Wyniki wyszukiwania

1

Prostaglandin-J2 induces the endothelial synthesis of IL-8 independently of PPARgamma activation

100%

Jozkowicz A., Huk I., Nigisch A., Grzenkowicz J., Podhajska A., Weigel G., Dulak J.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

2

Cyclooxygenase pathways

86%

Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.

Acta Biochimica Polonica

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2014

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tom 61

|

nr 4

3

Carvedilol and adrenergic agonists suppress the lipopolysaccharide-induced NO production in RAW 264.7 macrophages via the adrenergic receptors

86%

Pekarova M., Kralova J., Kubala L., Ciz M., Papezikova I., Macickova T., Pecivova J., Nosal R., Lojek A.

Journal of Physiology and Pharmacology

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2009

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tom 60

|

nr 1

143-150

The interaction of adrenergic agonists and/or antagonists with the adrenergic receptors expressed on immunologically active cells including macrophages plays an important role in regulation of inflammatory responses. Our study investigated the effects of carvedilol, a unique vasodilating b-adrenergic antagonist, and endogenous adrenergic agonists (adrenalin, noradrenalin, and dopamine) and/or antagonists (prazosin, atenolol) on lipopolysaccharide-stimulated nitric oxide (NO) production from murine macrophage cell line RAW 264.7. The production of NO was determined as the concentration of nitrites in cell supernatants (Griess reaction) and inducible nitric oxide synthase (iNOS) protein expression (Western blot analysis). Scavenging properties against NO were measured electrochemically. Carvedilol in a concentration range of 1, 5, 10 and 25 µM inhibited iNOS protein expression and decreased the nitrite concentration in cell supernatants. Adrenalin, noradrenalin or dopamine also inhibited the iNOS protein expression and the nitrite accumulation. Prazosine and atenolol prevented the effect of both carvedilol and adrenergic agonists on nitrite accumulation and iNOS expression in lipopolysaccharide-stimulated cells. These results, together with the absence of scavenging properties of carvedilol against NO, imply that both carvedilol and adrenergic agonists suppress the lipopolysaccharide-evoked NO production by macrophages through the activation and modulation of signaling pathways connected with adrenergic receptors.

4

Modulation of phagocytosis in Tetrahymena thermophila by histamine and the antihistamine diphenhydramine

86%

Buduma N., Balabanian J., Dalvi P., Chia S.-K., Dhaliwal A., Boothby J., Bros-Seemann S., Kibler R., Khuri S., Veregge S.

Acta Protozoologica

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2013

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tom 52

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nr 4

5

The effect of fiberoptic bronchoscopy on exhaled nitric oxide

86%

Krenke R., Przybylowski T., Hildebrand K., Fangrat A., Gorska K., Barnas M., Chazan R.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

|

nr 4

183-190

Nitric oxide has been extensively studied as a noninvasive marker of airway inflammation. Assuming that bronchoscopy can produce not only systemic but also local inflammatory response, we hypothesized that bronchofiberoscopy can be responsible for an increase in nitric oxide synthesis with resulting increase in fractional concentration of exhaled nitric oxide (FENO). Fifty five subjects (F/M-23/32; mean age 53.9 ±17.3 yr) undergoing diagnostic bronchoscopy participated in the study. The indications for bronchoscopy were as follows: interstitial lung diseases (n=13; 23.6%), lung cancer (n=11; 20.0%), hemoptysis (n=10; 18.2%), differential diagnosis of asthma/dyspnea (n=9; 16.4%), pulmonary infections (n=7; 12.7%), and others (n=5; 9.1%). During bronchoscopy bronchial washing (n=18), bronchoalveolar lavage (BAL) (n=26), and bronchial biopsies (n=24) were performed. FENO was analyzed on-line with chemiluminescence analyzer (NIOX, Aerocrine, Sweden) according to the ATS guidelines, before and at 1, 2, 3 and 24 h after bronchoscopy. The mean FENO before bronchoscopy was 21.0 ±3.31(SE) ppb, it decreased to 14.8 ±2.10 ppb 1 h after bronchoscopy, reached a nadir at 2 h (14.4 ±2.28 ppb; P<0.05), and was not different from baseline 24 h after bronchoscopy (22.8 ±2.90 ppb). There were no differences in the FENO profile in BAL patients compared with those in whom only the bronchial washing was performed. We conclude that bronchoscopy leads to a decrease in FENO. The underlying mechanisms are at present unclear.

