There is a strong interest in finding adequate biomarkers to aid in the diagnosis and prognosis of influenza A (H1N1)pdm09 virus infection. In this study, serum levels of inflammatory cytokines and laboratory markers were evaluated to assess their usefulness as biomarkers of influenza A (H1N1)pdm09 and their association with fatal cases. Serum samples of consecutive patients with a clinical presentation suggestive of influenza A (H1N1)pdm09 and progression to sepsis were evaluated. Serum inflammatory cytokines and routine laboratory tests were performed and correlated with positivity for influenza A (H1N1)pdm09 influenza by real time reverse transcription polymerase chain reaction and the results of three clinical severity scores (Sequential Organ Failure Assessment [SOFA], CURB-65, and Acute Physiology and Chronic Health Evaluation II [APACHE II]). High SOFA scores and some of its individual components, but not CURB-65 or APACHE II scores, correlate with fatal cases regardless of etiology. Total and unconjugated bilirubin, Ca + + , Cl -, prothrombin times, and partial thromboplastin times discriminate influenza A (H1N1)pdm09 from other causes of community-acquired pneumonia.
Cytokines and interferons are important molecules involved in influenza control. However, the relation between those cytokines and the outcome of those patients is not clear. The aim of this work was to analyze interferons, proinflammatory and anti-inflammatory cytokines in patients with influenza A H1N1 and other respiratory diseases. Methodology: Healthy controls (n=8), patients with influenza A H1N1 confirmed by PCR (n=14), and patients with other respiratory diseases (n=22) were enrolled. Blood samples were collected from each individual and sera were obtained for cytokines analysis. A panel of 14 cytokines was analyzed: IL-1b, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p40, IL-12p70, IL-15, IL-17, TNFa, IFNa and IFNg by Luminex; and IL-29 and TGF-b1 by ELISA. Results: IL-6, IL-8, and IL-10 were higher (P<0.05) in sera of patients with influenza A H1N1 and other respiratory diseases compared with control group at admission day. These cytokines were also higher in A H1N1 patients who deceased as compared to those that recovered (P<0.05). TGFb1 was lower in all patient groups compared with control (P<0.05). Interestingly, TGF-b1 increased in A H1N1 patients that recovered. This phenomenon was not observed in other respiratory diseases. No differences were found in the other analyzed cytokines. In conclusion, the anti-inflammatory response, under control of IL-10, is coadjuvated by TGF-b1 which seems important for A H1N1 patient survival.
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