Wyniki wyszukiwania - Biblioteka Nauki

1

Aktywność makrofagów i zmiany dystrybucji i koncentracji białek morfogenetycznych kości (BMP-4) oraz kolagenu typu II w sąsiedztwie wszczepów bioaktywnego szkła SZ2 : doniesienie wstępne

100%

Niedzielski K. , Koktysz R. , Bandurka W. , Woźniak J. , Łączka M. , Cholewa-Kowalska K. , Menaszek E.

Inżynieria Biomateriałów

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2006

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tom R. 9, nr 58-60

227-230

2

88%

Guevara-Lora I. , Florkowska M. , Kozik A.

Acta Biochimica Polonica

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2009

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tom 56

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nr 3

515-522

EN

Kinins, universal mediators of inflammation, are recognized by two kinds of receptors, B1 and B2, which have been found to be expressed in numerous cell types of several species. However, the knowledge of the regulation of these receptors in leukocytes is still not satisfactory. In the current work, we have demonstrated a constitutive production of B2 receptor mRNA in the human promonocyte U937 cells and its two-fold augmentation after cell differentiation with retinoic acid and phorbol ester. Bradykinin and des-Arg10-kallidin induced the expression of both B2 and B1 receptors in cells before and after differentiation. Generally, the undifferentiated cells were more susceptible to bradykinin-dependent induction of kinin receptors (increases by approximately 250% and 200% for B2 and B1 receptors, respectively). The induction, by approx. 200%, of B1 receptor by des-Arg10-kallidin was detected on both mRNA and protein levels. In addition, an unexpected strong induction of B2 receptor by this compound was observed in the retinoic acid- and phorbol ester-differentiated cells (by 150% and 200%, respectively) that suggests a possible autoregulation of kinin receptors by own agonists during the inflammatory state. On the other hand, a strong enhancement of the expression of both receptors by interleukin 1β, especially in the phorbol ester-differentiated cells, indicates the involvement of kinin receptors in the propagation of the inflammatory processes.

3

Semi-stable production of bovine IL-4 and GM-CSF in the mammalian episomal expression system

88%

Blanco F. C. , Vazquez C. L. , Garcia J. S. , Rocha R. V. , Gravisaco M. J. , Forrellad M. A. , Magistrelli G. , Bigi F.

Journal of Veterinary Research

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2021

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tom 65

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nr 3

4

Innate defenses to intestinal cell death in necrotizing enterocolitis – spotlight on macrophage efferocytosis and its efficacy in rescuing inflamed intestinal mucosa

88%

Kanuri S. H. , Bagang N. , Ulucay A. S. , Pandey P. , Singh G.

European Journal of Clinical and Experimental Medicine

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2023

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nr 2

365-396

EN

Introduction and aim. Necrotizing enterocolitis (NEC) is a grave gastrointestinal disease of preterm infants which is widely prevalent in the neonatal intensive care units. Current treatment options are very limited with high mortality and morbidity. With no disease specific interventions, understanding nascent cellular events that occur immediately after microbial insult can offer insights for devising novel treatment options for curtailing the disease progression in NEC. In this regard, intestinal cell death in NEC is a primordial cell-signaling event and is regarded as a harbinger of future pathological derangements such as increased intestinal permeability, intestinal dys-homeostasis, and systemic inflammation. Material and methods. We performed PubMed search of relevant articles that describes the host response to intestinal cell death in NEC by cellular battalion including dendritic cells, lymphocytes, neutrophils and macrophages which are important in containing intestinal inflammation. Analysis of the literature. We particularly focused this review on enumerating macrophage efferocytosis, and pertinent novel treatment modalities based on this physiological process that has inherent capability for down regulating inflammation and promoting tissue repair in NEC. We highlighted its mechanistic aspect including mediators, receptors and signaling mechanisms and its physiological significance. Conclusion. Macrophage efferocytosis is an overlooked and undervalued physiological defense mechanism to clear the dying intestinal epithelial cells for facilitating tissue healing and restoring the intestinal homeostasis. Any impairment of this critical defense mechanism can result in rapid clinical progression and systemic complications. Understanding its importance in the pathogenesis of NEC is important for designing novel therapeutic interventions to attenuate disease progression.

5

Thymocyte-macrophage interactions. Interleukin 6 produced by activated thymocytes induces interleukin 1 production by macrophages

88%

Zimecki M. , Wieczorek Z. , Kapp J. A.

Archivum Immunologiae et Therapiae Experimentalis

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1994

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tom 42

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nr 3

6

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

75%

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

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nr 1

143-150

EN

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.

