Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 18

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  eicosanoid
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Prostaglandins have been already pretty well rccognized as metabolic regulators in vertebebrata tissues mainly in mammals. Less reports concerned the occurrence of prostaglandins in invertebrates. In the present review we summarise literature data about the presence of prostaglandins and other eicosanoids in various groups of parasites and their possible role in hostparasite interaction. Prostaglandins have also been found in very primitive organisms as bacteria, varions plants and protozoa. We summarise that prostaglandins seem to be a very ancient group, going back to the roots of evolution. They are as universal in cell physiology as DNA in genetics. In host-parasiter eicosanoids also parasitic origin, play an important role as a modulators of hosts immune responsiveness.
The aim of the study was to investigate the influence of Mycoplasma bovis challenge in calves on the alteration of acute- phase response (APR). The study was performed on twelve calves aged 4-8 weeks. The animals were divided into two equal groups: experimental and control. Calves in the experimental group were intratracheally challenged with pathogenic strain of Mycoplasma bovis, whereas controls received sterile physiological saline as placebo. The blood samples were collected before (1st d) and after the mycoplasma challenge (3, 5, 7 and 9th d). The following parameters were assayed in serum: acute phase proteins (APPs), i.e. haptoglobin (Hp) and amyloid A (SAA), and eicosanoids such as prostaglandin E₂ (PGE₂), prostaglandin F₂ₐ (PGF₂ₐ), leukotrien B4 (LTB₄), and tromboxan B₂ (TXB₂). In calves of experimental group, a significant increase in concentrations of Hp and SAA was observed when compared with the controls. A decrease in both APPs to the initial values, i.e. before the challenge, was noted on the 9th d of experiment. On the other hand, the inoculation of Mycoplasma bovis caused a significant increase of the examined eicosanoids, which maintained elevated during the whole study. The stimulation of synthesis of APPs and eicosanoids in response to the challenge with Mycoplasma bovis probably indicates the effective activation of APR under these conditions.
COX-inhibitors promote nasal polyps or bronchial asthma in individuals susceptible to an alteration of the pattern of the eicosanoids, especially leukotrienes and prostaglandins. This is associated with an abnormal release of eicosanoids from white blood cells. Since COX-inhibitors also protect from colorectal cancer an analogous association may be suggested. The study was performed to detect abnormal patterns of eicosanoids in white blood cells of patients with intestinal cancer compared to healthy controls. Seventy patients with intestinal cancer (stomach = 5; colon = 25; sigma = 18; rectum = 22) were compared to 62 healthy controls. Blood leukocytes from patients in complete long-lasting remission were incubated with diluent, arachidonic acid or acetylsalicylic acid. The synthesis of prostaglandin E2 and peptido-leukotrienes was quantified using competitive enzyme-immuno-assays and calculated for individual eicosanoid patterns. The mean basal and arachidonic- or acetylsalicylic acid-modulated PGE2 synthesis in patients was significantly higher than in controls (4.8-fold, 9.4-fold, 3.7-fold, respectively) whereas pLT was generally less elevated. We conclude that the eicosanoid-pattern of white-blood-cells from patients with intestinal cancer differs significantly from that in healthy individuals. This abnormal cellular metabolism may contribute to the manifestation of cancer and help to detect individuals at risk.
4
Content available remote

Testing and typing of eicosanoid-patterns

72%
Eicosanoids are pleiotrope mediators with essential function in most biological processes. The network of inter- and intracellular signalling requires coordinated cellular information processing. The cross-talk is characterised by complex non-linear responses to combinations of different stimuli and cells, but little is known about the density of these interactions. Here I have analysed eicosanoid interactions carried out by functional eicosanoid testing and typing (FET) in leucocytes from healthy subjects and patients suffering from inflammatory diseases. The known eicosanoid pattern scoring was extended to metabolically linked prostaglandin E2 and peptido-leukotrienes pathways, both alone and in all pair wise combinations, for basal, maximal synthesis capacity, acetylsalicylic acid, and neuropeptide modification. Eicosanoids fluctuated over twenty minutes context-dependent dynamically, demanding further data integration. The integration suggested that many stimuli converge for quantitative discrimination applying a total eicosanoid pattern score (TEP). Varying cellular activities affect FET and thereby TEP. The non-additive metabolic interactions were consistent with known mechanisms of metabolic pathway cross-talk. FET-based modelling of eicosanoid circuits most suitably reflects the fundamental impact of eicosanoids in maintaining cellular integrity of organ and body function. This might improve our present understanding of complex cellular eicosanoid interactions of inflammatory diseases and might be applied for diagnostic considerations.
5
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Functional aspects of eicosanoid metabolism

