2057 Cytokine Profile Characterization in Patients Infected with AH1N1 Influenza Virus

Monday, 5 December 2011
Poster Hall (Cancún Center)

Nadia L Lopez-Espinosa , Research Unit, Institute of Ophthalmology, México D.F., Mexico

Lizet Vizuet-Garcia , Research Unit, Institute of Ophthalmology, México D.F., Mexico

Atzin Robles-Contreras, MSc , Research Unit and Department of Immunology, Institute of Ophthalmology, México D.F., Mexico

Maria C Jiménez-Martínez, MD, PhD , Research Unit and Department of Immunology, Institute of Ophthalmology, México D.F., Mexico

Victor M Bautista-de Lucio, PhD , Research Unit, Institute of Ophthalmology, México D.F., Mexico

Background: In 2009, an outbreak of severe respiratory infection caused by influenza AH1N1 virus affected Mexican people, previously in 1996 in Guangdong province (China) an outbreak of H5N1 influenza started spreading throughout Asia and the western Palearctic in 2004-2006. Chinese patients were studied and it was observed a deleterious immune response related to cytokine storm, mainly characterized by higher levels of IFN and other proinflammatory cytokines causing fatal infections or severe clinical outcome. Until now, is unknown the cytokine profile involved during AH1N1 infection, thus it was the aim of this study.

Methods: Serum samples were obtained from 39 infected patients and their close contacts from the first wave outbreak of influenza AH1N1 and were storage at -80°C until cytokine determination, Human Inflammatory and Th1/Th2/Th17 Cytometric Bead Array Kit was used to determine cytokine concentration in serum samples. Cytokine protein arrays were performed to know relative expression of 36 cytokines with the Profiler Array Membrane from R&D Systems. The results are reported on relative units (RU). It was performed with ANOVA test, considering p<0.05 as statistically significant.

Results: We did not find significative statistical differences between patients and their close contacts in IFN-γ, IL-1ß, IL-2, IL-4, IL-6, IL-8, IL-10, 12p70, IL-17A, and TNF evaluated with cytometry. However, the proteomic analysis showed a significant increased (p<0.05) in G-CSF, I-309, sICAM-1, IL-1Ra. IL-16, IL-23, IL-27, I-TAC, MIP-1α, and E1-Serpin compared with the closed contacts.

Conclusions: AH1N1 patients showed higher levels of IL-27. We observed more RU of sICAM expression in patients and closed contacts, possibly due to the IL-27 signaling. IL-23 were increased in AH1N1 patients, this cytokine is involved in the IFN-γ secretion and in the generation of memory CD4 T cells. These results suggest that AH1N1-patients developed an immune response characterized by IL-27 and IL-23. We need more studies to determine if this cytokines are related with the memory response induction.