Taghipour ◽  
Mohsen Roshani ◽  
Davar Amani ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Alveolar Macrophages ◽  
Critical Role ◽  
Peritoneal Macrophages ◽  
Considerable Effect ◽  
Epidemiologic Studies ◽  
Phagocytic Capacity ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Inflammatory Phenotype

The presence of ambient particulate matter (PM) poses more dangers to human health than that of other common air pollutants such as Carbon dioxide (Co2) and ozone.  Epidemiologic studies show a direct correlation between PM and the risk of respiratory and cardiovascular diseases. The immune system seems to play a critical role in the process of these diseases. The main goal of this study was to investigate the effect of Tehran particulate matter in two aerodynamic diameters (PM2.5 and PM10) on alveolar macrophages (AM) from C57/BL6 mice. To evaluate the inflammatory effects of PMs, cultured alveolar, and peritoneal macrophages were treated with PM2.5 & PM10 (concentrations of 5 µg/mL and 10 µg/mL). Tumor necrosis factor-alpha (TNF-α) and IL-10 (representatives of inflammatory and anti-inflammatory cytokines, respectively) were assessed in the culture supernatant by ELISA. Expression of arginase and inducible nitric oxide synthase (iNOS) genes was carried out by quantitative real-time PCR. Different functional types of cultured alveolar macrophages (M1, M2) were also determined in this study. Our results suggest that PM2.5 induces M1 inflammatory phenotype in comparison with PM10. We found Also, an increase in TNF-α and M1-related gene expression (iNOS), as well as a decrease in both IL-10 and M2 phenotype genes (Arginase). Moreover, a reduction in phagocytic capacity and increased apoptosis function of macrophage cells were detected. PM2.5 as a major component in hydrocarbons has a considerable effect on polarizing the alveolar macrophages to an inflammatory phenotype and eliciting lung inflammation in mice.

scholarly journals miRNA-486-5p Promotes COPD Progression by Targeting HAT1 to Regulate the TLR4-Triggered Inflammatory Response of Alveolar Macrophages

2020 ◽  
Author(s):  
Jie Zhang ◽  
Zhongneng Xu ◽  
Lianhua Kong ◽  
Hong Gao ◽  
Yueming Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Alveolar Macrophages ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Control Group ◽  
Down Regulation ◽  
Copd Patients ◽  
Tnf Α ◽  
Reporter Assays ◽  
Ifn Γ

Abstract Background: The aim of this study is to investigate the key regulatory miRNA-486-5p and underlying molecular mechanisms in chronic obstructive pulmonary disease (COPD) progression.Methods: Aberrant miRNA expression in smokers compared to non-smokers and COPD compared to normal was analyzed using microarray datasets and reverse-transcriptase quantitative polymerase chain reaction (qPCR). ELISA assay was used to determine the secretion of inflammatory cytokines in cell supernatants. Inflammatory cytokine expression, including HAT1, TLR4, and miR-486-5p, was determined using qPCR or western blotting. Luciferase reporter assays and fluorescence in situ hybridization were used to confirm the target regulation between miR-486-6p and HAT1. Results: Our results showed that miR-486-5p was significantly up-regulated in the COPD and smoker groups compared to the control group based on bioinformatics analysis and qPCR validation of alveolar macrophages and peripheral monocytes. miR-218-5p expression significantly correlated with IL-6, IL-8, TNF-α, and IFN-γ expression. Luciferase reporter assays confirmed that miR-486-5p directly targets HAT1, and cellular localization showed that miR-486-5p and HAT1 were highly expressed in the cytoplasm. miR-486-5p overexpression led to significant TLR4 up-regulation and significant HAT1 down-regulation. Inversely, miR-486-5p inhibition led to significant TLR4 down-regulation and significant HAT1 up-regulation. HAT1 knockdown using siRNA significantly increased TLR4, IL-6, IL-8, TNF-α, and IFN-γ expression. Conclusions: miR-486-5p was differentially expressed in alveolar macrophages of COPD patients. miR-486-5p overexpression might increase the TLR4-triggered inflammatory response in COPD patients by targeting HAT1.

scholarly journals Chemokine C10 Promotes Disease Resolution and Survival in an Experimental Model of Bacterial Sepsis

