Autacoids as modulators of the inflammatory and immune response

Melmon, Kenneth L.; Rocklin, Ross E.; Rosenkranz, Roberto P.

doi:10.1016/0002-9343(81)90264-3

Cited by 76 publications

(28 citation statements)

References 33 publications

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“…(i) PEA is predominately an H1 agonist but does have weaker H2 agonist effects (18). Preincubation ofregulatory cells with PEA thus may induce both I-J+ contrasuppressors and (4,7); and (iii) our findings were produced by a brief exposure to histamine, whereas all other effects have required the continuous presence of histamine, a situation unlikely to occur in vivo. Therefore, the potential for bidirectional effects and induction ofpreactivated antigen-specific regulatory cells after a brief exposure make histamine an ideal candidate for a mediator of local immune regulation in vivo.…”

Section: Tolerant Cells Expressmentioning

confidence: 69%

T-cell suppression and contrasuppression induced by histamine H2 and H1 receptor agonists, respectively.

Siegel¹,

Schwartz²,

Askenase³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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The intensity of Lyl T helper and delayed type hypersensitivity effector cell activities is governed, in part, by an interplay between two classes of immunoregulatory T cells: suppressor cells and contrasuppressor cells. We asked whether histamine, at concentrations and duration of exposure that we calculated might be achieved at local sites of inflammation, could activate either or both of these classes of regulatory cells in vitro.To answer this question we used spleen cells from mice treated in vivo with the toleragen trinitrobenzenesulfonic acid as regulators of in vitro generation of primary anti-trinitrophenyl self-cytotoxic T lymphocytes. Under the conditions used, these spleen cells had no major regulatory effects. However, if these cells were preincubated with histamine at 0.1 mM for 30-60 min, suppressor activity was induced, but this occurred inconsistently and with nonstoichiometric results. The use of synthetic histamine agonists revealed that histamine may activate both suppressor and contrasuppressor cell subsets. A histamine HI receptor agonist [2-(2-pyridyl)-ethylamine dihydrochloride] had a propensity to activate contrasuppression, whereas an H2 receptor. agonist (dimaprit) tended to activate suppressor cells. Thus, histamine may have opposing actions that obscure suppression. This duality was shown by treatment ofpyridylethylamine-induced contrasuppressor cells with complement and anti-I-J antibody that kills contrasuppressor cells. This treatment revealed a high level of suppressor cell activity that was not expressed until the opposing contrasuppressor cells were removed. Because histamine is released at local sites of delayed type hypersensitivity, these results indicate that histamine may serve as an inducer of microenvironmental immunomodulation by activating regulatory T cells at sites where immune responses are taking place.

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Section: Tolerant Cells Expressmentioning

confidence: 69%

T-cell suppression and contrasuppression induced by histamine H2 and H1 receptor agonists, respectively.

Siegel¹,

Schwartz²,

Askenase³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…see Rocklin et al, 1979;Rocklin et al, 1980a;Askenase etal., 1981;Melmon et al, 1981;Suzuki & Huchet, 1981;Thomas et al, 1981). Recently, helper T-cells have also been identified bearing histamine receptors (Siegal et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents

