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New products with tolerogenic properties on T cell response are necessary to improve current efficacy, cost and side effects of immunosuppressants. Prosopis strombuliferaaqueous extract (PsAE) have reported cytotoxic, antitumoral, antiatherogenic and antileishmanial activities, containing phytochemicals with immune-related activities. Despite these, there are no previous studies with respect to PsAE suppressive properties over T cell proliferation and their function.

One of the major goals in the research of autoimmune diseases is to develop specific therapies to regulate the expression and function of gene products that could contribute to restoring tolerance to self-constituents and replace conventional systemic immunosuppression, which is associated with important undesired side effects. Although significant progress has been made on the understanding of the pathogenesis of autoimmunity, therapies for these ailments have not seen a change. During the last decade, different strategies such as pharmacologic or gene therapy modulation of heme oxygenase-1 (HO-1) and the administration of its metabolic product, carbon monoxide (CO), have been shown to display beneficial immunoregulatory and cytoprotective properties. In different experimental autoimmune conditions, such as Experimental autoimmune encephalomyelitis, type-1 diabetes and systemic lupus erythematosus, genetic or pharmacological modulation of HO-1, as well as delivery of CO have shown to ameliorate disease progression. Furthermore, it has been demonstrated that dendritic cell and monocyte function can be modulated by HO-1 and/or CO. In this article, recent data related to the immunoregulatory properties of HO-1/CO will be discussed, focusing on their potential therapeutic use to treat autoimmune diseases.

It is surprising that despite the prevalence of prostate disease, little is known about the immunobiology of the prostate and its contribution to disease. The prostate is the target of many diseases like infection of the prostate gland, chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), benign hyperplasia and cancer. In this review we will focus on the relationship of the immune system with the prostate gland in two different scenarios: in the first one, the question of how prostate epithelial cells deal with inflammatory stimuli, like microorganisms, is addressed. Whereas the role of infiltrating innate immune cells like macrophages and neutrophils in prostate inflammation has been extensively studied, the particular contribution of prostate epithelial cells to an inflammatory setting has barely been investigated. Prostate epithelial cells can act as early sensors of infection, expressing Toll like receptors, the best well known innate immune receptors. Thus they become sentinels of the prostate gland, like the epithelial cells of other internal organs. The way these cells respond to infection up-regulating pro-inflammatory mediators is discussed. This topic is of particular interest since chronic inflammation has been postulated to be an important driving force to prostate carcinoma. In the second scenario, the situation in which the prostate gland becomes a target of an autoimmune response is analyzed. Chronic inflammatory prostate disease of noninfectious origin seems to be a good example of this situation, since at least 30 of the patients suffering from CP/CPPS exhibited IFN--secreting, proliferating lymphocytes against prostate antigens such as prostatic acid phosphatase (PAP), prostate specific antigen (PSA), and other antigens present in prostate homogenates and seminal plasma. We have dissected the immunological mechanisms that are involved in these patients and in experimental models of autoimmune prostatitis as well as analyzed its consequences on the fertility of these patients.

Although Chlamydia infections are widespread throughout the world, data about immunopathogenesis of genitourinary tract infections in males are very limited. In the present work we present an in vitro model of male genital tract-derived epithelial cells, more precisely prostate epithelial cells (PEC), to analyze if they are susceptible and able to respond to Chlamydia muridarum infection. Our results demonstrate that rat PEC are susceptible to C. muridarum infection and respond to this pathogen by up-regulating different proinflammatory cytokine and chemokine genes that could participate in the recruitment and local activation of immune cells, therefore influencing innate and adaptive immune responses during Chlamydia infection. Moreover, we analyzed the expression of Toll-like receptor 4 (TLR4), TLR2, and related molecules on PEC and the effect of C. muridarum infection on their expression. Our results demonstrate that PEC express significant levels of TLR4, CD14, TLR2, and the adaptor molecule MyD88 and up-regulate these proteins in response to C. muridarum infection. Indeed, TLR4, CD14, TLR2, and the adaptor MyD88 are specifically recruited to the vicinity of the bacterial inclusion, suggesting that these TLRs are actively engaged in signaling from this intracellular location in these cells. This is, to our knowledge, the first time that an in vitro model of infection with Chlamydia of male tract-derived epithelial cells has been achieved, and it provides the opportunity to determine how these cells respond and participate in modulating innate and adaptive immune response during Chlamydia infections.

ABSTRACTAlthough Chlamydiainfections are widespread throughout the world, data about immunopathogenesis of genitourinary tract infections in males are very limited. In the present work we present an in vitro model of male genital tract-derived epithelial cells, more precisely prostate epithelial cells (PEC), to analyze if they are susceptible and able to respond to Chlamydia muridaruminfection. Our results demonstrate that rat PEC are susceptible to C. muridaruminfection and respond to this pathogen by up-regulating different proinflammatory cytokine and chemokine genes that could participate in the recruitment and local activation of immune cells, therefore influencing innate and adaptive immune responses during Chlamydiainfection. Moreover, we analyzed the expression of Toll-like receptor 4 (TLR4), TLR2, and related molecules on PEC and the effect of C. muridaruminfection on their expression. Our results demonstrate that PEC express significant levels of TLR4, CD14, TLR2, and the adaptor molecule MyD88 and up-regulate these proteins in response to C. muridaruminfection. Indeed, TLR4, CD14, TLR2, and the adaptor MyD88 are specifically recruited to the vicinity of the bacterial inclusion, suggesting that these TLRs are actively engaged in signaling from this intracellular location in these cells. This is, to our knowledge, the first time that an in vitro model of infection with Chlamydiaof male tract-derived epithelial cells has been achieved, and it provides the opportunity to determine how these cells respond and participate in modulating innate and adaptive immune response during Chlamydiainfections.