2000 ◽  
Vol 68 (11) ◽  
pp. 6108-6114 ◽  
Author(s):  
M. L. Steinhauser ◽  
C. M. Hogaboam ◽  
A. Matsukawa ◽  
N. W. Lukacs ◽  
R. M. Strieter ◽  
...  
Keyword(s):  
Host Defense ◽  
Cecal Ligation ◽  
Peritoneal Macrophages ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tnf Α ◽  
Septic Peritonitis

ABSTRACT Previous studies have suggested that the C-C chemokine C10 is involved in the chronic stages of host defense reactions. The present study addressed the role of C10 in a murine model of septic peritonitis, induced by cecal ligation and puncture (CLP). Unlike other C-C chemokines, C10 levels in the peritoneal wash were increased approximately 30-fold above baseline levels at 48 h after CLP surgery. Immunoneutralization of peritoneal C10 levels with polyclonal anti-C10 antiserum during CLP-induced peritonitis negatively impacted mouse survival over 4 days. In contrast, when 500 ng of recombinant murine C10 was administered immediately after CLP surgery, the 4-day survival rate increased from 20% to over 60%. The C10 therapy appeared to facilitate a rapid and significant enhancement of the levels of tumor necrosis factor alpha (TNF-α) and monocyte chemoattractant protein-1 (MCP-1) and a later increase in interleukin-13 (IL-13) levels in the peritoneal cavity. In vitro studies showed that the combination of IL-1β and C10 markedly augmented TNF-α synthesis by peritoneal macrophages and that C10 synthesis was induced in these cells following their exposure to IL-13. At 24 h after CLP surgery, only 25% of C10-treated mice were bacteremic versus 85% of the control group that exhibited dissemination of bacteria into the circulation. The lack of bacteremia in C10-treated mice appeared to be related, in part, to in vitro evidence that C10 significantly enhanced the bacterial phagocytic activity of peritoneal macrophages. In addition, in vivo evidence suggested that C10 therapy significantly reduced the amount of material that leaked from the damaged gut. Taken together, the results of this study demonstrate that the C10 chemokine rapidly promotes disease resolution in the CLP model through its direct effects on the cellular events critically involved in host defense during septic peritonitis.

scholarly journals Caffeic Acid Phenethyl Ester: Consequences of Its Hydrophobicity in the Oxidative Functions and Cytokine Release by Leukocytes

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Luana Chiquetto Paracatu ◽  
Carolina Maria Quinello Gomes Faria ◽  
Camila Quinello ◽  
Camila Rennó ◽  
Patricia Palmeira ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Caffeic Acid ◽  
Superoxide Anion ◽  
Hypochlorous Acid ◽  
Inflammatory Diseases ◽  
Biological Effects ◽  
Caffeic Acid Phenethyl Ester ◽  
Nadph Oxidases ◽  
Tnf Α ◽  
Anti Inflammatory

Numerous anti-inflammatory properties have been attributed to caffeic acid phenethyl ester (CAPE), an active component of propolis. NADPH oxidases are multienzymatic complexes involved in many inflammatory diseases. Here, we studied the importance of the CAPE hydrophobicity on cell-free antioxidant capacity, inhibition of the NADPH oxidase and hypochlorous acid production, and release of TNF-α and IL-10 by activated leukocytes. The comparison was made with the related, but less hydrophobic, caffeic and chlorogenic acids. Cell-free studies such as superoxide anion scavenging assay, triene degradation, and anodic peak potential(Epa)measurements showed that the alterations in the hydrophobicity did not provoke significant changes in the oxidation potential and antiradical potency of the tested compounds. However, only CAPE was able to inhibit the production of superoxide anion by activated leukocytes. The inhibition of the NADPH oxidase resulted in the blockage of production of hypochlorous acid. Similarly, CAPE was the more effective inhibitor of the release of TNF-α and IL-10 byStaphylococcus aureusstimulated cells. In conclusion, the presence of the catechol moiety and the higher hydrophobicity were essential for the biological effects. Considering the involvement of NADPH oxidases in the genesis and progression of inflammatory diseases, CAPE should be considered as a promising anti-inflammatory drug.

