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This Article Full Text Full Text (PDF) All Versions of this Article: 68/5/1836    most recent biolreprod.102.013425v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Assreuy, A. M. S. Articles by Ribeiro, R. A. Search for Related Content PubMed PubMed Citation Articles by Assreuy, A. M. S. Articles by Ribeiro, R. A. Agricola Articles by Assreuy, A. M. S. Articles by Ribeiro, R. A.

Porcine Spermadhesin PSP-I/PSP-II Stimulates Macrophages to Release a Neutrophil Chemotactic Substance: Modulation by Mast Cells¹

Mestrado Acadêmico em Ciências Fisiológicas-CCS,⁴ Universidade Estadual do Ceará, Fortaleza-CE, Brazil Depto de Fisiologia e Farmacologia, Faculdade de Medicina,⁵ Depto de Bioquímica e Biologia Molecular,⁶ Universidade Federal do Ceará, Fortaleza-CE, Brazil Depto de Farmacologia,⁷ Faculdade de Medicina de Ribeirão Preto, Ribeirão Preto-SP, Brazil Instituto de Biomedicina de Valencia,⁸ C.S.I.C., Valencia, Spain

The complex of porcine seminal plasma heterodimers I and II (PSP-I/PSP-II), which are heterodimers of glycosylated spermadhesins, is the major component of porcine seminal fluid. The proinflammatory and immunostimulatory activities of this spermadhesin complex suggest its participation in modulation of the uterine immune activity that may ensure reproductive success. Spermadhesin PSP-I/PSP-II induced the migration of neutrophils into the peritoneal cavity of rats via activation of resident cells. In the present study, we have investigated the involvement of macrophages and mast cells in the neutrophil chemotactic activity of PSP-I/PSP-II and the underlying mechanism. Macrophages and mast cells were isolated, cultured, and stimulated with purified PSP-I/PSP-II. Pharmacological modulation was performed using the glucocorticoid dexamethasone, indomethacin (cyclooxygenase inhibitor), MK886 (leukotriene inhibitor), and the supernatant of spermadhesin-stimulated mast cells. Macrophages stimulated with PSP-I/PSP-II released into the culture supernatant a neutrophil chemotactic substance. This activity was partly inhibited by both dexamethasone (85%) and the supernatant of spermadhesin-stimulated mast cells (74%) but not by indomethacin and MK886. An anti-tumor necrosis factor (TNF) antibody neutralized (by 68%) the neutrophil chemotactic activity of PSP-I/PSP-II-stimulated macrophages. An anti-interleukin (IL)-4 antibody blocked the inhibitory activity of spermadhesin-stimulated mast cells on release of a neutrophil chemotactic substance by PSP-I/PSP-II-stimulated macrophages. As a whole, these data indicate that the neutrophil migration-inducing ability of spermadhesin PSP-I/PSP-II involves the release of the inflammatory cytokine TNF by stimulated macrophages and that this activity is modulated by the lymphokine IL-4 liberated by mast cells. The balance between these two cytokines may control onset of the local inflammatory reaction, avoiding excessive neutrophil recruitment that would lead to tissue damage.

¹ Supported by grants from Programa de Apoio ao Desenvolvimento Científico e Tecnológico (PADCT), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), and Fundação Cearense de Amparo à Pesquisa (FUNCAP) from Brazil and by grants PB98/0694 and BMC2001-3337 from Dirección General de Enseñanza Superior e Investigación Científica (Spain).

² Correspondence (Spain): Juan J. Calvete, Instituto de Biomedicina, C.S.I.C., Jaime Roig 11, 46010 Valencia, Spain. FAX: 34 96 3690800; jcalvete{at}ibv.csic.es

³ Correspondence (Brazil): Ronaldo A. Ribeiro, Depto de Fisiologia e Farmacologia, Universidade Federal do Ceará, R. Cel. Nunes de Melo, 1127-Rodolfo Teófilo, 60 430.270 Fortaleza, CE, Brazil. FAX: 55 85 2888333; ribeiror{at}ufc.br