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The role of leukotrienes in the pathophysiology of bronchial asthma - the perspective of therapy

100%

Wojnowski P. , Patkowski J.

Postępy Higieny i Medycyny Doświadczalnej

1997

tom 51

nr 5

499-514

Leukotrienes, products of the 5-lipoxygenase pathway of arachidonic acid, are pro-inflammatory mediators with various biological activities, including mechanisms relevant to the pathogenesis of bronchoobturation in bronchial asthma. This article reviews the evidence on their role in the pathophysiology of asthma as well as on the efficacy of recently developed antileukotriene agents. Leukotriene receptor antagonists and synthesis of inhibitors show promise as a new pharmacologic approach to the treatment of this disease.

Effect of recombinant IFN-gamma on IgE-dependent leukotriene generation by peripheral blood leukocytes in patients with pollinosis and asthma

80%

Krasnowska M. , Medrala W. , Malolepszy J. , Krasnowski R.

Archivum Immunologiae et Therapiae Experimentalis

2000

tom 48

nr 4

287-292

Interferon gamma (IFN-gamma) is considered one of the causative and intensifying factors in inflammation. The reaction to allergens releases IFN-gamma, an immunomodulatory cytokine known to inhibit IgE synthesis and Th cell proliferation. The aim of the study was to evaluate the influence of IFN-gamma on leukotriene (LT) release in vitro, from human leukocytes of atopic patients with pollinosis and asthma. Thirty-eight patients were enrolled in the study: 15 with pollinosis and 23 asthmatics. In the presence of IL-3, leukocytes were stimulated with specific allergens. Other samples of leukocytes were preincubated with different concentrations of IFN-gamma for 15 min before allergen stimulation. The concentration of LT in supernatants was measured according to the CAST-ELISA procedure. We stated that IFN-gamma had significantly diminished LT release in a dose-dependent mode from the leukocytes of pollinotics. IFN-gamma did not change LT release in the asthmatic group, although, in leukocytes the small and medium basic production of LT, IFN-gamma caused a statistically significant fall in LT generation.

Nuclear import of arachidonate 5-lipoxygenase

80%

Brock T. G. , Healy A. M.

Archivum Immunologiae et Therapiae Experimentalis

2000

tom 48

nr 5

481-486

Leukotrienes are lipid messenger molecules that are secreted by leukocytes to orchestrate a rapid and prolonged immune response. The enzyme 5-lipoxygnease catalyzes the rate-limiting first two steps in the synthesis of leukotrienes from arachidonic acid. Although it has long been known that 5-lipoxygenase moves from the cytoplasm to a membrane following activation, it has only recently been recognized that the enzyme may shuttle into and out of the nucleus before activation. The regulation of this movement of soluble 5-lipoxygenase between the cytoplasm and the nucleoplasm, as well as its impact on 5-lipoxygenase action, leukotriene synthesis and cell function, is only now being elucidated. This review details the state of our understanding of the nuclear import of 5-lipoxygenase and its potential importance in immunity.

Leukotrienes ? mediators of inflammation

80%

Woszczek G. , Pawliczak R. , Kowalski M. L.

Postępy Higieny i Medycyny Doświadczalnej

2003

tom 57

nr 5

593-610

Leukotrienes are biologically active metabolites derived from arachidonic acid playing an important role in inflammatory responses. There are two main groups of leukotrienes: dihydroxy-leukotrienes (LTB4) and cysteinyl-leukotrienes (LTC4, LTD4, LTE4). By activating specific G-protein coupled receptors, leukotrienes take part in immune responses, like activation and chemotaxis of leukocytes. Several studies have shown that leukotrienes may play a significant role in pathomechanisms of inflammatory diseases of human airways, skin, digestive tract and heart.

Eicosanoid regulation of pulmonary innate immunity post-hematopoietic stem cell transplantation

60%

Ballinger M. N. , McMillan T. R. , Moore B. B.

Archivum Immunologiae et Therapiae Experimentalis

2007

tom 55

nr 1

1-12

Hematopoietic stem cell transplantation (HSCT) is a therapeutic option for a number of malignant and inherited disorders. However, the efficacy of this therapy is limited by a number of serious infectious and noninfectious complications. Pulmonary infections represent a significant cause of morbidity and mortality post-HSCT and can occur both pre- and post-hematopoietic reconstitution. Susceptibility to Gram-negative bacterial infections despite full hematopoietic engraftment suggests that innate immunity remains impaired months to years post-HSCT. This review will describe the process and complications of HSCT and will summarize what is known about innate immune reconstitution post-HSCT. Data from the literature as well as our own laboratory will be presented to suggest that an eicosanoid imbalance characterized by over-production of prostaglandins and under-production of leukotrienes leads to impaired lung phagocyte function post-HSCT. Of therapeutic interest, strategies which limit production of prostaglandins can improve pulmonary host defense in animal HSCT models, which suggests that this may also be beneficial for human HSCT recipients.