Cytokine levels in bronchoalveolar lavage and serum in 3 patients with 2009 Influenza A(H1N1)v severe pneumonia

Abstract

Introduction: Pandemic Influenza A (H 1 N 1 )v pneumonia has led to a notable increase of admissions to intensive care units. A cytokinemediated inflammatory response has been well documented in pneumonia and acute respiratory distress syndrome. However, few studies have focused on the role of these inflammatory mediators in infections caused by the Influenza A (H 1 N 1 )v. In this study, we assess the inflammatory response mediated by cytokines at the local and systemic levels in three cases of severe pneumonia caused by Influenza A (H 1 N 1 ) virus. Methodology: Serum and bronchoalveolar lavage samples were obtained from three mechanically ventilated patients diagnosed with Influenza A (H1N1) virus pneumonia by bronchoscopic bronchoalveolar lavage. Levels of interleukin 6 (IL-6), interleukin 8 (IL-8), tumour necrosis factor alpha (TNFα) and interleukin 1 beta (IL-1ß) were meassured in these samples by enzyme-linked immunosorbent assay (ELISA). Results: High levels of C Reactive Protein, Procalcitonin below 1 ng/ml and absence of leukocytosis were common findings in all patients. TNF α and IL-1ß were not detected in the serum. IL-6 levels in serum were (94, pg/ml, 77 pg/ml and 84 pg/ml) respectively in the three patients, while IL-8 levels were (30,2 pg/ml, 128 pg/ml and 40,5 pg/ml). In the BAL samples, only one of the analysed cytokines, IL-1ß was present at detectable levels in two patients (21 pg/ml and 11 pg/ml respectively). Conclusions: Our results support previous findings which suggest that high levels of IL-6 and IL-8 in serum somehow participate in the inflammatory response in severe cases of pandemic influenza pneumonia.

Characterization In Vitro and In Vivo of a Pandemic H1N1 Influenza Virus from a Fatal Case

“…Accordingly, high levels of expression of a significant number of cytokines have been described in fatal cases of pH1N1 influenza virus infection [41]. The profile of cytokine response in severe pH1N1 influenza virus infections revealed a hyperactivation of the proinflammatory cytokines IL-6, IL-8, MCP-1, MIP-1β, GM-CSF and TNRF-1 that was not apparent in milder pH1N1 infections [42], [43], [44], [45], [46]. In addition an increase in RANTES whose natural receptor is CCR5, has been described in the bronchoalveolar lavage of patients with severe pneumonia associated with pH1N1 infections [47].…”

Osteopontin Exacerbates Pulmonary Damage in Influenza-Induced Lung Injury

“…During viral lung infection, the expression of many inflammatory cytokines, including TNF-a and IL-6, is increased, leading to inflammatory responses and further recruitment of infiltrating lymphocytes (21). TNF-a and IL-6, which are produced by macrophages exposed to respiratory viruses, influence the susceptibility to and severity of infection as well as recovery from respiratory virus infections (19).…”

IL-1βand IL-6 Upregulation in Children with H1N1 Influenza Virus Infection

“…Upregulation of inflammatory cytokines, such as the TNF-a, IL-1 β , IL-6, and IL-10, and a cytokine-mediated inflammatory response have also been documented as responsible of severity of viral lung infections [8]. Different viruses, such as respiratory syncytial virus (RSV) and adenovirus, enhanced the production of IL-6 by human macrophages influencing the susceptibility and severity of respiratory infections [9].…”