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. 2016 Nov 16;13(11):1144.
doi: 10.3390/ijerph13111144.

Effects of Asian Dust Particles on the Early-Stage Antigen-Induced Immune Response of Asthma in NC/Nga Mice

Jun Kurai  1 , Masanari Watanabe  2 , Hiroyuki Sano  3 , Degejirihu Hantan  4 , Yuji Tohda  5 , Eiji Shimizu  6
Affiliations

Effects of Asian Dust Particles on the Early-Stage Antigen-Induced Immune Response of Asthma in NC/Nga Mice

Jun Kurai et al. Int J Environ Res Public Health. .

Abstract

Asian dust (AD) can aggravate airway inflammation in asthma, but the association between AD and the development of asthma remains unclear. This study aimed to investigate the effects of AD on the early stage of antigen sensitization using a mouse model of asthma, as well as the role of leukotrienes (LTs) in antigen-induced airway inflammation potentiated by AD particles. NC/Nga mice were co-sensitized by intranasal instillation of AD particles and/or Dermatophagoides farinae (Df) for five consecutive days. Df-sensitized mice were stimulated with an intranasal Df challenge at seven days. Mice were treated with the type 1 cysteinyl LT (CysLT₁) receptor antagonist orally 4 h before and 1 h after the allergen challenge. At 24 h post-challenge, the differential leukocyte count, inflammatory cytokines, and LTs in bronchoalveolar lavage fluid were assessed, and airway inflammation was evaluated histopathologically. AD augmented neutrophilic and eosinophilic airway inflammation with increased CysLTs and dihydroxy-LT in a mouse model of asthma. The CysLT₁ receptor antagonist was shown to attenuate both neutrophilic and eosinophilic airway inflammation augmented by AD. Therefore, exposure to AD may be associated with the development of asthma and LTs may play important roles in airway inflammation augmented by AD.

Keywords: Asian dust; NC/Nga mouse model; airway inflammation; asthma; leukotrienes.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Experimental protocol. NC/Nga mice were sensitized using intranasal (i.n.) installation of a mixture (Asian dust (AD) particles and/or Dermatophagoides farina (Df), or CJ-1 soil and/or Df) for five consecutive days (days 0–4). Pranlukast (Prl)-treated mice received Prl orally (25 mg/kg/day) at 4 h before the allergen challenge and at 1 h after the challenge on day 11. At seven days after the last allergen sensitization, the mice were challenged using the allergen, which was followed by the collection of bronchoalveolar lavage fluid, lung tissue, and serum. Mice were divided into eight groups: normal saline (NS)/NS, NS/NS + Prl, Df/Df, Df/Df + Prl, AD/NS, AD/NS + Prl, AD + Df/Df, and AD + Df/Df + Prl.
Figure 2
Figure 2
Total and differential leukocyte counts in bronchoalveolar lavage fluid (BALF). The cell counts in BALF were obtained 24 h after the allergen challenge on day 11. The differential leukocyte counts included macrophages, lymphocytes, neutrophils, and eosinophils. Total cell counts in Asian dust (AD) + Dermatophagoides farina (Df)/Df + Pranlukast (Prl) mice were significantly decreased, as compared with AD + Df/Df mice. Data are expressed as the mean ± standard deviation, with eight mice per group. * p < 0.05.
Figure 2
Figure 2
Total and differential leukocyte counts in bronchoalveolar lavage fluid (BALF). The cell counts in BALF were obtained 24 h after the allergen challenge on day 11. The differential leukocyte counts included macrophages, lymphocytes, neutrophils, and eosinophils. Total cell counts in Asian dust (AD) + Dermatophagoides farina (Df)/Df + Pranlukast (Prl) mice were significantly decreased, as compared with AD + Df/Df mice. Data are expressed as the mean ± standard deviation, with eight mice per group. * p < 0.05.
Figure 3
Figure 3
Cytokine and chemokine levels in bronchoalveolar lavage fluid (BALF). BALF cytokine and chemokine expression profiles were analyzed using enzyme immunoassays for interferon (IFN)-γ, interleukin (IL)-5, IL-13, keratinocyte-derived chemokine (KC/CXCL1), macrophage inflammatory protein-2 (MIP-2/CXCL2), and IL-6. Data for each group are expressed as the mean ± standard deviation, with six mice per group. * p < 0.05.
Figure 3
Figure 3
Cytokine and chemokine levels in bronchoalveolar lavage fluid (BALF). BALF cytokine and chemokine expression profiles were analyzed using enzyme immunoassays for interferon (IFN)-γ, interleukin (IL)-5, IL-13, keratinocyte-derived chemokine (KC/CXCL1), macrophage inflammatory protein-2 (MIP-2/CXCL2), and IL-6. Data for each group are expressed as the mean ± standard deviation, with six mice per group. * p < 0.05.
Figure 4
Figure 4
Effects of Pranlukast (Prl) treatment on histopathological changes in the lungs. Light photomicrographs of representative lung sections were stained using hematoxylin and eosin (magnification: ×200). Representative light photomicrographs of normal saline (NS)/NS mice (A); NS/NS + Prl mice (B); Dermatophagoides farina (Df)/Df mice (C); Df/Df + Prl mice (D); Asian dust (AD)/NS mice (E); AD/NS + Prl mice (F); AD + Df/Df mice (G); and AD + Df/Df + Prl mice (H). Arrow heads show peribronchiolar and perivascular mixed inflammatory cell infiltration in AD + Df/Df mice.
Figure 5
Figure 5
Effects of Pranlukast (Prl) treatment on cysteinyl leukotrienes (CysLTs) and dihydroxy-LT (LTB4) levels in bronchoalveolar lavage fluid (BALF). BALF LT production was measured using enzyme immunoassays for CysLTs (A) and LTB4 (B). Data for each group are expressed as the mean ± standard deviation, with six mice per group. * p < 0.05.
Figure 6
Figure 6
Granulocyte-macrophage colony stimulating factor (GM-CSF) levels in serum and bronchoalveolar lavage fluid (BALF). GM-CSF levels in serum (A) and BALF (B) were analyzed using enzyme immunoassays. Data for each group are expressed as the mean ± standard deviation, with six mice per group.
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