You are here: Home Published Research Impaired innate immune alveolar macrophage response and the predilection for COPD exacerbations.

Charles S Berenson, Ragina L Kruzel, Ellana Eberhardt, Ree Dolnick, Hans Minderman, Paul K Wallace, and Sanjay Sethi (2014)

Impaired innate immune alveolar macrophage response and the predilection for COPD exacerbations.

Thorax, 69(9):811–818.

Alveolar macrophages (AM) in COPD have fundamentally impaired responsiveness to Toll-like receptor 2 (TLR2) and TLR4 ligands of non-typeable Haemophilus influenzae (NTHI). However, the contribution of innate immune dysfunction to exacerbations of COPD is unexplored. We hypothesised that impaired innate AM responses in COPD extend beyond NTHI to other pathogens and are linked with COPD exacerbations and severity.

Cells, Cultured, Coculture Techniques, Disease Progression, Female, Haemophilus influenzae, Humans, Immunity, Innate, Interleukin-8, Ligands, Lipopolysaccharides, Lipoproteins, Macrophages, Alveolar, Male, Middle Aged, Moraxella (Branhamella) catarrhalis, NF-kappa B, Pulmonary Disease, Chronic Obstructive, Severity of Illness Index, Signal Transduction, Streptococcus pneumoniae, Toll-Like Receptor 2, Toll-Like Receptor 4, Tumor Necrosis Factor-alpha, Up-Regulation
Cells, Cultured, Coculture Techniques, Disease Progression, Female, Haemophilus influenzae, Humans, Immunity, Innate, Interleukin-8, Ligands, Lipopolysaccharides, Lipoproteins, Macrophages, Alveolar, Male, Middle Aged, Moraxella (Branhamella) catarrhalis, NF-kappa B, Pulmonary Disease, Chronic Obstructive, Severity of Illness Index, Signal Transduction, Streptococcus pneumoniae, Toll-Like Receptor 2, Toll-Like Receptor 4, Tumor Necrosis Factor-alpha, Up-Regulation
 
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