7

Role of bronchoalveolar lavage in the initial diagnosis of smoking-related interstitial lung diseases

75%

Domagala-Kulawik J. , Maskey-Warzechowska M. , Krenke R. , Chazan R.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 6

243-251

8

Glial scar instability after brain injury

75%

Frontczak-Baniewicz M. , Walski M.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

|

nr 4

97-102

EN

Glial scar is formed following surgical damage to the cerebral cortex. In the present study we examined the ultrastructural status of the cerebral cortex 14 to 180 days following surgical damage to cerebral parenchyma. The results showed a contribution of astrocytes, but also mesodermal cells, to the process of scar formation. Furthermore, our study showed that the process initiated by trauma did not terminate with the formation of a glial scar. Late phases of repair following tissue damage were associated with lytic processes and a disassembly of the cerebral parenchyma. These findings indicate a changing and unstable nature of the glial scar and its components.

9

TCRalphabeta plus CD8plus and TCRgammadeltaplus lymphocytes inhibit the capability of peritoneal macrophages to induce contact hypersensitivity

75%

Majewska M. , Zajac K. , Zemelka M. , Sura P. , Gryglewski A. , Szczepanik M.

Folia Biologica

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2009

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tom 57

|

nr 1-2

23-27

10

Modulation of murine macrophages and T lymphocytes by lysozyme dimer

75%

Obminska-Mrukowicz B. , Szczypka M. , Gaweda B.

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nr 4

EN

The effects of lysozyme dimer (2 and 20 μg/kg) administered i.p. once and four times to mice on the phagocytic and killing ability of peritoneal macrophages, interleukin-1 (IL-1) production by murine macrophages stimulated in vitro with lipopolisaccharide of E. coli and expression of thymocyte, splenocyte and mesenteric lymphonode cell CD3+, CD4+ and CD8+ markers were studied. It was found that lysozyme dimer administered once or four times at doses of 2 (μg/kg and 20 μg/kg augments the phagocytic and killing activity of peritoneal macrophages. The strongest stimulating effect was noted after four injections of lysozyme dimer at a dose of 20 μg/kg. Moreover, lysozyme dimer is able to modulate the production of IL-1 by murine macrophages stimulated in vitro with LPS. Exposure to four doses of lysozyme dimer (20 μg/kg) enhances the synthesis and release of IL-1, but this drug administered once (2 μg/kg and 20 μg/kg) or four times (2 μg/kg) decreases IL-1 production by peritoneal macrophages. It was also found that administration of lysozyme dimer at a dose of 20 μg/kg, irrespective of the number of doses applied, increases the percentage of CD4+ thymocytes and splenocytes. Moreover, exposure to four doses of lysozyme dimer (2 and 20 μg/kg) increases the percentage of CD4+ and CD8+ mesenteric lymphonode cells.

11

Encephalitozoon intestinalis infection impacts the expression of apoptosis-related genes in U937 macrophage cells

75%

Cetinkaya U. , Caner A. , Charyyeva A. , Senturk M. , Eren M.

Acta Parasitologica

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2021

|

tom 66

|

nr 2

12

Electron microscope picture of the epithelium and epithelial-connective borderline in leukoplakia of the buccal mucous membrane

75%

Knychalska-Karwan Z. , Pawlicki R.

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nr 3

13

Cellular elements of the immune system in the larynx cancer, SEM study

75%

Kus J. , Miodonski A. J. , Olszewski E. , Sekula J.

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nr 3

14

Survival of Corynebacterium pseudotuberculosis within macrophages and induction of phagocytes death

75%

Stefanska I. , Gierynska M. , Rzewuska M. , Binek M.

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tom 13

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nr 1

143-149

EN

Since C. pseudotuberculosis is a facultative intracellular pathogen the aim of this study was focused on evaluating mechanisms that allowed these bacteria to survive in macrophages and determining their influence on induction of cell death. The influence of Corynebacteria on the programmed cell death of macrophages was determined on the basis of induction the autophagy and apoptosis in the cultures of murine macrophage cell lines J774 infected with bacteria. Corynebacterium pseudotuberculosis strains could survive within macrophages more than 48 hours. During that time bacteria were released as a result of the process that lead to death of phagocytes. This property varied among studied strains. There was no increase of micro- tubule-associated protein I light chain 3 (MAP I LC3) activity in macrophages infected with examined strains comparing with uninfected cultures and cultures treated with autophagy inducer (rapamycin) that served as negative and positive controls, respectively. The study with confocal microscopy did not show the increasing of caspase-3 activity in the infected macrophages and their nucleus did not reveal the fragmentation.

15

Macrophage profile in primary versus secondary liver tumors

75%

Avadanei E.-R. , Wierzbicki P. M. , Giusca S.-E. , Grigoras A. , Amalinei C. , Caruntu I.-D.

Folia Histochemica et Cytobiologica

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2014

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tom 52

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nr 2

16

Phagocytic and bactericidal properties of macrophages of mice immunized with outer membrane proteins (OMP) of Shigella

75%

Czarny A. , Witkowska D. , Mulczyk M.

