ABSTRACT
Introducción: Una de las complicaciones de la orquiepidédimitis (OE) aguda al largo plazo es la infertilidad secundaria a la atrofia testicular y el deterioro de la espermatogénesis. Los mecanismos fisiopatológicas exactos a través de los cuales la infección deteriora la espermatogénesis aún no están claros. Objetivo: Evaluar el impacto de la OE por Escherichia coli uropatógena (ECUP) sobre parámetros específicos de la espermatogénesis y esteroidogénesis. Materiales y método: El estudio incluyó 40 ratas Wistar macho. Post anestesia general se realizó una incisión escrotal media con posterior exposición de ambos epidídimos y conductos deferentes. Mediante la punción con una aguja 27G en el conducto deferente a un centímetro del epidídimo se inyectaron 50 ul de suspensión ECUP (10x6 UFC/ml) (grupo infectados) o suero fisiológico (grupo control). Las ratas fueron divididas en 4 grupos de 10 animales cada uno: el primer grupo infectado (n= 10) y control (n= 10) fue sacrificado a los 7 días y el segundo grupo infectado (n= 10) y control (n= 10) fue sacrificado a los 30 días post inoculación. Resultados: Respecto de los controles los animales infectados tuvieron menor (p< 0,05): concentración espermática (promedio +/- ds: 7 días = 100,2 +/- 56,8 vs 249,8 +/- 111,6; 30 días= 20,7 +/- 38,3 vs 75,3 +/- 98,7 millones/grm tejido en cola epidídimo); y mayor (p< 0,05): (i) degeneración del epitelio germinal e infiltración celular inflamatoria a los 30 días, y (ii) número de células espermatogénicas apoptóticas (índice apoptótico)detectadas por prueba de TUNEL a los 7 y a los 30 días. El ensayo inmunohistoquímico antivimentina reveló que las células apoptóticas dentro de los túbulos seminíferos fueron casi exclusivamente células germinales y no de Sertoli. No se observaron diferencias significativas en los niveles plasmáticos de testosterona entre el grupo infectado y control a los siete y treinta días de ser inyectados. Conclusiones: La OE aguda provocada...
Introduction: In the long term, one of the complications of epidydimo-orchitis (EO) is infertility due to testicular atrophy. The exact pathophisiologic mechanisms for impairment of spermatogenesis are not clear Objective: To evaluate the impact of infection by uropathogenic Escherichia coli (UPEC) on spermatogenesis and stereoidogenesis. Materials and method: The study included 40 Wistar male rats. Under general anesthesia a mid scrotal incision was performed. Both epidydimis and vas deferens were exposed. Using a 27G needle, 50 ul of either UPEC suspension (10x6 CFU/ml) or saline were injected. Rats were divided into 4 groups: the first study group (n =10) and controls ( n=10) were sacrificed at 7 days; the second study group (n =10) and controls (n =10) were sacrificed at 30 days post inoculation.Results: Compared to controls, infected animals had lower sperm concentration (p <0.05). The average +/- SD at 7 days was 100.2 +/- 56.8 vs 249.8 +/- 111.6 millions/gram of tissue from the tail of the epidydimis. At 30 days the results were 20.7 +/- 38.3 vs 75.3 +/- 98.7. The study group had more degeneration of germinal epithelium and inflammation at 30 days. The apoptotic index studied by TUNEL test at 7 and 30 days was higher. Immunohistochemistry with anti vimentin antibodies revealed that the apoptotic cells within seminifirous tubules were almost exclusively germ cells and not Sertoli cells. No significant differences on testosterone plasma levels between the study and control groups were found at 7 or 30 days post injection. Conclusions: Acute EO caused by retrograde inoculation of UPEC in rats generates a significant decrease in sperm concentration. This effect is secondary between others to an impairment of sperm activity at the seminiferous tubules generated by an increased apoptotic index of the sperm cells. The effect of EO on testosterone production seems irrelevant in the clinical setting.
Subject(s)
Animals , Male , Rats , Epididymitis/complications , Escherichia coli , Spermatogenesis , Orchitis/complications , TestosteroneABSTRACT
The packaging signal present in influenza viral RNA molecules is shown not to constitute a separate structural element, but to reside within the 5'-bulged promoter structure, as caused by the central unpaired residue A10 in its 5' branch. Upon insertion of two uridine residues in the 3' branch opposite A10, the minus-strand viral RNA (vRNA) promoter is converted into a 3'-bulged structure, whereas the plus-strand cRNA promoter instead adopts the 5'-bulged conformation. In this promoter variant it is exclusively the cRNA that is found packaged in the progeny virions. Upon insertion of only a single uridine nucleotide opposite 5'A10, the two debulged structures of the vRNA and cRNA promoters are rendered identical, and both vRNA and cRNA molecules are packaged indiscriminately, in a 1:1 ratio, but at lower rates. We propose that the binding interactions of viral polymerase with either of the two differently bulged vRNA and cRNA promoter structures result in two different conformations of the enzyme protein. Only the 5' bulged RNA-associated polymerase conformation appears to be recognized for nuclear export, which depends on nuclear matrix protein M1 and nonstructural protein NS2. And the respective wild-type vRNP- or insertion mutant cRNP complex is observed to enter the cytoplasm and hence is included in the viral encapsidation process, which takes place at the plasma membrane.
