Inhibition of macrophage phagocytic activity by SV-IV, a major protein secreted from the rat seminal vesicle epithelium

Galdiero, F; Tufano, Maria Antonietta; Martino, Luisa De; Capasso, Ciro; Porta, Raffaele; Ravagnan, G; Peluso, Gianfranco; Metafora, Salvatore

doi:10.1016/0165-0378(89)90056-9

Cited by 29 publications

(24 citation statements)

References 31 publications

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“…In addition, as a result of the known ability of anti-inflammatory drugs to control the inflammatory process through the downregulation of the NF-B gene expression pathway, the possible inhibition of NF-B (41) by SV-IV (an anti-inflammatory protein) could reasonably be involved in the process. The SV-IV-mediated reduction of phagocytosis observed in serovar Typhimurium-infected mice confirms previous data from our laboratory that have demonstrated the in vitro inhibitory effects of SV-IV on human macrophage and polymorphonucler leukocyte phagocytosis activities (11,21).…”

Section: Discussionsupporting

confidence: 78%

“…The reduction in the level of clearance of the bacteria from the spleens and livers and the decrease in the level of intracellular killing of the bacteria in the peritoneal macrophages of mice treated with SV-IV and serovar Typhimurium were probably related to a marked downregulation in the abilities of these macrophages to produce NO (a free radical involved in the intracellular killing of bacteria) and iNOS. The inhibitory effect of SV-IV on iNOS gene expression could be related, in turn, to the binding of SV-IV to SV-IV-specific tyrosine kinase-associated receptors (K d ϭ 10 Ϫ8 M; 80,000 to 100,000 SV-IV-specific binding sites/cell) (11,19,21,35;Metafora et al,unpublished data), with the subsequent production of a protein phosphorylation cascade following the plasma membrane signal transduction process. In addition, as a result of the known ability of anti-inflammatory drugs to control the inflammatory process through the downregulation of the NF-B gene expression pathway, the possible inhibition of NF-B (41) by SV-IV (an anti-inflammatory protein) could reasonably be involved in the process.…”

Section: Discussionmentioning

confidence: 99%

“…The biological function of SV-IV is multifaceted. SV-IV is a remarkable bioactive protein due to its powerful non-species-specific anti-inflammatory, procoagulant, and immunomodulatory properties (3,7,8,9,11,14,19,21,28,31,37,39). The anti-inflammatory activity of SV-IV is related to its ability to inhibit phospholipase A 2 , the first enzyme of the arachidonate cascade (3,19), while its procoagulant activity has been ascribed to its ability to inhibit antithrombin III (7)(8)(9).…”

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confidence: 99%

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Effect of Protein SV-IV on ExperimentalSalmonella entericaSerovar Typhimurium Infection in Mice

Romano-Carratelli

Bentivoglio

Nuzzo

et al. 2002

Clin Vaccine Immunol

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Seminal vesicle protein IV (SV-IV) is a secretory anti-inflammatory, procoagulant, and immunomodulatory protein produced in large amounts by the seminal vesicle epithelium of the rat under the strict transcriptional control of androgen. In particular, this protein was shown to possess the ability to markedly inhibit in vivo the humoral and cell-mediated immune responses of mice to nonbacterial cellular antigens (sheep erythrocytes and spermatozoa). We report data that demonstrate that in mice treated with SV-IV and infected with Salmonella enterica serovar Typhimurium, SV-IV is able to downregulate some important immunological and biochemical parameters that serovar Typhimurium normally upregulates in these animals. This event did not correlate with a lower bacterial burden but was associated with a markedly increased one (300%). Furthermore, the treatment of mice with SV-IV alone also produced a significant increase in the rate of mortality among serovar Typhimurium-infected animals. The mechanism underlying these phenomena was investigated, and the strong immunosuppression produced by SV-IV in serovar Typhimurium-infected mice was suggested to be the basis for the increased rate of mortality. The SV-IV-mediated immunosuppression was characterized by a decrease in the humoral and cell-mediated immune responses, altered lymphocyte-macrophage interaction, downregulation of cytokine and inducible nitric oxide synthase gene expression, inhibition of macrophage phagocytosis and intracellular killing activities, and absence of apoptosis in the splenocyte population of SV-IV-and serovar Typhimurium-treated mice. The immunosuppressive activity of SV-IV was specific and was not due to aspecific cytotoxic effects. SV-IV-specific receptors (K d ‫؍‬ 10 ؊8 M) occurring on the macrophage and lymphocyte plasma membranes may be involved in the molecular mechanism underlying the SV-IV-mediated immunosuppression. Some results obtained by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay also revealed a functional impairment of mitochondria (a decrease in mitochondrial dehydrogenase activity), thus indicating the possible implication of these organelles in the immunosuppressive process.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of Protein SV-IV on ExperimentalSalmonella entericaSerovar Typhimurium Infection in Mice