6

PDE4 inhibitors have no effect on eotaxin expression in human primary bronchial epithelial cells

86%

Paplinska-Goryca M., Chazan R., Grubek-Jaworska H.

Acta Biochimica Polonica

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2012

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tom 59

|

nr 3

The bronchial epithelium is a very important factor during the inflammatory response, it produces many key regulators involved in the pathophysiology of asthma and COPD. Local influx of eosinophils, basophils, Th2 lymphocytes and macrophages is the source of many cytotoxic proteins, cytokines and other mediators of inflammation. These cells are attracted by eotaxins (eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26). Inhibitors of phosphodiesterase 4 (PDE4) are new anti-inflammatory drugs which cause cAMP accumulation in the cell and inhibit numerous stages of allergic inflammation. The aim of our study was to evaluate the influence of PDE4 inhibitors: rolipram and RO-20-1724 on the expression of eotaxins in human primary bronchial epithelial cells. Cells were preincubated with PDE4 inhibitors for 1 hour and then stimulated with IL-4 or IL-13 alone or in combination with TNF-α. After 48 hours, eotaxin protein level was measured by ELISA and mRNA level by real time PCR. These cells produce CCL24 and CCL26. PDE4 inhibitors increased CCL24 and CCL26 mRNA level irrespectively of the used stimulators. Rolipram and RO-20-1724 had no effect on eotaxin protein production in our experimental conditions. Thus PDE4 inhibitors have no effect on eotaxin protein expression in human primary bronchial epithelial cells. In vitro experiments should be performed using a primary cell model rather than immortalized lines.

7

Protein kinase signalling cascade during nitric oxide-induced apoptosis, dedifferentiation and inflammatory responses of articular chondrocytes

86%

Chun J. S.

Cellular and Molecular Biology Letters

|

2003

|

tom 08

|

nr 2A

8

Helper-dependent adenoviral vectors in experimental gene therapy

86%

Jozkowicz A., Dulak J.

Acta Biochimica Polonica

|

2005

|

tom 52

|

nr 3

In the majority of potential applications gene therapy will require an effective transfer of a transgene in vivo resulting in high-level and long-term transgene expression, all in the absence of significant toxicity or inflammatory responses. The most efficient vehicles for delivery of foreign genes to the target tissues are modified adenoviruses. Adenoviral vectors of the first generation, despite the high infection efficacy, have an essential drawback: they induce strong immune response, which leads to short term expression of the transgene, and limits their usefulness in clinical trials. In contrast, helper-dependent adenoviral vectors (HdAd) lacking all viral coding sequences display only minimal immunogenicity and negligible side-effects, allowing for long-term transgene expression. Thus, HdAd vehicles have become the carrier of choice for adenoviral vector-mediated experimental gene therapy, effectively used in animal models for delivery of transgenes into the liver, skeletal muscle, myocardium or brain. Strong and long-lasting expression of therapeutic genes has allowed for successful treatment of dyslipidemias, muscular dystrophy, obesity, hemophilia, and diabetes. Additionally, the large cloning capacity of HdAd, up to 37 kb, facilitates the use of physiologically regulated, endogenous promoters, instead of artificial viral promoter sequences. This enables also generation of the single vectors expressing multiple genes, which can be potentially useful for treatment of polygenic diseases. In this review we characterize the basic features of HdAd vectors and describe some of their experimental and potential clinical applications.

9

The activation of complement system in different types of renal replacement therapy

72%

Stepniewska J., Dolegowska B., Golebiewska E., Marchelek-Mysliwiec M., Domanski M., Ciechanowski K., Zair L.

