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278 Interleukin and Neurotrophic Factor Plasma Expression are Related to Disease Severity in Children with Influenza A (H1N1) Virus Infection
  1. A Chiaretti1,
  2. S Pulitanò2,
  3. O Genovese2,
  4. D Buonsenso1,
  5. C Fantacci1,
  6. I Russo1,
  7. F Pierri1
  1. 1Department of Pediatrics
  2. 2Pediatric Intensive Care Unit, Catholic University of the Sacred Heart, A. Gemelli Hospital, Roma, Italy

Abstract

Background and Aims In the last years the world has been facing a new pandemic caused by a H1N1 influenza virus, showing particular virulence in children. Cytokines and neurotrophic factors seem to play an important role in severity and progression of this infection. In our study we evaluate cytokine (IL-1b and IL-6) and neurotrophic factor [Nerve Growth Factor (NGF), Brain Derived Neurotrophic Factor (BDNF), and Glial Derived Neurotrophic Factor (GDNF)] expression and their association with clinical-laboratory findings and outcome of children with H1N1 influenza virus infection.

Methods We performed a prospective observational clinical study on 15 children with H1N1 influenza virus infection and 15 controls with lower respiratory tract infection (LRTI). Cytokines and neurotrophic factor plasma levels were measured using an immunoenzymatic assay.

Results Significantly higher plasma levels of IL-1b, IL-6, NGF and BDNF were demonstrated in all patients with H1N1 infection respect to controls, while GDNF plasma levels did not undergo significant variations in the two groups. IL-6, NGF and BDNF expression was also significantly correlated with some laboratory and clinical findings, such as fever, cough, specific radiological lesions, and platelet count. No correlation was found between interleukin and neurotrophic factor expression and final outcome.

Conclusions H1N1 virus infection induces an early and significantly up-regulation of both interleukins (IL1b and IL-6) and neurotrophic factors (BDNF and NGF) respect to LRTI patients. The overexpression of these molecular markers is likely to play a neuro-immunomodulatory role in H1N1 infection and may contribute to airway inflammation and disease severity and progression.

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