Effects of co-exposure of lipopolysaccharide and β-glucan (Zymosan A) in exacerbating murine allergic asthma associated with Asian sand dust

During the 2000s, Asian sand dust (ASD) was implicated in the increasing prevalence of respiratory disorders, including asthma. We previously demonstrated that a fungus from ASD aerosol exacerbated ovalbumin (OVA)-induced airways inflammation. Exposure to heat-inactivated ASD (H-ASD) and either Zymosan A (ZymA, containing beta-glucan) or lipopolysaccharide (LPS) exacerbated allergic airways inflammation in a mouse model, but the effects of co-exposure of LPS and beta-glucan are unclear. We investigated the effects of co-exposure of LPS and ZymA in OVA-induced allergic airways inflammation with ASD using BALB/c mice. Exposure to OVA + LPS enhanced the recruitment of inflammatory cells to the lungs, particularly neutrophils; exposure to OVA + LPS + H-ASD potentiated this effect. Exposure to OVA + ZymA + H-ASD stimulated the recruitment of inflammatory cells to the lungs, particularly eosinophils, and serum levels of OVA-specific IgE and IgG1 antibodies, whereas exposure to OVA + ZymA did not affect most indicators of lung inflammation. Although exposure to OVA + LPS + ZymA + H-ASD affected a few allergic parameters additively or synergistically, most allergic parameters in this group indicated the same level of exposure to OVA + LPS + H-ASD or OVA + ZymA + H-ASD. These results suggest that LPS and ZymA play different roles in allergic airways inflammation with ASD; LPS mainly enhances neutrophil recruitment through H-ASD, and ZymA enhances eosinophil recruitment through H-ASD.