Journal of Physiology and Pharmacology

|

2020

|

tom 71

|

nr 2

10

Immune balance in critically ill patients

72%

Pinsky M. R.

Archivum Immunologiae et Therapiae Experimentalis

|

2000

|

tom 48

|

nr 6 Spec.Iss.

439-442

11

Evaluation of endothelial function by flow-mediated dilation: a comprehensive review in rheumatic disease

72%

Moroni L., Selmi C., Angelini C., Meroni P. L.

Archivum Immunologiae et Therapiae Experimentalis

|

2017

|

tom 65

|

nr 6

12

Increased cys-leukotrienes in exhaled breath condensate and decrease of PNIF after intranasal allergen challenge support the recognition of allergic rhinitis in children

72%

Zagorska W., Grzela K., Kulus M., Sobczynski M., Grzela T.

Archivum Immunologiae et Therapiae Experimentalis

|

2013

|

tom 61

|

nr 4

13

Exposure to air pollution and oxidative stress markers in patients with potentially malignant oral disorders

72%

Gregorczyk-Maga I., Celejewska-Wojcik N., Gosiewska-Pawlica D., Darczuk D., Kesek B., Maga M., Wojcik K.

Journal of Physiology and Pharmacology

|

2019

|

tom 70

|

nr 1

14

Functional analysis of eicosanoids from white blood cells in sepsis and SIRS

72%

Baenkler M., Leykauf M., John S.

Journal of Physiology and Pharmacology. Supplement

|

2006

|

tom 57

|

nr 12

25-33

Sepsis and SIRS are affections with major alterations in inflammatory activity. The impact of prostaglandins (PG) and leukotrienes (LT) produced from white blood cells (WBC) in this context is not completely understood. Thirty nine patients with sepsis or SIRS were investigated in comparison to 10 healthy controls. WBC were collected and separately exposed to arachidonic acid (AA) or to nothing else. After centrifugation, the generated PGE2 and LTCDE4 with or without stimulation were measured in the supernatant. LT-levels were significantly higher during sepsis/SIRS than in controls whereas PG-levels of patients were decreased to those of controls in basic condition. The relation between the level with and without stimulation showed a significant higher ratio in PG in contrast to LTs. The survivor’s ratio in LT levels was significantly higher than that of non-survivors, which did not differ from controls. Generation of LT from WBC is enhanced during sepsis/SIRS, but LT generation after stimulation only in survivors but not in non-survivors. This inability of WBC to generate LT during sepsis in non-survivors could be predictive regarding the outcome of sepsis/SIRS and may be part of the “immunoparalysis” seen during sepsis in association with bad outcome.

15

Caspases as the key effectors of inflammatory responses against bacterial infection

72%

Uchiyama R., Tsutsui H.

Archivum Immunologiae et Therapiae Experimentalis

|

2015

|

tom 63

|

nr 1

16

Chitin, a key factor in immune regulation: lesson from infection with fungi and chitin bearing parasites

72%

Brodaczewska K., Donskow-Lysoniewska K., Doligalska M.

Acta Parasitologica

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2015

|

tom 60

|

nr 2

17

MiR-143 mediates the TLR2/NF-kappaB pathway to attenuate AngII-induced damage to VSMCs

72%

Wang Z., Lin F., Cai Z., Lyu G.

Folia Biologica

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2021

|

tom 69

|

nr 2

18

Influence of leptin administration on the course of acute ischemic pancreatitis

72%

Warzecha Z., Dembinski A., Ceranowicz P., Jaworek J., Konturek P. C., Dembinski M., Bilski J., Konturek S. J.

