Enhancement of Mite Allergen-Induced Eosinophil Infiltration in the Murine Airway and Local Cytokine/Chemokine Expression by Asian Sand Dust

Abstract

Data on the effects of sand dust toward allergic asthma produced by indoor allergens, such as house dust mites, are not currently available. This study was undertaken to clarify the role of Asian sand dust on mite allergen, Dermatophagoides farinae (D. farinae)-induced eosinophilic inflammation in the murine lung, using sand dusts from the Maowusu Desert (Inner Mongolia) (SD-1) and the Tengger Desert (China) (SD-2). ICR mice were intratracheally administered saline; SD-1 alone; SD-2 alone; D. farinae alone; D. farinae + SD-1; and D. farinae + SD-2, 4 times at 2-wk intervals. The two sand dusts enhanced infiltration of eosinophil in the airway, along with goblet-cell proliferation related to D. farinae. The degree of eosinophil infiltration induced with SD-2 was greater than with SD-1. The SD-1, which contained higher amounts of β-glucan, increased the expression of interferon (IFN)-γ in bronchoalveolar lavage fluids (BALF) with or without D. farinae, but SD-2 did not. Synergistically or cumulatively elevated levels of interleukin (IL)-5, eotaxin, and monocyte chemotactic protein in BALF related to D. farinae were higher with D. farinae + SD-2 than with D. farinae + SD-1. These results suggest that increased cytokine and chemokines in BALF play an important role in the enhancement of eosinophil infiltration in the airway induced by D. farinae + sand dusts. The reduced eosinophil infiltration in the SD-1-treated mice could be due to suppression of Th-2 cytokine and eotaxin via interferon-γ induced by microbial materials, such as β-glucan.

The authors thank Kaori Tokugasaki and Aya Yakushiji, Oita University of Nursing and Health Sciences. This study was supported in part by a grant from the Ministry of Education, Science, and Culture of Japan, and by the Environmental Agency in Japan.

Notes

^a Six groups of mice were treated intratracheally with normal saline (control), SD-1 (sample from Maowusu desert), SD-2 (sample from Shapotou desert), Dermatophagoides farinae (D. farinae), D. farinae + SD-1, and D. farinae + SD-2, 4 times at 2-wk intervals. The values are mean ± SD (n = 8).

^b Significant at p < .05 vs. control.

^c Significant at p < .05 vs. SD-1.

^d Significant at p < .05 vs. D. farinae.

^e Significant at p < .05 vs. SD-2.

^a Six groups of mice were treated intratracheally with normal saline (control), SD-1 (sample from Maowusu desert), SD-2 (sample from Shapotou desert), Dermatophagoides farinae (D. farinae), D. farinae + SD-1, and D. farinae + SD-2, 4 times at 2-wk intervals. Bronchoalveolar lavage (BAL) was obtained 24 h after the last intratracheal instillation. The values are mean ± SE (n = 8).

^b Significant at p < .05 vs. control.

^c Significant at p < .05 vs. SD-1.

^d Significant at p < .05 vs. D. farinae.

^e Significant at p < .05 vs. SD-2.

^a Six groups of mice were treated intratracheally with normal saline (control), SD-1 (sample from Maowusu desert), SD-2 (sample from Shapotou desert), Dermatophagoides farinae (D. farinae), D. farinae + SD-1, and D. farinae + SD-2, 4 times at 2-wk intervals. Bronchoalveolar lavage (BAL) was conducted 24 h after the last intratracheal instillation. The values are mean ± SE (n = 8).

^b Significant at p < .05 vs. control.

^c Significant at p < .05 vs. SD-1.

^d Significant at p < .05 vs. SD-2.

^e Significant at p < .05 vs. D. farinae.

^a Six groups of mice were treated intratracheally with normal saline (control), SD-1 (sample from Maowusu desert), SD-2 (sample from Shapotou desert), Dermatophagoides farinae (D. farinae), D. farinae + SD-1, and D. farinae + SD-2, 4 times at 2-wk interval. Bronchoalveolar lavage (BAL) was conducted 24 h after the last intratracheal instillation. The values are mean ± SE (n = 8).

^b Significant at p < .05 vs. control.

^c Significant at p < .05 vs. SD-1.

^d Significant at p < .05 vs. D. farinae.

^e Significant at p < .05 vs. SD-2.