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Background: Respiratory syncytial virus infection (RSV) alone or associated to rhinovirus (RV) in the infant has been linked with more likelihood to develop asthma and atopy. Aim: Analyze clinical and immunological markers of patients with RSV or RV bronchiolitis that determine their evolution. Patients and Methods: We studied previously healthy infants hospitalized for bronchiolitis during the fall-winter period of2009 and 2010. RSV and RV by qPCR, and proinflammatory interleukins (IL). IL-6, IL-8, TNF-a, IL-1fl and IL-12, were determined in nasopharyngeal aspirate (NPA). A follow-up clinical, indoor pollution and immunological study was done at 4 or 5 years. Results are expressed in median and range. Mann-Whitney’s test was used in the nonparametric statistical analysis. Results: Eight out of 22patients (36%) are currently with recurrent wheezing (RW) in treatment with budesonide 400 yg per day as a mean dose. In the IL assessment significant changes were detected only in IL-1fl that was increased and in IL-12 that was decreased in the RWgroup versus the non RW (NRW) group. There were not significant differences in both groups in age at hospitalization, infection severity, presence of personal or family atopy, co-infection with RSV and RV, presence of older siblings or indoor air pollution. Conclusions: The determination of IL-1fl and IL-12 in NPA for bronchiolitis could be an early marker of subsequent inflammation of the airway. Co-infection of RSV and RV does not get worse the clinical evolution. The group RW ofpreschool children had no further development of atopy than the NRW group. There could be other factors that contribute to the manifestation of bronchial inflammation in the RW group.

Introducción: Se ha relacionado la infección por Virus Respiratorio Sincicial (VRS) solo o asociado a Rinovirus (RV) en el período de lactante con mayor probabilidad de desarrollar atopia y asma. Objetivo: Analizar marcadores clínicos e inmunológicos de pacientes con bronquiolitis por VRS y/o RV que determinen su evolución. Material y Método: Lactantes previamente sanos hospitalizados por bronquiolitis, en el hospital Roberto del Río en el período de otoño-invierno de 2009 y 2010. Se determinó en aspirado nasofaríngeo (ANF) VRS y RV por qPCR, e interleuquinas (IL) proinflamatorias (IL-6, IL-8, TNF-a, IL-1fl e IL-12). Seguimiento clínico y estudio inmunológico a los 4 o 5 años. Los resultados se expresan en medianas y rango. Análisis estadístico no paramétrico con test de Mann-Whitney Resultados: 22 pacientes seguidos hasta ahora, 8 (36%) son actualmente sibilantes recurrentes (SR) en tratamiento con budesonida dosis mediana de 400 fg/día. De las ILs evaluadas sólo la elevación de la IL-1fi y la disminución de la IL-12 se objetivaron con diferencias significativas en el grupo de SR versus el grupo No SR. No hubo diferencias significativas en estos dos grupos en edad de hospitalización, gravedad de la infección, presencia de atopia personal o familiar, coinfección de VRS y RV, presencia de hermanos mayores ni contaminación intradomiciliaria. Conclusiones: La determinación de IL-1fi y de IL-12 en ANF durante la bronquiolitis podría ser un marcador precoz de inflamación posterior de la vía aérea. La co-infección de VRS y RV no empeora la evolución clínica. Este grupo de preescolares SR no tiene mayor desarrollo de atopia que los no SR. En este grupo de SR podrían existir otros factores que ayuden a contribuir a la manifestación de inflamación bronquial.

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BACKGROUND: The etiology of acute exacerbations of chronic obstructive pulmonary disease (COPD) is heterogeneous and still under discussion. Inflammation increases during exacerbation of COPD. The identification of inflammatory changes will increase our knowledge and potentially guide therapy. AIM: To identify which inflammatory parameters increase during COPD exacerbations compared to stable disease, and to compare bacterial and viral exacerbations. MATERIAL AND METHODS: In 85 COPD patients (45 males, mean age 68 ± 8 years, FEV1 46 ± 17% of predicted) sputum, nasopharyngeal swabs and blood samples were collected to identify the causative organism, during a mild to moderate exacerbation. Serum ultrasensitive C reactive protein (CRP), fibrinogen and interleukin 6 (IL 6), neutrophil and leukocyte counts were measured in stable conditions, during a COPD exacerbation, 15 and 30 days post exacerbation. RESULTS: A total of 120 mild to moderate COPD exacerbations were included. In 74 (61.7%), a microbial etiology could be identified, most commonly Mycoplasma pneumoniae (15.8%), Rhinovirus (15%), Haemophilus influenzae (14.2%), Chlamydia pneumoniae (11.7%), Streptococcus pneumoniae (5.8%) and Gram negative bacilli (5.8%). Serum CRP, fibrinogen and IL 6, and neutrophil and leukocyte counts significantly increased during exacerbation and recovered at 30 days post exacerbation. Compared to viral exacerbations, bacterial aggravations were associated with a systemic inflammation of higher magnitude. CONCLUSIONS: Biomarkers of systemic inflammation increase during mild to moderate COPD exacerbations. The increase in systemic inflammation seems to be limited to exacerbations caused by bacterial infections.

