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Inhalation Toxicology
International Forum for Respiratory Research
Volume 34, 2022 - Issue 9-10
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Research Articles

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

ORCID Icon, , &
Pages 231-243 | Received 16 Nov 2021, Accepted 27 May 2022, Published online: 13 Jun 2022
 

Abstract

Aims

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.

Methods

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.

Results and Discussion

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.

Conclusions

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.

Acknowledgments

The authors are grateful for the contributions of the technical staff and students at Oita University of Nursing and Health Sciences to this research study.

Ethical approval

This study was approved by the Research Ethics Committee of the Oita University of Nursing and Health Sciences in Oita, Japan (permit number: 893). This study did not involve human participants.

Disclosure statement

The authors report there are no competing interests to declare.

Additional information

Funding

This work was supported by the Japan Society for the Promotion of Science (JSPS) KAKENHI under grant number JP17H01616 from the Ministry of Education, Culture, Sports, Science and Technology of Japan. The funding agency played no role in the study design, data collection, analysis, data interpretation, or manuscript writing.

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