Inhibitions of metabolic responses of polymorphonuclear leukocytes by antiallergic drugs.

Taniguchi, Katsuhiko; Takanaka, Koichiro

doi:10.1248/bpb1978.12.37

Cited by 13 publications

(4 citation statements)

References 22 publications

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“…On the other hand, the acidic agents were developed on the basis of ob servations that DSCG (disodium cromogly cate), bicalein and caffeic acid are inhibitors of chemical mediator release (12,15). We have previously shown that superoxide generation, arachidonic acid release as well as changes of membrane potential were sup pressed by one of the basic antiallergic agents, azelastine (16)(17)(18). In this study, we attemped to compare the inhibitory effects of antial lergic drugs on the release of arachidonic acid, leukotriene B4 and superoxide from ac tivated human neutrophils to clarify the action sites of the various basic and acidic anti allergic drugs.…”

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confidence: 99%

Action sites of antiallergic drugs on human neutrophils.

1990

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Abstract-Sites of the inhibitory action of antiallergic drugs (azelastine, oxatomide, tranilast, repirinast and amlexanox) on human neutrophils were investigated by measuring leukotriene B4 formation, arachidonic acid release and superoxide generation. Results obtained in this study were as follows: (1) Formations of leukotriene B4 by neutrophils activated with a calcium ionophore (A23187) were effectively inhibited by all types of antiallergic drugs examined here, although the required concentrations were within a range of 20-200 /tM. (ii) Releases of arachidonic acid from activated cells were diminished by azelastine and oxatomide that were classified as basic antiallergic drugs. On the contrary, acidic antiallergic agents including repirinast, amlexanox and tranilast enhanced the arachidonic acid liberation. (iii) Generations of superoxide from neutrophils activated with either phorbol 12-myristate 13-acetate or n-formyl-methionyl-leucyl-phenylalanine were effectively diminished only by the basic antiallergic drugs.

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confidence: 99%

Action sites of antiallergic drugs on human neutrophils.

1990

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“…Moreover, ketotifen may act on inflammatory cells other than mast cells. For example, it may reduce the functions of mobility and phagocytosis of polymorphonuclear cells [43], it may reduce the chemotaxis of neutrophils [44] or it may inhibit their metabolic responses [45]. It also inhibits leukotriene C 4 release and PAF-induced chemotaxis of eosinophils [46].…”

Section: Discussionmentioning

confidence: 99%

Development and Sequels of Intestinal Inflammation in Nematode-Infected Rats: Role of Mast Cells and Capsaicin-Sensitive Afferents

Gay¹,

Fioramonti²,

Garcia‐Villar³

et al. 2000

Neuroimmunomodulation

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Objectives: To determine whether intestinal mast cells and capsaicin-sensitive afferent nerves are involved in the development and sequels of Nippostrongylus brasiliensis-induced intestinal inflammation in rats. Methods: Two series of experiments were performed. In the first series, six groups of 8 rats were used to study the effects of mast cell stabilization by ketotifen. In the second series, six groups of 6 rats were used to study the effects of gut extrinsic sensory neuron depletion by capsaicin. For each series, four groups of rats were infected with N. brasiliensis and two groups were not infected. Results: Infection with N. brasiliensis resulted in an increase of myeloperoxidase (MPO) activity and mast cell numbers at day 12 postinfection; MPO returned to preinfection levels by day 35 while mast cell numbers remained elevated at that time. In ketotifen-treated infected rats, the increase of MPO at day 12 was less pronounced, but MPO activity remained elevated and mast cell numbers were increased at day 35. In capsaicin-treated infected rats, the MPO increase at day 12 was augmented, and MPO was still not returned to preinfection values by day 35; in contrast, the increase of mast cell numbers at days 12 and 35 was not modified by afferent nerve depletion. Conclusion: Mast cell stabilization decreased jejunal inflammation during the acute stage (day 12), but prolonged the inflammatory process until at least day 35 postinfection. The data also confirmed the protective role of gut extrinsic sensory neurons against intestinal inflammation in a model of nematode infection and revealed that these afferent nerves do not seem crucial for the development of nematode-induced hypermastocytosis.

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“…It has been shown that it prevents the synthesis/release of mediators such as histamine (Chand et al, 1985), leukotrienes (Chand et al, 1989;Nishihira et al, 1989), superoxide anions (Busse et al, 1989;Taniguchi & Takanaka, 1989), arachidonic acid (Taniguchi & Takanaka, 1989), and that it antagonizes the effect of some of these mediators on target organs (Rafferty et al, 1989). In addition, Nakamura et al (1988) have shown that azelastine inhibits the release of Ca2+ from intracellular storage sites in guinea-pig peritoneal macrophages stimulated by PAF or by FMLP.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, Nakamura et al (1988) have shown that azelastine inhibits the release of Ca2+ from intracellular storage sites in guinea-pig peritoneal macrophages stimulated by PAF or by FMLP. Azelastine was also described as an inhibitor of leukocyte (Chand et al, 1985;Taniguchi & Takanaka, 1989;Busse et al, 1989), and platelet functions (Achterrath-Tuckermann et al, 1988). Azelastine is effective in animals (Chand et al, 1986;AchterrathTuckermann et al, 1988), and has been claimed to reduce allergic rhinitis (Meltzer et al, 1988) and asthma Kemp et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Interference of anti‐inflammatory and anti‐asthmatic drugs with neutrophil‐mediated platelet activation: singularity of azelastine

Renesto

Balloy

Vargäftig

et al. 1991

British J Pharmacology

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1 The capacity of various drugs (acetylsalicylic acid (ASA), ketoprofen, diclofenac, piroxicam, BW 755C, BW A4C, nedocromil sodium and azelastine) to inhibit human polymorphonuclear neutrophil (PMN)-mediated platelet activation was investigated. In this model, stimulated PMN release cathepsin G (Cat G), a serine proteinase which, in turn, induces platelet activation. 2 Among the different tested drugs, azelastine (100pM for 1 min) was the only one able to prevent platelet aggregation. The cyclo-oxygenase inhibitors were all inactive, although used at effective concentrations as judged by inhibition of thromboxane B2 (TxB2) formation. Inhibition of platelet aggregation by azelastine was concentration-dependent, the range of active concentrations being of 20-70pM. Release from platelets of 5-hydroxytryptamine was also inhibited at 3OpM and above, but never reached 100%. 3 The inhibition by azelastine is due to an effect on both cells. Indeed, f-glucuronidase release from activated PMN and platelet activation by purified Cat G were both affected.4 However, used at high concentrations (>100,UM) azelastine was toxic since it released significant amounts of lactate dehydrogenase (LDH) from PMN and platelets. 5 These results show the capacity of azelastine, an anti-allergic and anti-asthmatic compound, to inhibit the cell-to-cell communication between PMN and platelets, an effect which may be relevant for its therapeutic efficacy or for a new application in diseases in which PMN and platelets are involved.

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Inhibitions of metabolic responses of polymorphonuclear leukocytes by antiallergic drugs.

Cited by 13 publications

References 22 publications

Action sites of antiallergic drugs on human neutrophils.

Action sites of antiallergic drugs on human neutrophils.

Development and Sequels of Intestinal Inflammation in Nematode-Infected Rats: Role of Mast Cells and Capsaicin-Sensitive Afferents

Interference of anti‐inflammatory and anti‐asthmatic drugs with neutrophil‐mediated platelet activation: singularity of azelastine

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