Inhibition of pre-B cell colony-enhancing factor attenuates inflammation and apoptosis induced by pandemic H1N1 2009 in lung endothelium
- Resource Type
- Authors
- Xin Su; Qing Mao; Ai-Wen Feng; Wen-Kui Sun; Xin Lu; Wei Gao; Hui-Ming Sun; Yi Shi
- Source
- Respiratory Physiology & Neurobiology. 178:235-241
- Subject
- Pulmonary and Respiratory Medicine
Endothelium
Physiology
Acute Lung Injury
Cell
Apoptosis
Inflammation
Respiratory Mucosa
Lung injury
Fas ligand
Proinflammatory cytokine
Dogs
Influenza A Virus, H1N1 Subtype
Influenza, Human
Animals
Humans
Medicine
Gene silencing
Child
Nicotinamide Phosphoribosyltransferase
Pandemics
Cells, Cultured
business.industry
Microcirculation
General Neuroscience
respiratory tract diseases
medicine.anatomical_structure
Gene Knockdown Techniques
Immunology
Cytokines
Inflammation Mediators
medicine.symptom
Apoptosis Regulatory Proteins
business
- Language
- ISSN
- 1569-9048
The recent pandemic influenza A (H1N1 2009) virus infection has caused acute lung injury in susceptible population resulting in high mortality in ICU patients. In this report, we observed the effect of pre-B cell colony-enhancing factor (PBEF) on the inflammation and apoptosis in H1N1-infected human pulmonary microvascular endothelial cells (HPMECs). We constructed an in vitro HPMEC monolayer model. The results showed that H1N1 2009 induced the increased expression of inflammatory cytokines (IL-6/IL-8/TNF-α/IP-10) and apoptosis factors (FasL/TRAIL) in infected HPMECs. However, PBEF silencing with siRNA inhibited the expression of some inflammatory cytokines and decreased the apoptosis mediated by FasL. We conclude that PBEF might be partially responsible for the localized inflammatory response to H1N1 2009 in the lung microvascular endothelium and the H1N1-induced endothelial cell apoptosis probably through the FasL-mediated pathway.