@Article{,
AUTHOR = {Robin W. Freeburn, Lynne Armstrong, Ann B. Millar},
TITLE = {Cultured alveolar macrophages from patients with idiopathic pulmonary fibrosis (IPF) show dysregulation of lipopolysaccharide-induced tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) inductions},
JOURNAL = {European Cytokine Network},
VOLUME = {16},
YEAR = {2005},
NUMBER = {1},
PAGES = {5--16},
URL = {http://www.techscience.com/ECN/v16n1/66231},
ISSN = {1952-4005},
ABSTRACT = {Regulation of the pulmonary host defence mechanism is crucial for protection of the lung without
pathological consequences. This is exemplified in the normal lung by the induction of both the pro-inflammatory
cytokine TNF-α, its receptors and the anti-inflammatory cytokine IL-10 by bacterial lipopolysaccharide (LPS). We
have evaluated this mechanism in patients with idiopathic pulmonary fibrosis (IPF). Alveolar macrophages (AM)
were obtained by bronchoalveolar lavage from 21 subjects with IPF and 12 healthy volunteers. Constitutive and
LPS-stimulated AM production of TNF-α, TNF soluble receptors CD120a and CD120b, and IL-10 at the protein
and mRNA level were measured by bioassay, ELISA and competitive PCR respectively. AM from IPF subjects
were more susceptible to LPS induction of TNF-α protein (P = 0.03) and transcription of IL-10 mRNA (P = 0.01)
and IL-10R1 (P = 0.01) expression in comparison to controls. In contrast, increased CD120b was present as
protein and mRNA compared to controls (P = 0.02). AM from IPF subjects were at least as susceptible to
down-regulation of LPS-induced TNF-α levels by exogenous IL-10 as normal controls (94% versus 63%). These
data suggest that there is dysregulation of LPS-induced TNF-α and IL-10 in AM from IPF subjects. Further
studies are required to elucidate these observations, which may, in turn, give additional insight into the
pathogenesis of this disease.},
DOI = {}
}