Effects of two Asian sand dusts transported from the dust source regions of Inner Mongolia and northeast China on murine lung eosinophilia

He, Miao; Ichinose, Takamichi; Song, Yuan; Yoshida, Yasuhiro; Arashidani, Keiichi; Yoshida, Seiichi; Liu, Boying; Nishikawa, Masataka; Takano, Hirohisa; Sun, Guifan

doi:10.1016/j.taap.2013.07.010

Cited by 37 publications

(39 citation statements)

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“…Among the other cytokines produced by Th2 cells, IL-5 has important roles in the terminal maturation of eosinophils [138,139]. On the other hand, pro-inflammatory cytokines are also involved in mucus production, airway remodeling, and release fibrosis factors such as TGF-β1 [140][141][142]. In addition to Th2 cells, Th17 cells are a T cell effector subset that produces high levels of IL-17 and IL-22 cytokines and thus plays an important role in the pathogenesis of asthma and allergic airway disease [142][143][144].…”

Section: Pathogeny Of Desert Dust On Respiratory Diseasesmentioning

confidence: 99%

A Systematic Review of Global Desert Dust and Associated Human Health Effects

et al. 2016

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Dust storms and sandy dust events originating in arid and semi-arid areas can transport particulate material, pollutants, and potential transport long distances from their sources. Exposure to desert dust particles is generally acknowledged to endanger human health. However, most studies have examined anthropogenic particulate sources, with few studies considering contributions from natural desert dust. A systematic literature review was undertaken using the ISI Web of Knowledge and PubMed databases with the objective of identifying all studies presenting results on the potential health impact from desert dust particles across the world. This review reveals an imbalance between the areas most exposed to dust and the areas most studied in terms of health effects. Among the human health effects of dust storms are mortality and morbidity, arising from respiratory system, circulatory system, and other diseases. We summarize the quantitative results of current scientific health research and possible pathological mechanisms, and describe some of the many challenges related to understanding health effects from exposures to desert dust particles. Overall, for respiratory and circulatory mortality, both positive and negative associations have been reported for PM 10 of desert dust, but only a positive relationship was reported between PM 2.5-10 and mortality, and a positive relationship was also reported between PM 2.5 and human mortality. Future pathological studies should continue to focus on those mechanisms causing the most harmful effect of desert dust on respiratory and cardiovascular diseases. More attention should also be paid to the association between desert dust and the morbidity of other diseases, such as those affecting the reproductive system and nervous system.

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Section: Pathogeny Of Desert Dust On Respiratory Diseasesmentioning

confidence: 99%

A Systematic Review of Global Desert Dust and Associated Human Health Effects

et al. 2016

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“…Slides were prepared by Cytospin (Sakura Co., Ltd., Tokyo, Japan) and stained with Diff-Quik (International Reagents Co., Kobe, Japan). A total of 300 cells were counted under oil immersion microscopy [18,19,20]. …”

Section: Methodsmentioning

confidence: 99%

“…Sections were also stained with periodic acid-Schiff (PAS) to evaluate the degree of goblet cell proliferation in the bronchial epithelium. A pathological analysis of inflammatory cells and epithelial cells in the airways was performed using a Nikon ECLIPSE light microscope (Nikon Co., Tokyo, Japan) [18,19,20]. The degree of infiltration of neutrophils, eosinophils, and lymphocytes in the airways or proliferation of goblet cells in the bronchial epithelium was graded in a blinded fashion as follows: 0, not present; 1, slight; 2, mild; 3, moderate; 4, moderate to marked, and 5, marked.…”