72%
The sequential metabolism of eicosanoids by AA oxygenases confers biological properties that may have significant functional implications. Further- the interpretation of the effects of cyclooxygenase inhibitors on eicosanoid, dependent mechanisms needs to be reevaluated. Previously, if cyclooxygenase inhibitors affected the biological action of AA, it was considered to be due to elimination of a prostanoid-mediated component. This interpretation is no longer valid if a cell or tissue has significant P450 and cyclooxygenase activity. The cellular proximity of the P450-dependent monooxygenases and cyclooxygenase, described in tubules, interstitial cells, and blood vessels, may confer a unique ability of A A metabolites to coordinate tubular and vascular function.
Conjugated linoleic acid (CLAs) are positional and geometric isomers of linoleic acid with have a potential anti-atherosclerotic and anti-inflammation properties. Metabolites of arachidonic acid - prostaglandins and thromboxans are endogenous mediators of inflammation. Prostaglandin E2 and thromboxan A2 which are a products of two izoformes of cyclooxygenases (COX-1 and COX-2) in macrophages, play an important role in this process. COX - 1 is a constitutive enzyme, whereas the COX - 2 is inducible and its amount in the cell rapidly increases during inflammation (e.g. via NF B pathway). The aim of the study was to test the effect of CLAs on cyclooxygenases (COX-1 and COX-2) activity, their mRNA expression and protein content in macrophages. Additionally the active form of the kB (NF B) transcription factor was measured. For the experiments monocytes from monocytic cell line (THP-1) and from human venous blood were used. Monocytes were differentiated to macrophages and cultured with 30 µM CLAs or linoleic acid for 48 h. The COX-1 and COX-2 products - PGE2 and TXB2, were measured by ELISA method. The enzymes (COX-s) activity were estimated by spectroscopic method. mRNA expression and protein analysis were analysed by real-time PCR and Western blot technique. In macrophages cultured with CLAs reduction of TXB2 and PGE2 concentration was observed. Significant change in COX-2 expression in cells cultured with trans-10, cis-12 CLA (in macrophages obtained from peripheral blood) was observed. COX-1 inhibition was resulting from competition of CLA and linoleic acid with arachidonic acid.
8
Content available remote

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

72%
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.
12
Content available remote

Functional-eicosanoid-test (FET) and disease

58%
Eicosanoids are involved in most cellular activities. Measurement of their levels in tissue or blood renders information about the function of activated cells. An extended analysis will improve the conclusions regarding eicosanoid-related diseases. Peripheral white blood cells (WBC) were used for the test. Stimulating or inhibiting substances to influence the generation and the metabolism of eicosanoids were separately added to the samples. Prostaglandins (PG) and leukotrienes (LT) were measured after incubation in culture medium for 20 minutes at room temperature. Healthy controls rendered normal data. Patients with intolerance to acetylsalicylic acid (ASS) showed an elevated output of PG and LT upon stimulation. Addition of ASS shifted from PG to LT. An altered pattern of eicosanoids also was found in patients suffering from gastroduodenal ulcer and in intestinal malignancy. The senstivity regarding the ASS-intolerance is >80% and the specifity in the same group >70%. We concluded that the FET is a suitable test for the demonstration and verification of intolerance to ASS. It also detects an imbalance of the eicosanoids in intestinal malignancy. This makes the FET a helpful tool for diagnosis and for the elucidation of pathogenic mechanisms.
In 1922, Widal et al. were the first to describe intolerance reactions to acetylsalicylic acid (ASA, e.g. in aspirin) and to other nonsteroidal anti-inflammatory drugs (NSAIDs). The full clinical picture reveals a classic triad of symptoms (Samters Triad): aspirin induced bronchial asthma (with severe acute asthma attacks), aspirin-sensitivity and chronic rhinosinusitis with nasal polyps. In many cases, nasal polyps reveal as the first symptom of ASA sensitivity indicating that the upper airways are predominantly involved in the pathogenetic process. Therefor, emphasis of this article mainly focuses on the upper airways in ASA-intolerant patients. In the last decade, clear evidence has been pointed out that ASA-intolerance is related to the abnormal metabolism of arachidonic acid leading towards excessive leukotriene (LTs) production. The resulting dysbalance of the eicosanoids leukotrien and prostaglandine might be the crucial pathophysiologic keypoint of the disease. The incidence of aspirin hypersensitivity in the general population ranges from 0.6 % to 2.5% and in adult astmatics from 4,3 % to 11%. Besides the patients history, challenge tests with Lysin-aspirin are performed as the diagnostic tool of choice. Apart from surgical or pharmacological therapy, ASA desensitization therapy is the only specific treatment of choice. As first described by Stevensson et al. in the early 1984, oral administration by means of an initial desensitization with gradually ascending doses of aspirin is followed by a daily maintenance-dose. In the last years, many publications on various desensitization protocols and routes of administration have been worked out. Recently, the intravenous route for the inititial increment desensitization has been described which might offer new therapeutical possibilities in the treatment of ASA-intolerant patients.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.