title: Asian sand dust enhances ovalbumin-induced eosinophil recruitment in the alveoli and airway of mice.
abstract: Asian sand dust (ASD) containing sulfate (SO4(2-)) reportedly causes adverse respiratory health effects but there is no experimental study showing the effect of ASD toward allergic respiratory diseases. The effects of ASD and ASD plus SO4(2-) toward allergic lung inflammation induced by ovalbumin (OVA) were investigated in this study. ICR mice were administered intratracheally with saline; ASD alone (sample from Shapotou desert); and ASD plus SO4(2-) (ASD-SO4); OVA+ASD; OVA+ASD-SO4. ASD or ASD-SO4 alone caused mild nutrophilic inflammation in the bronchi and alveoli. ASD and ASD-SO4 increased pro-inflammatory mediators, such as Keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-1 alpha, in bronchoalveolar lavage fluids (BALF). ASD and ASD-SO4 enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. However, a further increase of eosinophils by addition of SO4(2-) was not observed. The two sand dusts synergistically increased interleukin-5 (IL-5) and monocyte chemotactic protein-1 (MCP-1), which were associated with OVA, in BALF. However, the increased levels of IL-5 were lower in the OVA+ASD-SO4 group than in the OVA+ASD group. ASD caused the adjuvant effects to specific-IgG1 production by OVA, but not to specific-IgE. These results suggest that the enhancement of eosinophil recruitment in the lung is mediated by synergistically increased IL-5 and MCP-1. IgG1 antibodies may play an important role in the enhancement of allergic reaction caused by OVA and sand dust. However, extra sulfate may not contribute to an increase of eosinophils.
authors.affiliation: Major of Human Care Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan.
authors.forename: Kyoko
authors.initials: K
authors.lastname: Hiyoshi
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Kaori
authors.initials: K
authors.lastname: Sadakane
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Ikuko
authors.initials: I
authors.lastname: Mori
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yoshida
authors.forename: Yoshito
authors.initials: Y
authors.lastname: Kumagai
authors.forename: Shigeo
authors.initials: S
authors.lastname: Tomura
authors.forename: Takayuki
authors.initials: T
authors.lastname: Shibamoto
mesh_terms: D000818:Animals; D001208:Asia; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000276:immunology; D018932:Chemokine CCL2 / Q000096:biosynthesis; D004391:Dust / Q000276:immunology*; D004804:Eosinophils / Q000502:physiology*; D007074:Immunoglobulin G / Q000032:analysis; D015848:Interleukin-5 / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000276:immunology*; D012822:Silicon Dioxide; D013431:Sulfates / Q000633:toxicity*
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D004391:Dust; D007074:Immunoglobulin G; D015848:Interleukin-5; D013431:Sulfates; D012822:Silicon Dioxide