Archivum Immunologiae et Therapiae Experimentalis

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1988

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tom 36

|

nr 6

17

Inhibition of NOS-2 induction in LPS-stimulated J774.2 cells by 1,5-isoquinolinediol, an inhibitor of PARP

75%

Olszanecki R. , Gebska A. , Jawien J. , Jakubowski A. , Korbut R.

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nr 1

EN

Activation of both poly (ADP-ribose) polymerase (PARP) and inducible nitric oxide synthase (NOS-2) have been implicated in the pathogenesis of various forms of inflammation, therefore compounds which may simultaneously inhibit both pathways are of potential therapeutic interest. We tested the influence of potent inhibitor of PARP, 1, 5-isoquinolinediol (ISO), on NOS-2 induction in model of mouse macrophages (cell line J774.2) stimulated with lipopolysaccharide (1 µg/ml). Pretreatment with ISO (1-300 µM) resulted in dose-dependent inhibition of accumulation of NOS-2-derived nitrite in culture medium (IC50 = 9,3 µM) as well as inhibition of NOS-2 protein induction in cultured J774.2 cells; ISO given 10 hours after LPS did not influence activity of NOS-2. Interestingly, another PARP inhibitor, 3-aminobenzamide (3-AB, 10-3000 µM), did not influence 24-hr nitrite accumulation in J774.2 cell culture, either administered 15 minutes prior to LPS or 10 hrs after LPS. Scavenging of reactive oxygen species by use of mixture of SOD and catalase (SOD/Cat, 100/300 - 1000/3000 U/ml) as well as cell permeable SOD-mimetic [Mn(III)TBAP, 1- 100 µM], did not influence NOS-2 induction in J774.2 cells. In summary, we identified 1, 5-isoquinoline as potent inhibitor of induction of NOS-2 in LPS-treated mouse macrophages. The exact mechanism of inhibitory action of this compound on NOS-2 induction requires further investigation.

18

High molecular mass dextran sulfate increases expression of HIV-1 coreceptor CCR-5 in macrophage-monocytes in culture

75%

Jagodzinski P. P. , Trzeciak W. H.

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nr 1

EN

It has been reported that high molecular mass dextran sulfate (HMDS) enhances the infection of monocyte-macrophages by HIV-1. We observed that in monocyte-macrophages maintained in the presence of HMDS the expression of HIV-1 coreceptor CCR-5 was increased approximately 5-fold at the transcriptional level. We postulate that the increased expression of CCR-5 might be responsible for HMDS-enhanced infectivity of monocyte-macrophages by HIV-1.

19

Flavonoids and nitric oxide synthase

75%

Olszanecki R. , Gebska A. , Kozlovski V. I. , Gryglewski R. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

EN

Induction of NOS-2 in macrophages and smooth muscles within vascular wall with concomittant suppression of endothelial NOS-3 activity is considered to be a hallmark of vascular inflammation that triggers atherogenesis. Accordingly, drugs designed to reverse these changes should not only support vaning function of NOS-3 but also suppress proinflammatory NO production by NOS-2. It means that using selective inhibitors of induction of NOS-2 (they spare ex definitione constitutive activity of NOS-3) is a more rational approach than using isselectivel. inhibitors of activity of previously induced NOS-2. First of all, those drugs are never sufficiently selective. In our work we tried to identify inhibitors of NOS-2 induction within the group of flavonoids, known stimulators of NOS-3 with putative antiatherogenic effects. Representatives of four main groups of flavonoids: flavonols (kaempferol, quercetin, rutin), flavones (apigenin, primuletin), flavanols (catechine) and flavanones (hesperetin, hesperidin, naringenin) were tried on NOS-2 induction and activity in the in vitro model of LPS-treated macrophages (cell line J774.2). While none of these compounds inhibited activity of NOS-2, all with unexpectedly scattered potencies inhibited induction of NOS-2 protein in LPS-treated J774.2 cells, as evidenced by Western blotting technique. Subsequently, RT-PCR and Northern blotting methods revealed that so far the most potent compounds, kaempferol and apigenin, at micromolar concentrations did inhibit NOS-2 induction at the level of NOS-2 gene transcription. We conclude that some of flavonoids are potent inhibitors of NOS-2 induction. At the same time they may increase endothelial NOS-3 activity. Could these flavonoids become natural parents of future drugs, which will be used for reversal of inflammatory component of atherothrombosis?

20

Genetical control on Lentinan - induced acute phase responses and vascular responses

75%

Maeda Y. Y. , Sakaizumi M. , Moriwaki K. , Chihara G. , Yonekawa H.

Folia Histochemica et Cytobiologica

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1992

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tom 30

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nr 4