Showing posts with label BAL. Show all posts
Showing posts with label BAL. Show all posts

Sunday, October 2, 2011

Immunoglobulin free light chains are increased in hypersensitivity pneumonitis and IPF

from PLoSOne
PLoS One. 2011;6(9):e25392. Epub 2011 Sep 28.
Immunoglobulin free light chains are increased in hypersensitivity pneumonitis and idiopathic pulmonary fibrosis.
Groot Kormelink T, Pardo A, Knipping K, Buendía-Roldán I, García-de-Alba C, Blokhuis BR, Selman M, Redegeld FA.
Source
Division of Pharmacology and Pathophysiology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands.
Abstract
BACKGROUND:
Idiopathic pulmonary fibrosis (IPF), a devastating lung disorder of unknown aetiology, and chronic hypersensitivity pneumonitis (HP), a disease provoked by an immunopathologic reaction to inhaled antigens, are two common interstitial lung diseases with uncertain pathogenic mechanisms. Previously, we have shown in other upper and lower airway diseases that immunoglobulin free light chains (FLCs) are increased and may be involved in initiating a local inflammation. In this study we explored if such a mechanism may also apply to HP and IPF.

METHODS:
In this study we examined the presence of FLC in serum and BAL fluid from 21 IPF and 22 HP patients and controls. IgG, IgE and tryptase concentrations were measured in BAL fluid only. The presence of FLCs, plasma cells, B cells and mast cells in lung tissue of 3 HP and 3 IPF patients and 1 control was analyzed using immunohistochemistry.

RESULTS:
FLC concentrations in serum and BAL fluid were increased in IPF and HP patients as compared to control subjects. IgG concentrations were only increased in HP patients, whereas IgE concentrations were comparable to controls in both patient groups. FLC-positive cells, B cells, plasma cells, and large numbers of activated mast cells were all detected in the lungs of HP and IPF patients, not in control lung.

CONCLUSION:
These results show that FLC concentrations are increased in serum and BAL fluid of IPF and HP patients and that FLCs are present within affected lung tissue. This suggests that FLCs may be involved in mediating pathology in both diseases.

PMID: 21980441 [PubMed - in process] PMCID: PMC3182208

Tuesday, May 24, 2011

FIZZ2 and lung fibrosis

A recent study by Dr. Phan and associates of Michigan identified that FIZZ2 was highly induced in lungs of rodents with bleomycin-induced pulmonary fibrosis in vivo and of human patients with idiopathic pulmonary fibrosis. FIZZ2 expression was induced in rodent and human lung epithelial cells by Th2 cytokines in vitro.

FIZZ2 deficiency significantly attenuated pulmonary fibrosis in bleomycin model.

FiZZ2 is down stream of IL-13 signaling.  It is unclear whether deletion of FIZZ2 abolishes IL-13 Th2 response.

Reference
[1] Liu, T., et al., J Immunol. 2011 May 20. [Epub ahead of print] PMID 21602491