Background: Pneumonitis induced by pandemic influenza A H1N1 has a potential to cause respiratory failure, which is a risk factor for death. The underlying immunopathological mechanisms, however, have not yet been fully elucidated.
Patients and Methods: We investigated changes in plasma cytokines, T cell subsets, and C-reactive protein (CRP) in 16 hospitalized patients with pneumonia caused by 2009 H1N1 influenza infection. The patients were classified into a severe disease group and a mild disease group according to PaO2.

Results: Cytokine profiles showed no changes in interferon γ (IFN-γ), interleukin 6 (IL-6), IL-8, or transforming necrosis factor α (TNF-α) levels throughout the observation period. Transforming growth factor ß (TGF-ß1) was overproduced in the severe group but not in the mild group. Accordingly, we also found some signs of pulmonary fibrosis during the recovery period. Elevated CRP levels and lymphopenia were common in both the severe and the mild group. After treatment, there was a significant elevation in lymphocytes in both groups, but a significant decrease in CRP in the mild group. Lymphocyte counts and CRP levels rapidly recovered to normal levels in all survivors posttreatment; otherwise it seemed to be related to poor prognosis.

Conclusions: Serial measurements of cytokines showed that only TGF-ß1 was overproduced, possibly in relation to the early use of corticosteroids, which may have downregulated immune responses to H1N1 infection. Pretreatment TGF-ß1 plasma concentrations and absolute lymphocyte counts were independent predictors of severity. However, the role of elevated TGF-ß1 in H1N1 infection-associated pulmonary fibrosis requires further investigation.

Key words: Cytokines. Immunological features. Influenza A H1N1. Pneumonitis.