Abstract
BackgroundA previous study has shown that the aggravation of Asian sand dust (ASD) on ovalbumin (OVA)-induced lung eosinphilia was more severe in lipopolysaccharide (LPS)-rich ASD than in SiO2-rich ASD. Therefore, the effects of different LPS contamination levels in ASD on the aggravation of OVA-induced lung eosinophilia were investigated in the present study.MethodsBefore beginning the in vivo experiment, we investigated whether the ultra-pure LPS would act only on TLR4 or not using bone marrow-derived macrophages (BMDMs) of wild–type, TLR2-/-, TLR4-/- and MyD88-/- BALB/c mice. ASD collected from the desert was heated to remove toxic organic substances (H-ASD). BALB/c mice were instilled intratracheally with 12 different testing samples prepared with LPS (1 ng and 10 ng), H-ASD, and OVA in a normal saline solution. The lung pathology, cytological profiles in the bronchoalveolar lavage fluid (BALF), the levels of inflammatory cytokines/chemokines in BALF and OVA-specific immunoglobulin in serum were investigated.ResultsThe LPS exhibited no response to the production of TNF-α and IL-6 in BMDMs from TLR4-/-, but did from TLR2-/-. H-ASD aggravated the LPS-induced neutrophilic lung inflammation. In the presence of OVA, LPS increased the level of eosinophils slightly and induced trace levels of Th2 cytokines IL-5 and IL-13 at the levels of 1 ng and 10 ng. In the presence of OVA and H-ASD, LPS induced severe eosinophil infiltration and proliferation of goblet cells in the airways as well as remarkable increases in Th2 cytokines IL-5 and IL-13 in BALF. The mixture containing LPS (1 ng) showed adjuvant activity on OVA-specific IgE and IgG1 production.ConclusionsThe results suggest that H-ASD with naturally-occurring levels of LPS enhances OVA-induced lung eosinophilia via increases in Th2-mediated cytokines and antigen-specific immunoglobulin. These results indicate that LPS is a strong candidate for being a major aggravating substance in ASD.
Highlights
A previous study has shown that the aggravation of Asian sand dust (ASD) on ovalbumin (OVA)-induced lung eosinphilia was more severe in lipopolysaccharide (LPS)-rich ASD than in SiO2-rich ASD
High levels of IL-6, Monocyte chemotactic protein-1 (MCP-1), Macrophage inflammatory protein-1α (MIP-1α) and Tumor necrosis factor-α (TNF-α) were found in WT cells, ranging from 136 ± 19.4 pg/ml (MIP-1α) to 2,080 ± 297 pg/ml (IL-6), and TLR2−/− cells, ranging from 96.0 ± 16.0 pg/ml (MIP-1α) to 1,763 ± 223 pg/ml (IL-6)
IL-6 and TNF-α were not detected in TLR4−/− cells
Summary
A previous study has shown that the aggravation of Asian sand dust (ASD) on ovalbumin (OVA)-induced lung eosinphilia was more severe in lipopolysaccharide (LPS)-rich ASD than in SiO2-rich ASD. The effects of different LPS contamination levels in ASD on the aggravation of OVA-induced lung eosinophilia were investigated in the present study. Our previous studies have shown that ASD had aggravating effects on ovalbumin (OVA) - induced lung eosinophilia, whereas ASD heated at 360°C to exclude organic substances and chemicals (H-ASD) caused fewer effects [8,9]. Our recent study has shown that the aggravation of murine lung eosinophilia was more severe in LPS-rich ASD than in SiO2-rich ASD [18]. Experimental study as to whether the levels of LPS contamination in ASD are significantly related to the degree of aggravation of the lung eosinophilia is in order
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