Release of adenosine from human neutrophils stimulated by platelet activating factor, leukotriene B4 and opsonized zymosan
نویسندگان
چکیده
Isolated human polymorphonuclear leukocytes (PMNL) stimulated by platelet activating factor (PAF), leukotriene B(4) (LTB(4)) or opsonized zymosan (OZ) released adenosine measured by thermospray high performance liquid chromatography mass spectrometry in the cell-free supernatants. Stimulation by PAF or LTB(4) resulted in a bellshaped concentration-effect curve; 5 x 10(-7) M PAF, 10(-8) M LTB(4) and 500 mug ml(-1) OZ induced peak adenosine release, thus cytotoxic concentrations did not elevate adenosine level in the supernatants. Therefore adenosine release was characteristic of viable cells. As calculated from concentration-effect curves, the rank order of potency for adenosine release was PAF > LTB > OZ. These resuits suggest that adenosine, when bound specifically to membrane receptor sites, may initiate signal transduction, and, in co-operation with other inflammatory mediators, may modulate phagocyte function, e.g. production of chemoluminescence (CL).
منابع مشابه
Exogenous leukotriene B4 (LTB4) inhibits human neutrophil generation of LTB4 from endogenous arachidonic acid during opsonized zymosan phagocytosis.
The effect of exogenous leukotriene B4 (LTB4) on opsonized zymosan-stimulated human neutrophil formation of 5-lipoxygenase products and arachidonic acid release was directly assessed using reverse-phase HPLC/tandem mass spectrometric methods for quantitation. Stable isotopically labeled LTB4, [1,2-13C2]LTB4, caused a dose-dependent inhibition of LTB4 production in isolated human neutrophils wit...
متن کاملFormation and release of nitric oxide from human neutrophils and HL-60 cells induced by a chemotactic peptide, platelet activating factor and leukotriene B4.
Vascular endothelial cells and neutrophils synthesize and release potent vasodilatatory factors, i.e. endothelium-derived relaxing factors (EDRF) and neutrophil-derived relaxing factors (NDRF). One EDRF has been identified as nitric oxide (NO) derived from arginine. We studied the synthesis and release of NO from human neutrophils stimulated with the chemotactic peptide N-formyl-L-methionyl-L-l...
متن کاملEffects of adhesins from mannose-resistant Escherichia coli on mediator release from human lymphocytes, monocytes, and basophils and from polymorphonuclear granulocytes.
We investigated the role of Escherichia coli expressing mannose-resistant hemagglutination and adhesins with regard to the induction of leukotrienes from a suspension of human lymphocytes, monocytes, and basophils (LMBs) compared with human polymorphonuclear granulocytes (PMNs). Genetically cloned E. coli strains expressing various types of mannose-resistant hemagglutination (MRH+) were phagocy...
متن کاملConstitutive apoptosis in equine peripheral blood neutrophils in vitro
The aim of this study was to characterise constitutive apoptosis in equine peripheral blood neutrophils, including assessment of factors that potentially modulate neutrophil survival through alteration of the rate of constitutive apoptosis. Cells underwent spontaneous time-dependent constitutive apoptosis when aged in culture for up to 36 h, developing the structural and functional features of ...
متن کاملStimulus-specific induction of phospholipid and arachidonic acid metabolism in human neutrophils
Phospholipid remodeling resulting in arachidonic acid (AA) release and metabolism in human neutrophils stimulated by calcium ionophore A23187 has been extensively studied, while data obtained using physiologically relevant stimuli is limited. Opsonized zymosan and immune complexes induced stimulus-specific alterations in lipid metabolism that were different from those induced by A23187. [3H]AA ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Mediators of Inflammation
دوره 1 شماره
صفحات -
تاریخ انتشار 1992