Abstract
BackgroundLipopolysaccharide (LPS) often presents in high concentrations in particulate matter (PM), few studies have reported the enhancing effects of both LPS and PM on airway inflammation in mice and the role of toll-like receptors (TLRs) in this process. Asian sand dust (ASD) is observed most frequently during the spring. This study aimed to clarify the role of TLRs in murine lung eosinophilia exacerbated by ASD and LPS.MethodsThe effects of LPS and ASD co-treatment on ovalbumin (OVA)-induced lung eosinophilia were investigated using wild-type (WT), TLR2−/−, TLR4−/−, and adaptor protein myeloid differentiation factor 88 (MyD88)−/− BALB/c mice. ASD was heated (H-ASD) to remove the toxic organic substances. WT, TLR2−/−, TLR4−/− and MyD88−/− BALB/c mice were intratracheally instilled with four different combinations of LPS, H-ASD and OVA treatment. Subsequently, the pathological changes in lungs, immune cell profiles in bronchoalveolar lavage fluid (BALF), inflammatory cytokines/chemokines levels in BALF and OVA-specific immunoglobulin (Ig) in serum were analyzed.ResultsIn WT mice, H-ASD + LPS exacerbated OVA-induced lung eosinophilia. This combination of treatments increased the proportion of eosinophils and the levels of IL-5, IL-13, eotaxin in BALF, as well as the production of OVA-specific IgE and IgG1 in serum compared to OVA treatment alone. Although these effects were stronger in TLR2−/− mice than in TLR4−/− mice, the expression levels of IL-5, IL-13, eotaxin were somewhat increased in TLR4−/− mice treated with OVA + H-ASD + LPS. In MyD88−/− mice, this pro-inflammatory mediator-induced airway inflammation was considerably weak and the pathological changes in lungs were negligible.ConclusionsThese results suggest that LPS and H-ASD activate OVA-induced Th2 response in mice, and exacerbate lung eosinophilia via TLR4/MyD88, TLR4/TRIF and other TLR4-independent pathways.
Highlights
Lipopolysaccharide (LPS) often presents in high concentrations in particulate matter (PM), few studies have reported the enhancing effects of both LPS and PM on airway inflammation in mice and the role of toll-like receptors (TLRs) in this process
The changes in the distributions of macrophages, neutrophils, eosinophils and lymphocytes in TLR2−/− mice were relatively similar to those in WT mice, while the change in macrophage distribution in TLR4−/− mice were similar to that in WT mice. The numbers of these inflammatory cells were reduced by OVA + H-Asian sand dust (ASD) + LPS treatment in myeloid differentiation factor 88 (MyD88)−/− mice compared to WT and T LR2−/− mice
The results of our study indicate that the murine lung eosinophilia exacerbated by co-exposure of LPS and H-ASD is mediated by TLR4/MyD88 signaling pathway, and TLR4independent signaling pathways
Summary
Lipopolysaccharide (LPS) often presents in high concentrations in particulate matter (PM), few studies have reported the enhancing effects of both LPS and PM on airway inflammation in mice and the role of toll-like receptors (TLRs) in this process. Asian sand dust (ASD) is observed most frequently during the spring. This study aimed to clarify the role of TLRs in murine lung eosinophilia exacerbated by ASD and LPS. Epidemiological studies have demonstrated that LPS exposure is a significant risk factor for increased asthma prevalence [1, 2]. LPS often presents in high concentrations in particulate matter (PM) [3]. Ren et al Allergy Asthma Clin Immunol (2019) 15:82 is observed most frequently during the spring. Epidemiological studies suggest that ASD events are associated with increased mortality rates due to respiratory and circulatory diseases [5, 6]
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