Interleukin-1 Release by Alveolar Macrophages in Asthmatic Patients and Healthy Subjects

Pujol, Jean-Louis; Cosso, B.; Daurès, Jean‐Pierre; Clot, J; Michel, François‐Bernard; Godard, P.

doi:10.1159/000235117

Cited by 51 publications

(26 citation statements)

References 4 publications

(5 reference statements)

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“…Similar results have previously been observed for other mediators, namely that the spontaneous release of mediators by "resting cells" may be very high, without modification of the total release after PMA-stimulation. This has been observed with alveolar macrophages, either for interleukin-1 (IL-1) release by PUJOL et al [27], or for phosphoinositide turnover by DAMON et al [28].…”

Section: Discussionmentioning

confidence: 88%

Enhancement of reactive oxygen species formation in stable and unstable asthmatic patients

Vachier

Chanez²,

Doucen³

et al. 1994

Eur Respir J

107

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E En nh ha an nc ce em me en nt t o of f r re ea ac ct ti iv ve e o ox xy yg ge en n s sp pe ec ci ie es s f fo or rm ma at ti io on n i in n s st ta ab bl le e a an nd d u un ns st ta ab bl le e a as st th hm ma at ti ic c p pa at ti ie en nt ts s ABSTRACT: There is increasing evidence to suggest that human blood polymorphonuclear neutrophils (PMNs) and monocytes play an important role in the inflammatory processes of asthma. In asthmatic patients, PMNs and monocytes were shown to be activated more than in healthy subjects. We investigated the capacity of these two cell populations to generate reactive oxygen species (ROS) in stable and unstable asthmatic patients. The two populations of asthmatic patients were identified by asthma activity, as expressed by clinical events occurring within 2 weeks prior to the study. Oxygen species formation was analysed for isolated purified PMNs and monocytes (Mos) by chemiluminescence (CL) using lucigenin and luminol as luminescent probes. CL was determined on nonstimulated and on phorbol myristate acetate (PMA)-stimulated cells. The stimulatability coefficient (PMA-stimulated/nonstimulated cell ratio) of each cell population was then calculated.Resting PMNs and Mos generated significantly greater amounts of ROS in stable asthmatic patients, and much more in unstable asthmatic patients, as compared to healthy subjects, both in lucigenin and luminol enhanced CL. Non O 2 · -ROS production from PMA-stimulated PMNs and Mos was identical in unstable asthmatic patients and in healthy subjects, whereas a significant decrease was observed in stable asthmatic patients, as assessed by luminol enhanced CL. PMA-stimulated cells showed no difference in O 2 · -generation, as assessed by lucigenin enhanced CL. However, the stimulatability coefficient of all asthmatic patients was always significantly lower than that of healthy subjects.These results suggest that there are differences in priming and stimulation of Ros production from PMNs and Mos between stable and unstable asthmatic patients. Release of oxygen species from these cells may be implicated in the pathophysiology of unstable asthma.

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Section: Discussionmentioning

confidence: 88%

Enhancement of reactive oxygen species formation in stable and unstable asthmatic patients

Vachier

Chanez²,

Doucen³

et al. 1994

Eur Respir J

107

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“…In recent years, substantial evidence has been accumulated in support of the concept that cytokines are key regulators of the cascade of cellular events associated with airway inflammation in atopic asthma (2,27,(35)(36)(37)(38). In this regard, some studies have demonstrated elevated levels of various cytokines in the bronchoalveolar lavage fluid from asthmatic patients (8-10).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of cytokine-induced modulation of beta-adrenoceptor responsiveness in airway smooth muscle.

Hákonarson

Herrick²,

Serrano³

et al. 1996

J. Clin. Invest.

128

112

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To elucidate the role of specific proinflammatory cytokines in regulating airway responsiveness, we examined the effects and mechanisms of action of IL-1 ␤ , TNF-␣ , and IL-2 on the ␤ -adrenoceptor-and postreceptor-coupled transmembrane signaling mechanisms regulating relaxation in isolated rabbit tracheal smooth muscle (TSM) segments. During half-maximal isometric contraction of the tissues with acetylcholine, relaxation responses to isoproterenol, PGE 2 , and forskolin were separately compared in control (untreated) TSM and tissues incubated for 18 h with IL-1 ␤ (10 ng/ml), TNF-␣ (100 ng/ml), or IL-2 (200 ng/ml). Relative to controls, IL-1 ␤ -and TNF-␣ -treated TSM, but not IL-2-treated tissues, depicted significant attenuation of their maximal relaxation and sensitivity (i.e., Ϫ log dose producing 50% maximal relaxation) to isoproterenol ( P Ͻ 0.001) and PGE 2 ( P Ͻ 0.05); whereas the relaxation responses to direct stimulation of adenylate cyclase with forskolin were similar in the control and cytokine-treated tissues. Further, the attenuated relaxation to isoproterenol and PGE 2 was ablated in the IL-1 ␤ -treated TSM that were pretreated with either the muscarinic M 2 -receptor antagonist, methoctramine (10

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“…There is increasing evidence that a range of pro-inflammatory cytokines play an important role in orchestrating and perpetuating the airway inflammatory response in asthma (3). Among these pro-inflammatory cytokines, interleukin-1 ␤ (IL-1 ␤ ) which is an important mediator controlling inflammatory and immune responses (4,5) has been implicated in asthma. IL-1 has been measured in increased amounts in bronchoalveolar lavage fluid and in supernatants of alveolar macrophages from asthmatic patients (4,6).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of impaired beta-adrenoceptor-induced airway relaxation by interleukin-1beta in vivo in the rat.

Kojima

Mak²,

Haddad³

et al. 1996

J. Clin. Invest.

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We studied the in vivo mechanism of ␤ -adrenergic receptor ( ␤ -AR) hyporesponsiveness induced by intratracheal instillation of interleukin-1 ␤ (IL-1 ␤ , 500 U) in Brown-Norway rats. Tracheal and bronchial smooth muscle responses were measured under isometric conditions ex vivo. Contractile responses to electrical field stimulation and to carbachol were not altered, but maximal relaxation induced by isoproterenol (10 Ϫ 6 -10 Ϫ 5 M) was significantly reduced 24 h after IL-1 ␤ treatment in tracheal tissues and to a lesser extent, in the main bronchi. Radioligand binding using [

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Interleukin-1 Release by Alveolar Macrophages in Asthmatic Patients and Healthy Subjects

Cited by 51 publications

References 4 publications

Enhancement of reactive oxygen species formation in stable and unstable asthmatic patients

Enhancement of reactive oxygen species formation in stable and unstable asthmatic patients

Mechanism of cytokine-induced modulation of beta-adrenoceptor responsiveness in airway smooth muscle.

Mechanisms of impaired beta-adrenoceptor-induced airway relaxation by interleukin-1beta in vivo in the rat.

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