CONICET | Buscador de Institutos y Recursos Humanos

Purpose: An autoimmune etiology is proposed in some patients with chronic nonbacterial prostatitis since they show IFN- secreting lymphocytes specific to prostate antigens in the periphery and increased IFN- in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. investigated the involvement of IFN- in an animal model of autoimmune prostatitis. prostate antigens in the periphery and increased IFN- in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. investigated the involvement of IFN- in an animal model of autoimmune prostatitis. nonbacterial prostatitis since they show IFN- secreting lymphocytes specific to prostate antigens in the periphery and increased IFN- in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. investigated the involvement of IFN- in an animal model of autoimmune prostatitis. prostate antigens in the periphery and increased IFN- in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. investigated the involvement of IFN- in an animal model of autoimmune prostatitis. An autoimmune etiology is proposed in some patients with chronic nonbacterial prostatitis since they show IFN- secreting lymphocytes specific to prostate antigens in the periphery and increased IFN- in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. investigated the involvement of IFN- in an animal model of autoimmune prostatitis. prostate antigens in the periphery and increased IFN- in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. investigated the involvement of IFN- in an animal model of autoimmune prostatitis. secreting lymphocytes specific to prostate antigens in the periphery and increased IFN- in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. investigated the involvement of IFN- in an animal model of autoimmune prostatitis. in seminal plasma. We investigated the involvement of IFN- in an animal model of autoimmune prostatitis. in an animal model of autoimmune prostatitis. Materials and Methods: Experimental autoimmune prostatitis was studied in the no-obese diabetic and C57Bl/6 (Harlan, Zeist, The Netherlands) susceptible mouse strains, and in the IRF-1 KO and STAT-1 KO mouse strains deficient in transcription factors involved in IFN- signaling. the no-obese diabetic and C57Bl/6 (Harlan, Zeist, The Netherlands) susceptible mouse strains, and in the IRF-1 KO and STAT-1 KO mouse strains deficient in transcription factors involved in IFN- signaling. Experimental autoimmune prostatitis was studied in the no-obese diabetic and C57Bl/6 (Harlan, Zeist, The Netherlands) susceptible mouse strains, and in the IRF-1 KO and STAT-1 KO mouse strains deficient in transcription factors involved in IFN- signaling. signaling. Results: Experimental autoimmune prostatitis was characterized by prostate specific IFN-secreting cells in the periphery and by T-helper 1 related cytokines in the target organ. Increased IFN- and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. in the target organ. Increased IFN- and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. specific IFN-secreting cells in the periphery and by T-helper 1 related cytokines in the target organ. Increased IFN- and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. in the target organ. Increased IFN- and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. Experimental autoimmune prostatitis was characterized by prostate specific IFN-secreting cells in the periphery and by T-helper 1 related cytokines in the target organ. Increased IFN- and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. in the target organ. Increased IFN- and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. secreting cells in the periphery and by T-helper 1 related cytokines in the target organ. Increased IFN- and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. and IL-12 were observed in the prostate of autoimmune animals while IL-10 and IL-4 were decreased and unaltered, respectively. The absence of transcription factors involved in the IFN- signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. signaling cascade, IRF-1 and STAT-1 made mice resistant to experimental autoimmune prostatitis. IRF-1-KO and STAT-1-KO mice immunized with prostate antigens did not show infiltration or alterations in the prostate. They did not have the typical prostate specific autoimmune response and showed decreased IFN-, IL-12 and IL-10, and enhanced of IL-4 in the prostate. IL-12 and IL-10, and enhanced of IL-4 in the prostate. , IL-12 and IL-10, and enhanced of IL-4 in the prostate. Conclusions: Our results argue for a crucial role of IFN- as a key factor in the pathogenesis of the disease. Intense research is promptly required to identify the pathogenic mechanisms underlying chronic prostatitis/chronic pelvic pain syndrome to find a more rational therapy. pathogenesis of the disease. Intense research is promptly required to identify the pathogenic mechanisms underlying chronic prostatitis/chronic pelvic pain syndrome to find a more rational therapy. Our results argue for a crucial role of IFN- as a key factor in the pathogenesis of the disease. Intense research is promptly required to identify the pathogenic mechanisms underlying chronic prostatitis/chronic pelvic pain syndrome to find a more rational therapy. Key Words: prostate, prostatitis, pain, autoimmunity, miceprostate, prostatitis, pain, autoimmunity, mice