Romano-Carratelli

Bentivoglio

Nuzzo

et al. 2002

Clin Vaccine Immunol

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“…SV-IV is a highly flexible molecule that in aqueous solution behaves as a concentration-dependent self-associating system in which the degree of association (monomer & dimer & trimer equilibrium) is apparently related to its biological activities (Stiuso et al, 1989;Vuotto et al, 1993;data not shown). We have shown that this protein possesses anti-inflammatory properties and a potent, nonspecies-specific modulatory activity on the humoral and cellmediated immune responses to antigens and mitogens, both in vitro and in vivo (Galdiero et al, 1989;Metafora et al, 1989a,b;Vuotto et al, 1993;Romano-Carratelli et al, 1995). The protein SV-IV is a good substrate of the enzyme transglutaminase (TGase; EC 2.3.2.13) (Porta et al, 1991) and inhibits phospholipase A 2 (PLA 2 ) activity (Metafora et al, 1989a).…”

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confidence: 96%

SV-IV, a major protein secreted from rat seminal vesicle epithelium, promotes lymphocyte cytotoxic activity against the lymphoblastoid Raji cell line in human peripheral blood mononuclear cells

et al. 1997

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The treatment of human peripheral blood mononuclear cells (PBMC) with micromolar concentrations of SV-IV, a major protein secreted from the rat seminal vesicle epithelium, promotes in this cell population a marked cytotoxic activity against the Raji lymphoblastoid cell line. This activity is apparently due to cell-to-cell contact interactions. The expression of HLA DR on Raji cells has a modulatory effect on the SV-IV-induced cytotoxic activity. The experimental evidence strongly suggests that the cytotoxic effector cells are functionally activated NK cells.

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“…SV-IV exerts a non-species-specific inhibitory activity on inflammation, cell-mediated and humoral immunity, and apoptosis [13,17,18,19,20,21,22,23,24,25]. In addition, it possesses a stimulatory effect on purified peroxidases [25,26] and protects cells against oxidative-stress-induced damage, by acting as an indirect reactive-oxygen-species scavenger [25].…”

Section: Introductionmentioning

confidence: 99%

Antiapoptotic Seminal Vesicle Protein IV Induces Histamine Release from Human FcεRI+ Cells

Prevete

Rossi

Triggiani

et al. 2009

Int Arch Allergy Immunol

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Background: Seminal vesicle protein number 4 (SV-IV) is a small, basic, multifunctional, intrinsically disordered secretory protein synthesized in large amounts by rat seminal vesicle epithelium under androgen transcriptional control. SV-IV-immunorelated proteins occur in other rat tissues and in humans. Methods: The in vitro effect of SV-IV on human FcΕRI+ cells was investigated by standard immunologic, biochemical and molecular biology procedures. Results: SV-IV-induced histamine release from human basophils and lung mast cells without any influence on leukotriene C₄ release and cell migration. The histamine release rate was slower compared with that induced by anti-IgE, the temperature dependence of the event being similar. SV-IV-induced histamine release was Ca²⁺-dependent, suggesting a physiological interaction of the protein with FcΕRI+ cells. SV-IV and anti-IgE acted synergistically on the histamine release. SV-IV did not induce de novo synthesis of cytokines and growth factors (transforming growth factor-β₁, interleukin-10, interleukin-13, tumor necrosis factor-α, vascular endothelial growth factor A) in FcΕRI+ cells. Conclusions: SV-IV protein induces in human FcΕRI+ cells the release of histamine, a proinflammatory, antiapoptotic and immunosuppressive biogenic amine. These data: (1) are consistent with the antiapoptotic and immunosuppressive properties of SV-IV; (2) confirm a regulatory feature of SV-IV on mammal inflammatory reactivity by either inhibiting the arachidonate cascade pathway or stimulating proinflammatory cytokine release from lymphocyte/monocytes and histamine from FcΕRI+ cells; (3) raise the possibility of a protective role of SV-IV on implanting hemiallogenic blastocysts against maternal reactive oxygen species and immunological attacks at the uterine implantation site.

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Inhibition of macrophage phagocytic activity by SV-IV, a major protein secreted from the rat seminal vesicle epithelium

Cited by 29 publications

References 31 publications

Effect of Protein SV-IV on ExperimentalSalmonella entericaSerovar Typhimurium Infection in Mice

Effect of Protein SV-IV on ExperimentalSalmonella entericaSerovar Typhimurium Infection in Mice

SV-IV, a major protein secreted from rat seminal vesicle epithelium, promotes lymphocyte cytotoxic activity against the lymphoblastoid Raji cell line in human peripheral blood mononuclear cells

Antiapoptotic Seminal Vesicle Protein IV Induces Histamine Release from Human FcεRI+ Cells

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