[Late T-lymphocyte and monocyte activation in coronary restenosis. Evidence for a persistent inflammatory/immune mechanism?]. / Linfocitos T y monocitos activados en la reestenosis coronaria. ¿Reflejan la persistencia de un mecanismo inflamatorio?

AIMS: This study was made to determine if restenosis after percutaneous coronary angioplasty is associated with acute or chronic inflammatory/immunologic activity, and explored possible relationships with latent infection. PATIENTS AND METHOD: Forty-six consecutive patients underwent elective PTCA and 6 months of angiographic follow-up. Peripheral venous blood samples were obtained at baseline, 24-48 h, and 4-6 months post-intervention. Flow-cytometric methods were used to measure early and late circulating leukocyte activation status. Il-6 and TNF-alpha cytokines, and Il-2 soluble receptor concentrations were determined in all plasma samples. Chlamydia pneumoniae and Cytomegalovirus antibody assays were performed to detect infectious disease. RESULTS: Angiographic coronary stenosis developed in 27 out of 46 patients. At 6 months of follow-up, these patients showed a significant increase in circulating cytotoxic T-lymphocytes CD3+/CD56+ (18.8 7.1 vs 6.12 2.7%; p = 0.005) and activated monocytes (CD11b: 1,383 624 vs 990 484 MFI, p = 0.025; CD64: 76.0 28.7 vs 56.7 21.8 MFI; p = 0.014), with no apparent relation to increased cytokines or latent infectious disease. CONCLUSIONS: Restenosis appears to be associated to inflammatory and immunological activity that persists 6 months after coronary intervention. No relationship was found with the infections studied. The presence of inflammatory activity 4-6 months after PTCA suggess that pharmacological therapeutic interventions to prevent restenosis should be maintained for months.

Linfocitos T y monocitos activados en la reestenosis coronaria. ¿Reflejan la persistencia de un mecanismo inflamatorio? / Late T-Lymphocyte and monocyte activation in coronary restenosis. Evidence for a persistent inflammatory/immune mechanism?

Objetivos. El objetivo de este trabajo ha sido estudiar la relación de la reestenosis coronaria postangioplastia con la actividad inflamatoria e inmunitaria en la sangre periférica, y explorar su posible asociación con infecciones latentes. Pacientes y método. Se estudiaron 46 pacientes consecutivos con angina a los que se practicó una angioplastia coronaria percutánea y un control angiográfico a los 6 meses. Se tomaron muestras de sangre venosa antes de la intervención, 24-48 h después y a los 6 meses. Se determinó la expresión de las moléculas de adhesión en los leucocitos mediante la técnica de la citometría de flujo. Se cuantificaron las concentraciones de las citocinas proinflamatorias interleucina (IL) 6 y factor de necrosis tumoral (TNF) alfa, así como los receptores solubles de la IL-2 en el plasma, y se utilizaron las reacciones antigénicas para detectar la infección por Chlamydia pneumoniae y Cytomegalovirus. Resultados. Los pacientes con reestenosis coronaria angiográfica (27 de 46) presentaron un aumento significativo de los linfocitos T citotóxicos CD3+/CD56+ (18,8 ñ 7,1 frente a 6,12 ñ 2,7 por ciento; p = 0,005) y de monocitos activados (CD11b: 1.383 ñ 624 frente a 990 ñ 484 MFI; p = 0,025; CD64: 76,0 ñ 28,7 frente a 56,7 ñ 21,8 MFI; p = 0,014) a los 6 meses, sin relación aparente con el aumento de las citocinas o la positividad de las reacciones antigénicas infecciosas. Conclusiones. La reestenosis coronaria se asocia a una reacción inflamatoria/inmunitaria persistente, que no parece estar relacionada con las infecciones latentes estudiadas. La persistencia de actividad inflamatoria a los 4-6 meses sugiere que las intervenciones destinadas a prevenir la reestenosis deberían mantenerse durante meses (AU)

Differences in virulence factors among clinical isolates of Escherichia coli causing cystitis and pyelonephritis in women and prostatitis in men.

Differences in the presence of nine urovirulence factors among clinical isolates of Escherichia coli causing cystitis and pyelonephritis in women and prostatitis in men have been studied. Hemolysin and necrotizing factor type 1 occur significantly more frequently among isolates causing prostatitis than among those causing cystitis (P < 0.0001) or pyelonephritis (P < 0.005). Moreover, the papGIII gene occurred more frequently in E. coli isolates associated with prostatitis (27%) than in those associated with pyelonephritis (9%) (P < 0.05). Genes encoding aerobactin and PapC occurred significantly less frequently in isolates causing cystitis than in those causing prostatitis (P < 0.01 and P < 0.0001, respectively) and pyelonephritis (P < 0.01 and P < 0.0001, respectively). No differences in the presence of Sat or type 1 fimbriae were found. Finally, AAFII and Bfp fimbriae are no longer considered uropathogenic virulence factors since they were not found in any of the strains analyzed. Overall, the results showed that clinical isolates producing prostatitis need greater virulence than isolates producing pyelonephritis in women or, in particular, cystitis in women (P < 0.05). Overall, the results suggest that clinical isolates producing prostatitis are more virulent that those producing pyelonephritis or cystitis in women.