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Background: The etiology of acute exacerbations of chronic obstructive pulmonary disease (COPD) is heterogeneous and still under discussion. Inflammation increases during exacerbation of COPD. The identification of inflammatory changes will increase our knowledge and potentially guide therapy. Aim: To identify which inflammatory parameters increase during COPD exacerbations compared to stable disease, and to compare bacterial and viral exacerbations. Material and Methods: In 85 COPD patients (45 males, mean age 68 ± 8 years, FEV1 46 ± 17% of predicted) sputum, nasopharyngeal swabs and blood samples were collected to identify the causative organism, during a mild to moderate exacerbation. Serum ultrasensitive C reactive protein (CRP), fibrinogen and interleukin 6 (IL 6), neutrophil and leukocyte counts were measured in stable conditions, during a COPD exacerbation, 15 and 30 days post exacerbation. Results: A total of 120 mild to moderate COPD exacerbations were included. In 74 (61.7%), a microbial etiology could be identified, most commonly Mycoplasma pneumoniae (15.8%), Rhinovirus (15%), Haemophilus influenzae (14.2%), Chlamydia pneumoniae (11.7%), Streptococcus pneumoniae (5.8%) and Gram negative bacilli (5.8%). Serum CRP, fibrinogen and IL 6, and neutrophil and leukocyte counts significantly increased during exacerbation and recovered at 30 days post exacerbation. Compared to viral exacerbations, bacterial aggravations were associated with a systemic inflammation of higher magnitude. Conclusions: Biomarkers of systemic inflammation increase during mild to moderate COPD exacerbations. The increase in systemic inflammation seems to be limited to exacerbations caused by bacterial infections.

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It is well fnown that an immunosuppresive rsponse occuts after acute trauma. Some cellular mediators participate in the pathogenesis of septic shock. However, the exact role of the lymphocyte subsets and natural killer (NK) activity in this condition is not clear. We studied NK cytolytic activity through a 51Cr liberation assay using K-562 target cells in 20 patients with initial septic shock (10 men and 10 females, mean age 41 years old). Lymphocyte subsets CD3 (T3), CD4 (T4), CD8 (T8), CD16 (Leu-11) and CD56 (Leu-19) wetre also studied by indirect immunofluorescence. Compared to tesults obtained in 20 healthy volunteers, patient's NK activity was decreased (4.6 ñ 3.9 vs 26.1 ñ 10, p < 0.025), CD16 was lower (10%/187 vs 15%/280 per ul) and CD56 was also lower (6%/120 vs 12%/224 per ul), p < 0,05. T lymphocyte subsers were also decreased: CD3 cells (1100 vs 1352 per ul) and CD4 cells (634 vs 873 per ul), p < 0.05. Thus, a severe decrease in NK cells and NK cell function as well as decreases in CD3 and CD4 lymphocyte subsets are present in the initial stages of septic shock. The predictive value of these findings is currently under study

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We evaluated the usefulness of the direct immunofluorescence test with monoclonal antibodies and the enzyme immunoassay in comaprison with isolation in cell cultures for the diagnosis of Chlamydia trachomatis in 55 endocervica specimens from female prostitutes and 21 urethral specimens fro men with diagnosis of nongonococcal urethritis. In comparison with culture, the enzyme immunoassay had a sensitivity of 100% and a specificity of 95%. The immunofluorescence test had a sensitivity of 92% and a specificity of 98%. The positive and negative predictive values for the enzyme immunoassay were 81% and 100% and for immunofulorescence 92% and 98% respectively. The immunologic methods appear to be satisfactory alternatives to culture for detecting C trachomatis in genital specimens in the studied populations

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