Zinc deficiency is an independent risk factor for prehypertension in healthy subjects.

Objective: To assess whether zinc deficiency is associated with prehypertension (preHTN) in apparently healthy subjects. Design: Apparently healthy women and men, aged 20 to 60 years were enrolled into a case-control study. Individuals with and without preHTN were allocated into the case and control groups, respectively. Hypertension, liver disease, renal disease, smoking, pregnancy, diabetes, malignancy, hypernatremia, hypomagnesemia, medical treatment, and use of supplements containing zinc were exclusion criteria. PreHTN was defined by systolic blood pressure (SBP) and/or diastolic blood pressure (DBP) of 120-139 mmHg and/or of 80-89 mmHg, respectively, and the zinc deficiency by serum zinc levels < 74 µg/dL in men and < 70 µg/dL in women. Results: In total, 142 subjects (90 women and 52 men) were enrolled and allocated in the case (n = 71) and control (n = 71) groups. In the overall population, the frequency of zinc deficiency was 11.1%; individuals in the case group showed significant higher frequency of zinc deficiency as compared with the control group (16.9% vs 5.5%, p = 0.04). The logistic regression analysis showed a significant association between zinc deficiency and preHTN (OR = 4.61; 95% CI: 1.24-17.12, p = 0.02). Conclusion: Our results suggest that zinc deficiency is associated with the presence of preHTN in apparently healthy subjects.

Actinobacillus pleuropneumoniae possesses an antiviral activity against porcine reproductive and respiratory syndrome virus.

Pigs are often colonized by more than one bacterial and/or viral species during respiratory tract infections. This phenomenon is known as the porcine respiratory disease complex (PRDC). Actinobacillus pleuropneumoniae (App) and porcine reproductive and respiratory syndrome virus (PRRSV) are pathogens that are frequently involved in PRDC. The main objective of this project was to study the in vitro interactions between these two pathogens and the host cells in the context of mixed infections. To fulfill this objective, PRRSV permissive cell lines such as MARC-145, SJPL, and porcine alveolar macrophages (PAM) were used. A pre-infection with PRRSV was performed at 0.5 multiplicity of infection (MOI) followed by an infection with App at 10 MOI. Bacterial adherence and cell death were compared. Results showed that PRRSV pre-infection did not affect bacterial adherence to the cells. PRRSV and App co-infection produced an additive cytotoxicity effect. Interestingly, a pre-infection of SJPL and PAM cells with App blocked completely PRRSV infection. Incubation of SJPL and PAM cells with an App cell-free culture supernatant is also sufficient to significantly block PRRSV infection. This antiviral activity is not due to LPS but rather by small molecular weight, heat-resistant App metabolites (<1 kDa). The antiviral activity was also observed in SJPL cells infected with swine influenza virus but to a much lower extent compared to PRRSV. More importantly, the PRRSV antiviral activity of App was also seen with PAM, the cells targeted by the virus in vivo during infection in pigs. The antiviral activity might be due, at least in part, to the production of interferon γ. The use of in vitro experimental models to study viral and bacterial co-infections will lead to a better understanding of the interactions between pathogens and their host cells, and could allow the development of novel prophylactic and therapeutic tools.

Las hormonas esteroides y la etiopatogénesis de padecimientos hepáticos de naturaleza fibrótica / Fibrotic liver disease and steroid hormones

Existen hipótesis en el sentido de que el estatus hormonal está involucrado en la distinta susceptibilidad entre el hombre y la mujer en el desarrollo de enfermedad hepatobiliar, ya que el hígado es órgano blanco para hormonas esteroides. En el desarrollo del fenómeno fibrogénico durante la cirrosis hepática de diversa etiología están involucradas las células de Ito, los miofibroblastos y diversas citocinas como factor transformador de crecimiento-ß, interleucina-6 y factor de necrosis tumoral-alfa. Se sabe que en el organismo existen asas de regulación mutua entre citocinas, glucocorticoides y esteroides sexuales; en el hígado, esta interacción pudiera afectar el proceso fibrogénico a través de diferenciación de células de Ito. El conocimiento del papel preciso de los glucocorticoides y las hormonas esteroides sexuales sobre los mecanismos fibrogénicos, permitiría sustentar racionalmente la viabilidad de la manipulación hormonal en el tratamiento de padecimiento hepático de natulareza fibrótica