Volume 19, Issue 2 pp. 225-230
ORIGINAL ARTICLE

Inflammatory markers and pulmonary granuloma infiltration in sarcoidosis

Marjeta Terčelj

Corresponding Author

Marjeta Terčelj

Clinic of Pulmonary Diseases and Allergy, University Medical Centre, Ljubljana, Slovenia

Correspondence: Marjeta Terčelj, Clinic of Pulmonary Disease and Allergy, University Medical Center, Zaloska 7, 1000 Ljubljana, Slovenia. Email: [email protected]Search for more papers by this author
Barbara Salobir

Barbara Salobir

Clinic of Pulmonary Diseases and Allergy, University Medical Centre, Ljubljana, Slovenia

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Mirjana Zupancic

Mirjana Zupancic

Laboratory Department, Children's Hospital, University Medical Center, Ljubljana, Slovenia

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Branka Wraber

Branka Wraber

Institute of Microbiology and Immunology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia

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Ragnar Rylander

Ragnar Rylander

BioFact Environmental Health Research Center, Lerum, Sweden

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First published: 24 December 2013
Citations: 11
(Associate Editor: Yuben Moodley).

Abstract

Background and objective

Previous studies have demonstrated increases of inflammatory mediators in sarcoidosis while epidemiological studies have also demonstrated an association with increased fungi exposure. This study measured the level of β-glucan in the lungs and of inflammatory mediators in serum, and correlated both with the extent of pulmonary granuloma infiltration.

Methods

This is a cross-sectional study of 98 patients with sarcoidosis and 26 controls. β-glucan, a cell wall constituent of fungi, was measured in bronchoalveolar lavage. Inflammatory mediator levels were determined in serum. The extent of granuloma infiltration was estimated on the chest X-ray. Exposure to fungi at home was determined by taking air samples in bedrooms and analysing for the presence of β-N-acetylhexosaminidase.

Results

Significantly, higher levels of β-glucan were found in broncho-alveolar lavage in subjects with sarcoidosis as compared with controls. There were significant positive relationships between the extent of granuloma infiltration and the levels of the different inflammatory mediators, except for interleukin-10. Domestic fungal exposure was higher among subjects with sarcoidosis.

Conclusions

This is the first time that a specific agent, previously suspected to be related to the risk of sarcoidosis, has been detected in the lung of subjects with sarcoidosis and related to the levels of inflammatory mediators and the degree of home exposure to fungi. The results suggest that exposure to fungi should be explored when investigating patients with sarcoidosis.

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