PURPOSE: Interstitial lung diseases (ILD) are an heterogeneuos group of illnesses characterized by the chronic inflammation of the lung parenchyma. Hyaluronan (HA) is a major glycosaminoglycan of the extracellular matrix (ECM), recently described as an immune regulator. It participates in many inflammatory processes and contributes to cell recruitment at inflammatory sites. The aim of this study was to determine the concentration of HA in BAL from ILD patients and to evaluate the role of HA as a chemotactic agent for BAL cells.
METHODS: Patient population: 28 patients with ILD were diagnosed on the basis of ATS and ERS criteria. Controls: 13 persons with healthy lungs, to whom bronchoscopy was performed as follow up for post-intubation tracheal stenosis surgery. Analysis of HA levels: an enzyme immunoassay using HA binding protein (bHABP, Calbiochem) was performed. Sample concentrations of HA were calculated from a standard curve generated by plotting the absorbance at 450 nm against a HA concentration curve. Migration assay: a chemotaxis assay using a transwell system was used. The results were expressed as a migration index (MI) = number of cells stimulated by HA that migrated to the lower chamber/number of unstimulated cells that migrated to the lower chamber.
RESULTS: The levels of HA were significantly higher in BAL samples from ILD patients compared to controls: 1997.0 ± 124.8 vs 569.9 ± 56.5 ng/ml, p<0.001. Similar results were observed when the serum samples were analzyed: 274.6 ± 23.9 vs 26.1 ± 1.9 ng/ml, p<0.05. Moreover, we observed a significant migration of the cells harvested from the BAL samples from ILD patients: MI = 1.85 ± 0.11 vs 1.00, p<0.001.
CONCLUSIONS: We found a significant increase in HA levels in BAL harvested from ILD compared to controls. Furthermore, we show that HA is able to induce the chemotaxis of BAL cells. These results support that HA might play a role in the inflammatory responses underlying the development of ILD.
CLINICAL IMPLICATIONS: This work might contribute to the understanding of the role of HA role in the pathogenesis of ILD.
DISCLOSURE: The following authors have nothing to disclose: Pedro Grynblat, Glenda Ernst, Santiago Auteri, Fernando Galíndez, Jorge Geffner, Silvia Hajos
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