Journal of Physiology and Pharmacology

|

2002

|

tom 53

|

nr 4,2

Leptin is involved in the regulation of food intake and previous studies have shown that leptin affects the inflammatory response in various tissues. The objective of this study was to examine the influence of leptin administration on the development and the course of acute ischemic pancreatitis. Acute pancreatitis was induced by limitation of pancreatic blood flow by clamping of inferior splenic artery for 30 min, followed by reperfusion. Leptin was administered three times daily at the dose 10 or 50 µg/kg. Animals were sacrificed 1, 3, 5, 10 and 21 days after removal of vascular clips. Administration of leptin reduced development of pancreatic damage and accelerated pancreatic regeneration what was manifested by the improvement of pancreatic histology, the decrease in serum lipase and amylase activity, and the reduction in serum interleukin-1ß concentration. Also, treatment with leptin caused the increase in the pancreatic blood flow and pancreatic DNA synthesis. Leptin administration was without effect on serum interleukin-10 concentration. Leptin at the dose 50 µg/kg was more effective than 10 µg/kg. We conclude that leptin reduces the pancreatic damage in the course of ischemic pancreatitis and accelerates the pancreatic tissue repair. The beneficial effects of leptin appear to be dependent on the improvement of pancreatic blood flow, the increase in pancreatic cell growth, and the limitation of pro-inflammatory interleukin-1ß release.

19

The annexin-1 knockout mouse: what it tells us about the inflammatory response

72%

Roviezzo F., Getting S. J., Paul-Clark M. J., Yona S., Gavins F. N. E., Perretti M., Hannon R., Croxtall J. D., Buckingham J. C., Flower R. J.

Journal of Physiology and Pharmacology

|

2002

|

tom 53

|

nr 4,1

The 37kDa protein annexin 1 (Anx-1; lipocortin 1) is a glucocorticoid-regulated protein that has been implicated in the regulation of phagocytosis, cell signalling and proliferation, and postulated to be a mediator of glucocorticoids action in inflammation and in the control of anterior pituitary hormone release. Immuno-neutralisation or antisense strategies support this hypothesis as they can reverse the effect of glucocorticoids in several systems. We recently generated a line of mice lacking the Anx-1 gene noting that some tissues taken from such animals exhibited an increased expression of several proteins including COX-2 and cPLA2. In models of experimental inflammation, Anx-1-/- mice exhibit an exaggerated response and a partial or complete resistance to the anti-inflammatory effects of glucocorticoids. Several other anomalies were noted including abnormal leukocyte adhesion molecule expression, an increased spontaneous migratory behaviour of PMN in Anx-1-/- mice and a resistance in Anx-1-/- macrophages to glucocorticoid inhibition of superoxide generation. This paper reviews these and other data in the light of the development of the ‚second messenger™ hypothesis of glucocorticoid action.

20

Effect of cardiopulmonary bypass on neutrophil activity in pediatric open-heart surgery

72%

Pasnik J., Siniewicz K., Moll J. A., Moll J., Baj Z., Sysa A., Zeman K.

Archivum Immunologiae et Therapiae Experimentalis

|

2005

|

tom 53

|

nr 3

Ograniczanie wyników

Prostaglandin-J2 induces the endothelial synthesis of IL-8 independently of PPARgamma activation

Cyclooxygenase pathways

Carvedilol and adrenergic agonists suppress the lipopolysaccharide-induced NO production in RAW 264.7 macrophages via the adrenergic receptors

Modulation of phagocytosis in Tetrahymena thermophila by histamine and the antihistamine diphenhydramine

The effect of fiberoptic bronchoscopy on exhaled nitric oxide

PDE4 inhibitors have no effect on eotaxin expression in human primary bronchial epithelial cells

Protein kinase signalling cascade during nitric oxide-induced apoptosis, dedifferentiation and inflammatory responses of articular chondrocytes

Helper-dependent adenoviral vectors in experimental gene therapy

The activation of complement system in different types of renal replacement therapy

Immune balance in critically ill patients

Evaluation of endothelial function by flow-mediated dilation: a comprehensive review in rheumatic disease

Increased cys-leukotrienes in exhaled breath condensate and decrease of PNIF after intranasal allergen challenge support the recognition of allergic rhinitis in children

Exposure to air pollution and oxidative stress markers in patients with potentially malignant oral disorders

Functional analysis of eicosanoids from white blood cells in sepsis and SIRS

Caspases as the key effectors of inflammatory responses against bacterial infection