Section: Methodsmentioning

confidence: 99%

“…The degree of infiltration of neutrophils, eosinophils, and lymphocytes in the airways or proliferation of goblet cells in the bronchial epithelium was graded in a blinded fashion as follows: 0, not present; 1, slight; 2, mild; 3, moderate; 4, moderate to marked, and 5, marked. ‘Slight' was defined as less than 20% of the airway exhibiting an eosinophilic inflammatory reaction or goblet cells stained with PAS, ‘mild' as 21-40%, ‘moderate' as 41-60%, ‘moderate to marked' as 61-80%, and marked as more than 80% [18,19,20,21]. The degree of thickening of the subepithelial layer in the main bronchus was graded on the following scale: 0, not present; 1, slight; 2, mild; 3, moderate; 4, moderate to marked, and 5, marked.…”

Section: Methodsmentioning

confidence: 99%

“…After 6 days in culture, adherent BMDM were collected via addition of 5 ml of 0.02% EDTA, after which the loose cells were scraped off the plates. BMDM were replated at a concentration of 3 × 10 5 cells/ml into 24-well plates at 1 ml/well [20]. BMDM were incubated with PBS and B. adusta (final concentration 20 μg/ml) for 12 h. Cytokines secreted into the culture medium by BMDM were measured via enzyme-linked immunosorbent assay (ELISA).…”

Section: Methodsmentioning

confidence: 99%

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The Role of Toll-Like Receptors and Myeloid Differentiation Factor 88 in <b><i>Bjerkandera adusta-</i></b>Induced Lung Inflammation

Ichinose²,

Song³

et al. 2015

Int Arch Allergy Immunol

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Background: Recently, a cluster of patients with an intractable allergic fungal cough who were characterized by sensitization to Bjerkandera adusta was reported. In the present study, the role of Toll-like receptors and myeloid differentiation factor 88 (MyD88) in B. adusta-induced lung inflammation was investigated. Methods: Wild-type (WT), TLR2^-/-,TLR4^-/-, and MyD88^-/- BALB/c mice were intratracheally challenged with B. adusta 4 times at 2-week intervals. Lung pathology, bronchoalveolar lavage fluid (BALF) cytological profiles, and inflammatory mediators in BALF were investigated. Bone marrow-derived macrophages (BMDM) from TLR2^-/-,TLR4^-/-, TLR2/4^-/-, TLR7/9^-/-,MyD88^-/-, and WT C57BL/6J mice were stimulated with B. adusta for 12 h, and inflammatory mediators in the culture medium were measured. Results:B. adusta caused lung inflammation along with Th2 cytokine [interleukin (IL)-5 and IL-13] and eosinophil-related chemokine [eotaxin and monocyte chemotactic protein (MCP-3)] production, an increase in eosinophils in BALF, and eosinophil infiltration in the airways in WT and TLR4^-/- mice. However, Th2 and eosinophil-related responses in TLR2^-/- and MyD88^-/- mice were low or undetectable. The induction of neutrophils and IL-6, IL-12, IL-17A, and MCP-1 in the BALF of MyD88^-/- mice was attenuated compared to that in WT mice. The induction of IL-6, TNF-α, MCP-1, and macrophage inflammatory protein-1α was reduced or undetectable in B. adusta-stimulated BMDM from TLR7/9^-/- and MyD88^-/- mice compared to WT mice. Conclusions: These results suggest that TLR2 and the adapter protein MyD88 may play an important role in the induction of eosinophils by B. adusta. However, TLR7/9-MyD88 might be important in the induction of neutrophils and the relevant inflammatory mediators, especially IL-17A.

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

Sadakane

Ichinose

Nishikawa

2018

J of Applied Toxicology

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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 β‐glucan) or lipopolysaccharide (LPS) exacerbated allergic airways inflammation in a mouse model, but the effects of co‐exposure of LPS and β‐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.

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Effects of two Asian sand dusts transported from the dust source regions of Inner Mongolia and northeast China on murine lung eosinophilia

Cited by 37 publications

References 33 publications

A Systematic Review of Global Desert Dust and Associated Human Health Effects

A Systematic Review of Global Desert Dust and Associated Human Health Effects

The Role of Toll-Like Receptors and Myeloid Differentiation Factor 88 in <b><i>Bjerkandera adusta-</i></b>Induced Lung Inflammation

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

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