AdultBrugia malayimitochondrial and nuclear fractions impart Th1-associated sizeable protection against infective larval challenges inMastomys coucha

2009 ◽  
Vol 83 (1) ◽  
pp. 83-95 ◽  
Author(s):  
S. Shakya ◽  
A.K. Srivastava ◽  
S. Misra-Bhattacharya
Keyword(s):  
Interleukin 1 ◽  
Peritoneal Macrophages ◽  
Control Group ◽  
Rodent Host ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Antibody Isotypes ◽  
Factor Alpha ◽  
Mastomys Coucha

AbstractProtective immunity to the subperiodic human filariid,Brugia malayi, was explored in the rodent host,Mastomys couchaafter vaccination with subcellular fractions derived from the adult stage of the parasite. The highest level of protection was conferred in animals vaccinated with the ‘mitochondria rich’ (MT) fraction, in which microfilaraemia and worm burden were markedly reduced by 67.2 and 65.9%, respectively, followed by the ‘nucleus rich’ (NR) fraction, showing reductions of 62 and 52.3%, respectively, over the non-immunized control group. Mastomys vaccinated with MT and NR, displayed a significant increase in the level of antigen-specific serum immunoglobulin G (IgG). The levels of IgG2a, IgG2b and IgM antibody isotypes were remarkably elevated in both the MT and NR immunized groups, while IgG1 and IgG3 levels were low. Apart from antibodies, both these fractions also led to marked antigen-specific lymphoproliferationin vitro, along with enhanced release of nitric oxide by peritoneal macrophages. There was an increased population of CD4+ and CD8a+T-cells in MT immunized animals, as measured by flow cytometry, accompanied by elevated levels of proinflammatory cytokines; interferon gamma (IFN-γ), tumour necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in the culture supernatants of the activated splenocytes. The results suggest that both NR and MT contain proinflammatory molecules which evoke a protective Th1 type of immune response.

Urethan anesthesia protects rats against lethal endotoxemia and reduces TNF-α release

1996 ◽  
Vol 81 (5) ◽  
pp. 2304-2311 ◽  
Author(s):  
Anastasia Kotanidou ◽  
Augustine M. K. Choi ◽  
Richard A. Winchurch ◽  
Leo Otterbein ◽  
Henry E. Fessler
Keyword(s):  
Mrna Expression ◽  
Biological Effects ◽  
Lethal Dose ◽  
Peritoneal Macrophages ◽  
Organ Injury ◽  
In Vivo Studies ◽  
Myeloperoxidase Activity ◽  
Neutrophil Sequestration ◽  
Tnf Α

Kotanidou, Anastasia, Augustine M. K. Choi, Richard A. Winchurch, Leo Otterbein, and Henry E. Fessler. Urethan anesthesia protects rats against lethal endotoxemia and reduces TNF-α release. J. Appl. Physiol. 81(5): 2304–2311, 1996.—Urethan is a commonly used animal anesthetic for nonrecovery laboratory surgery. However, urethan has diverse biological effects that may complicate the interpretation of experimental findings. This study examined the effect of urethan on the response to an intravenous bolus of lipopolysaccharide (LPS; 30 mg/kg) in rats. In instrumented rats, urethan (1.2 gm/kg ip) completely prevented the fall in arterial pressure immediately after LPS administration but did not prevent late cardiovascular collapse. In uninstrumented rats, urethan also attenuated indexes of organ injury measured 4 h after LPS administration, including mural bowel hemorrhage, hemoconcentration, hypoglycemia, metabolic acidosis, and lung myeloperoxidase activity, a measure of neutrophil sequestration. The peak increase in tumor necrosis factor-α (TNF-α) 90 min after LPS administration was reduced 88% by urethan (2,060 ± 316 vs. 16,934 ± 847 pg/ml; P < 0.001). In uninstrumented animals, urethan at 1.2 gm/kg reduced the 90% mortality rate of a lethal dose of LPS to 0–10% when given up to 24 h before LPS administration but did not reduce mortality when given 2 h after LPS. Urethan neither directly bound LPS by Limulus assay nor inhibited LPS-stimulated TNF-α mRNA expression in cultured mouse peritoneal macrophages, but TNF-α mRNA expression was suppressed by serum from a urethan-treated rat. Moreover, rauwolscine, which shares α2-adrenoceptor-blocking activity with urethan, also prevented death from a subsequent 90% lethal dose LPS bolus. We conclude that urethan or its metabolites protect against LPS, in part, by reducing TNF-α release and speculate that this may be mediated by α2-adrenoceptors. These actions of urethan make it an undesirable anesthetic agent for in vivo studies of sepsis or LPS.

