1991
DOI: 10.1016/0162-3109(91)90043-x
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Benzodiazepines inhibit neutrophil chemotaxis and superoxide production in a stimulus dependent manner; PK-11195 antagonizes these effects

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Cited by 38 publications
(19 citation statements)
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“…Indeed, synthetic pBR ligands modulate neutrophil chemotaxis and superoxide production [12,13], monocyte chemotaxis and production of cytokines [14][15][16], and peripheral blood mononuclear cell proliferation and cytokine secretion [17]. At present, however, the immune effects of DBI-derived peptides have received little attention, although at least some of them seem to affect important mechanisms in host defense and inflammation, such as cytokine production by human monocytes [15,16,18].…”
Section: Introductionmentioning
confidence: 99%
“…Indeed, synthetic pBR ligands modulate neutrophil chemotaxis and superoxide production [12,13], monocyte chemotaxis and production of cytokines [14][15][16], and peripheral blood mononuclear cell proliferation and cytokine secretion [17]. At present, however, the immune effects of DBI-derived peptides have received little attention, although at least some of them seem to affect important mechanisms in host defense and inflammation, such as cytokine production by human monocytes [15,16,18].…”
Section: Introductionmentioning
confidence: 99%
“…Most cellular components of the immune system are endowed with pBZrs, such as the thymus gland, spleen and lymph nodes [5], neutrophils [6], monocytes and macrophages [7][8][9], and lymphocytes [10]. Experimental evidence indicates that pBZrs are involved in the modulation of leukocyte function [9,[11][12][13][14], providing a possible explanation for the immunologic side effects of anticonvulsant drugs [15].…”
Section: Introductionmentioning
confidence: 99%
“…A densidade de RPBs nas células do sistema imune, é maior que a concentração destes receptores no sistema neuroendócrino (Zavala et al, 1990), o que poderia explicar a ação imunomoduladora de alguns benzodiazepínicos, como a redução da resistência às infecções, redução do burst oxidativo e da fagocitose por macrófagos, inibição da quimiotaxia de células inflamatórias e diminuição da produção do ânion superóxido e de algumas interleucinas (Finnerty et al, 1991;Galdiero et al, 1995;Lazzarini et al, 2001Lazzarini et al, , 2003Massoco, Palermo-Neto, 1999Zhang, Morrison, 1993).…”
Section: Introductionunclassified