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Asian sand dust (ASD) comprises soil particles, microorganisms, and various chemical components. We examined whether peptidoglycan (PGN), a structural cell wall component of Gram-positive bacteria, exacerbates ASD-induced allergic airway inflammation in mice. The ASD (median diameter ∼4 µm) used was a certified reference material from the National Institute for Environmental Studies in Japan, derived from Gobi Desert surface soil collected in 2011. BALB/c mice were intratracheally exposed to PGN, heat-inactivated ASD (H-ASD), and ovalbumin (OVA), individually and in combination. Twenty-four hours after the final intratracheal administration, bronchoalveolar lavage fluid (BALF) and serum samples were collected. Inflammatory cell count, cytokine levels in the BALF, OVA-specific immunoglobulin levels in the serum, and pathological changes in the lungs were analyzed. After OVA + PGN + H-ASD treatment, the number of eosinophils, neutrophils, and macrophages in the BALF and of eosinophils in the lung tissue was significantly higher than that after OVA + PGN or OVA + H-ASD treatment. Moreover, levels of chemokines and cytokines associated with eosinophil recruitment and activation were significantly higher in the BALF of this group than in that of the OVA + PGN group, and tended to be higher than those in the OVA + H-ASD group. Pathological changes in the lungs were most severe in mice treated with OVA + PGN + H-ASD. Our results indicate that PGN is involved in the exacerbation of ASD-induced allergic airway inflammation in mice. Thus, inhalation of ASD containing Gram-positive bacteria may trigger allergic bronchial asthma.

Co-exposure of peptidoglycan and heat-inactivated Asian sand dust exacerbates ovalbumin-induced allergic airway inflammation in mice