Inflammatory proteins in nasal lavage of workers exposed to occupational agents

Abstract

Background

Low-molecular-weight (LMW) and high-molecular-weight (HMW) agents have been recognized as causes of occupational rhinitis (OR). Immunological mechanisms underlying OR differ according to the type of exposure. While HMW agents act mainly through IgE-mediated mechanisms, LMW agents appear to act through both immunologic and non-immunologic mechanisms.

Objective

The objective of this study was to identify potential differences in the upper airways inflammatory response after exposure to LMW and HMW agents by specific inhalation challenge test (SIC).

Methods

Nasal lavage (NL) samples from 20 subjects who were exposed to HMW (n=10, Group I) and LMW (n=10, Group II) at their workplaces were collected after SIC with control and specific occupational agents. These samples were analyzed for 47 inflammatory markers using multiplex bead technology.

Results

After exposure to specific agent, Group I exhibited higher concentrations of the following proteins compared to Group II: fibrinogen (median (interquartile range) Group I: 0.09 (0.00) μg/ml, Group II: 0.04 (0.05) μg/ml, p=0.05); haptoglobin (Group I: 0.86 (0.01) μg/ml, Group II: 0.14 (0.20) μg /ml, p=0.02); vascular cell adhesion molecule-1 (VCAM-1) (Group I: 0.34 (0.67) ng/ml, Group II: 0.11(0.11) ng/ml, p=0.01); vascular endothelial growth factor (VEGF) (Group I: 157.0 (154.0) pg/ml, Group II: 98.0 (20.25) pg/ml, p=0.01) and vitamin D (VDBP) (Group I: 0.06 (0.13) μg /ml, Group II: 0.03 (0.03) μg /ml, p=0.04). No statistically significant differences in proteins profiles were observed between the groups after exposure to control agent. Also, subjects exposed to HMW agents showed a significant increase in NL levels of C-reactive protein compared to control day exposure.

Conclusions and clinical relevance

Exposure to HMW and LMW agents by SIC induced a differential nasal airway response including acute-phase reactants proteins (fibrinogen, haptoblobin and CRP), cell adhesion molecules (VCAM-1), endothelial growth factors (VEGF) and VDBP.

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