Somatostatin and macrophage function: modulation of hydrogen peroxide, nitric oxide and tumor necrosis factor release

https://doi.org/10.1016/0167-0115(95)00051-CGet rights and content

Abstract

Recent studies have shown that somatostatin modulates lymphocyte function, but the effects of somatostatin on macrophage function are not clearly defined. In the present study, peritoneal macrophages (M∅) obtained from male rats were treated in vitro with somatostatin or octreotide and their effects on the release of hydrogen peroxide (H2O2), nitrite, and tumor necrosis factor (TNF) determined. Macrophages treated with somatostatin (10−9 M to 10−7 M) or octreotide (10−8 M and 10−7 M) released significantly greater amounts of PMA-stimulated H2O2 than did the untreated controls. In addition, 10−9 M of somatostatin significantly enhanced PMA-stimulated H2O2 release by LPS-treated M∅. Octreotide had no effect on H2O2 release by LPS-treated M∅. At concentrations of 10−14 M, 10−13 M, or greater than 10−8 M, somatostatin or octrectide suppressed nitrite release by M∅. Somatostatin or or octreotide did not affect nitrite release by LPS-treated M∅. On the other hand, M∅ treated with 10−11 M of somatostatin or octreotide released greater amounts of TNF than did the untreated controls. In contrast, TNF release by M∅ treated with 10−9 M to 10−5 M of somatostatin or 10−7 M to 10−5 M of octreotide was less than that of the controls. Anti-TNF antibody (1:1000) caused a reduction in the release of H2O2 and nitrite. These findings demonstrate that somatostatin and octreotide modulate the release of H2O2, nitric oxide, and TNF by M∅ depending on the concentration of hormones used.

References (60)

  • C.J. Wiedermann et al.

    Stimulation of monocyte chemotaxis by human growth hormone and its deactivation by somatostatin

    Blood

    (1993)
  • S. Efendic et al.

    Inhibition by somatostatin of glucose induced 3′,5-monophosphate (cyclic AMP) accumulation and insulin release in isolated pancreatic islets of the rat

    FEBS Lett.

    (1975)
  • C. Gespach et al.

    Selective inhibition by somatostatin of cyclic AMP production in rat gastric glands

    FEBS Lett.

    (1980)
  • J.J. Segura et al.

    Somatostatin inhibition of VIP- and isoproterenol-stimulated cyclic AMP production in rat peritoneal macrophages

    Neuropeptides

    (1992)
  • R.L. Smith et al.

    Reactive oxygen production associated with arachidonic acid metabolism by peritoneal macrophages

    Biochem. Biophys. Res. Commun.

    (1980)
  • L.K. Lim et al.

    Reactive oxygen production, arachidonic metabolism and cyclic AMP in macrophages

    Biochem. Biophys. Res. Commun.

    (1983)
  • Y. Bromberg et al.

    Unsaturated fatty acids as second messengers of superoxide generation by macrophages

    Cell. Immunol.

    (1983)
  • S. Reichlin et al.

    Engl. J. Med.

    (1983)
  • S. Reichlin et al.

    Engl. J. Med.

    (1983)
  • S.J. Bhathena et al.

    Identification of human mononuclear leukocytes bearing receptors for somatostatin and glucagon

    Diabetes

    (1981)
  • R. Scicchitano et al.

    The murine IgA-secreting plasmocytoma MOPC-315 expresses somatostatin receptors

    J. Immunol.

    (1988)
  • A.M. Blum et al.

    Granuloma T lymphocytes in murine schistosomiasis mansoni have somatostatin receptors and respond to somatostatin with decreased IFN-gamma secretion

    J. Immunol.

    (1992)
  • S. Yousefi et al.

    The effect of somatostatin on the production of human interferons by mononuclear cells

  • L.E. Bermudez et al.

    Effect of stressrelated hormones on macrophage receptors and response to tumor necrosis factor

    Lymphokine Res.

    (1990)
  • H. Kimata et al.

    Effect of vasoactive intestinal peptide, somatostatin, and substance P on spontaneous IgE and IgG4 production in atopic patients

    J. Immunol.

    (1993)
  • A.M. Stanisz et al.

    Differential effects of vasoactive intestinal peptide, substance P, and somatostatin on immunoglobulin synthesis and proliferations by lymphocytes from Peyer's patches, mesenteric lymph nodes, and spleen

    J. Immunol.

    (1986)
  • D.A. Nio et al.

    Modulation of T lymphocyte function by neuropeptides

    J. Immunol.

    (1993)
  • O. Johansson et al.

    Effect of the neuropeptides beta-MSH, neurotensin, NPY, PHI, somatostatin and substance P on proliferation of lymphocytes in vitro

    Acta Physiol. Scand.

    (1989)
  • C.F. Nathan et al.

    The macrophages as an effector cell

    N. Engl. J. Med.

    (1980)
  • D.O. Adams et al.

    The cell biology of macrophage activation

    Annu. Rev. Immunol.

    (1984)
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