Andersson¹,

Bergstrand²

1984

British J Pharmacology

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Guinea‐pigs were sensitized to ovalbumin (OA) by immunization regimens chosen to cause antigen‐induced bronchial anaphylactic responses mediated mainly either by IgE‐like antibodies or by IgG1‐like antibodies. Treatment of the IgE‐producing animals for three weeks with the histamine H2‐receptor antagonist cimetidine (1 mg kg−1 i.p. once a day) or with the H2‐agonist dimaprit (0.1, 1.0, or 10 mg kg−1 i.p. once a day) led to a significantly reduced bronchial response capacity compared with that of the saline‐treated controls challenged intravenously with antigen one week after the end of treatment. The changes were biphasic and not strictly dose‐dependent. In contrast, acute treatment of immunized animals with a single dose of cimetidine (10 or 30 mg kg−1 i.v.) or dimaprit (1 or 10 mg kg−1 i.v.) 2 min before challenge with OA did not significantly affect the bronchial anaphylactic response. However, long‐term treatment with cimetidine (10 mg kg−1) or the dimaprit analogue, S‐[4‐(N, N‐dimethylamino)‐butyl] isothiourea (SKF Compound 91488) (1 mg kg−1), which is reported not to activate H2‐receptors, had no effect on the response capacity. Treatment with cimetidine (1 mg kg−1) or dimaprit (1 mg kg−1) did not influence the response capacity to antigen challenge in IgG1‐ type animals. Dimaprit (1 mg kg−1) did not affect the responsiveness to intravenous provocation with histamine in ‘IgE‐type’ animals. Antigen‐induced release of histamine from chopped lung tissue in vitro was not significantly affected in ‘IgE‐type’ animals treated with cimetidine (1 mg kg−1) or dimaprit (1 mg kg−1). Treatment of immunized animals with cimetidine or dimaprit one week before and one week after a booster injection of antigen also led to reduced response capacity compared with that of saline‐treated controls. However, the serum levels of IgE‐like homocytotropic antibodies of these animals were not reduced; on the contrary, those of IgG1‐antibody were increased in dimaprit‐treated animals. These data show that intermittent treatment with histamine H2‐agents reduces reagin‐mediated anaphylactic response capacity in vivo in actively sensitized guinea‐pigs by an as yet undefined mode of action.

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“…More recently, histamine has been shown to stimulate renin release by isolated perfused rat kidneys, an effect primarily mediated by an H2 receptor (10,11,33). In addition to its hemodynamic effects on the renal and other regional circulations, histamine is an important regulator of the immune-infl ammatory response in many tissues (34).…”

Section: Discussionmentioning

confidence: 99%

The effect of histamine on kidney by fasting in rats

Gürgen¹,

Erdoğan²,

Take-Kaplanoglu³

2013

BLL

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Abstract:Background: The aim of this study was to investigate ultrastructural and apoptotic changes occurring in the kidneys in fasting individuals and to examine the effects of histamine treatment at the electron-microscopic and immunohistochemical levels. Methods: Eighteen adult Wistar male rats were randomly divided into three groups (n=6 for each). Control group (1), fasting group (12 h) (2), and fasting+histamine injection (0.5 mg/kg) (3) group. Expression of caspase-3 and caspase-9 was determined in the tissue sections using immunohistochemical techniques. Quantitative data were obtained using H-SCORE, and statistical evaluations were then performed. The ultrastructure of the kidney tissues was examined using transmission electron microscopy. Results: Weak caspase-3 and caspase-9 expression was observed in the renal tubules and glomeruli in the control group, while immunoreactivity was more intense in the fasting group (p < 0.05). In the fasting+histamine group, caspase-3 and caspase-9 immunostaining was signifi cantly positive in both renal tubules and glomeruli (p <0.05). At electron microscopic evaluation, degenerative changes were seen in the glomeruli of the fasting group, as well as partial vacuolization and disruption at the basal foldings in the tubular epithelial cells. In the fasting+histamine group, in addition to signifi cant dilatation of all glomerular capillaries, there were degenerative changes in all tubular and canalicular epithelial cells in the proximal tubules. Conclusions: Fasting, an important metabolic stress factor, accompanied by histamine treatment may cause signifi cant disruptions in the kidneys, particularly in the glomerular capillaries and proximal and distal tubules (Tab. 1, Fig. 2 Acknowledgements: We confi rm that we have read the Journal's position on issues involved in ethical publication and affi rm that this report is consistent with those guidelines.

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Autacoids as modulators of the inflammatory and immune response

Cited by 76 publications

References 33 publications

T-cell suppression and contrasuppression induced by histamine H2 and H1 receptor agonists, respectively.

T-cell suppression and contrasuppression induced by histamine H2 and H1 receptor agonists, respectively.

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents

The effect of histamine on kidney by fasting in rats

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Autacoids as modulators of the inflammatory and immune response

Cited by 76 publications

References 33 publications

T-cell suppression and contrasuppression induced by histamine H2 and H1 receptor agonists, respectively.

T-cell suppression and contrasuppression induced by histamine H2 and H1 receptor agonists, respectively.

Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H2‐agents

The effect of histamine on kidney by fasting in rats

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Changes in bronchial anaphylactic reactivity induced in guinea‐pigs by long‐term treatment with histamine H₂‐agents