Effect of Resveratrol on NF-κB Activity in Rat Peritoneal Macrophages

2006 ◽  
Vol 34 (04) ◽  
pp. 623-630 ◽  
Author(s):  
Zhen-Hua Ma ◽  
Qing-Yong Ma ◽  
Lian-Cai Wang ◽  
Huan-Chen Sha ◽  
Sheng-Li Wu ◽  
...  
Keyword(s):  
Culture Medium ◽  
Interleukin 1 ◽  
Peritoneal Macrophages ◽  
Inflammatory Factors ◽  
Future Application ◽  
Control Group ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Significant Difference

This study was to investigate the inhibitive effect of resveratrol (RESV) on nuclear factor kappa B (NF-κB) expression and activity induced by lipopolysaccharide (LPS) in rat peritoneal macrophages (PMA). Male Sprague-Dawley (SD) rats were randomly divided into 7 groups, including control group, LPS group and RESV I-V group. In the LPS group, PMA were incubated in DMEM containing LPS (10 μg/ml), whereas in control group, PMA were incubated in DMEM only. In the RESV I-V groups, PMA were incubated in DMEM containing LPS (10 μg/ml) and different concentrations of RESV. After 24 hours of incubation, NF-κB activity in PMA, and the levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1) and nitric oxide (NO) in the culture medium were measured. In the concentrations of 1.25-5 μg/ml, RESV had a dose- dependent inhibitive effect on NF-κB activity in PMA as well as the expressions of TNF-α, IL-1 and NO in the culture medium contrasted with the LPS group. There was no significant difference in the levels of these pro-inflammatory factors between the groups of 5 μg/ml and 10 μg/ml RESV. In conclusion, RESV has the potential for the future application of preventing inflammatory diseases involving PMA.

Molecular imaging of lung glucose uptake after endotoxin in mice

2005 ◽  
Vol 289 (5) ◽  
pp. L760-L768 ◽  
Author(s):  
Zhaohui Zhou ◽  
James Kozlowski ◽  
Andrea L. Goodrich ◽  
Nathaniel Markman ◽  
Delphine L. Chen ◽  
...  
Keyword(s):  
Molecular Imaging ◽  
Glucose Uptake ◽  
Biological Effects ◽  
Control Group ◽  
New Paradigm ◽  
Influx Rate ◽  
Positron Emission ◽  
Tnf Α ◽  
Drug Inhibition ◽  
Additional Agent

Positron emission tomographic imaging after administration of the glucose analog fluorine-18 fluorodeoxyglucose ([18F]FDG) may be useful to study neutrophilic inflammation of the lungs. In this study, we sought to determine the specificity of the increase in lung [18F]FDG uptake after intraperitoneal endotoxin (Etx) for neutrophil influx into mouse lungs and to determine the regulation of glucose uptake after Etx by Toll-like receptors (TLRs) and TNF-α. Lung tissue radioactivity measurements by imaging were validated against counts in a gamma well counter. Glucose uptake was quantified as the [18F]FDG tissue-to-blood radioactivity ratio (TBR) after validating this measure against the “gold standard” measure of glucose uptake, the “net influx rate constant.” TBR measurements were made in a control group (no intervention), a group administered Etx, and a group administered Etx plus an additional agent (e.g., vinblastine) or Etx administered to a mutant mouse strain. The glucose uptake measurements were compared with measurements of myeloperoxidase. Increases in TBR after Etx were significantly but not completely eliminated by neutrophil depletion with vinblastine. Increases in TBR after Etx were consistent with signaling via either TLR-4 or TLR-2 (the latter probably secondary to peptidoglycan contaminants in Etx preparation) and were decreased by drug inhibition of TLR-4 but not by inhibition of TNF-α. Thus molecular imaging can be used to noninvasively monitor biological effects of Etx on lungs in mice, and changes in lung glucose uptake can be used to monitor effects of anti-inflammatory agents. Such imaging capacity provides a powerful new paradigm for translational “mouse-to-human” pulmonary research.

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