干旱区生态环境知识资源中心(Arid): Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways

Arid

DOI	10.1186/s13223-019-0396-4
	Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways
	Ren, Yahao; Ichinose, Takamichi; He, Miao; Youshida, Seiichi; Nishikawa, Masataka; Sun, Guifan
通讯作者	Ren, YH (corresponding author), China Med Univ, Sch Publ Hlth, Dept Nutr & Food Hyg, Shenyang 110122, Peoples R China.
来源期刊	ALLERGY ASTHMA AND CLINICAL IMMUNOLOGY
ISSN	1710-1492
出版年	2019
卷号	15 期号:1
英文摘要	Background 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. Methods The 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. Results In 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. Conclusions These 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.
英文关键词	Lipopolysaccharide Airway-inflammation TLR4 MyD88 TRIF
类型	Article
语种	英语
开放获取类型	Green Published, gold
收录类别	SCI-E
WOS记录号	WOS:000512065300001
WOS关键词	PATTERN-RECOGNITION RECEPTORS ; TOLL-LIKE RECEPTORS ; MURINE LUNG ; DENDRITIC CELLS ; DAILY MORTALITY ; TNF-ALPHA ; ASTHMA ; ENDOTOXIN ; EOSINOPHILIA ; INTERLEUKIN-5
WOS类目	Allergy ; Immunology
WOS研究方向	Allergy ; Immunology
资源类型	期刊论文
条目标识符	http://119.78.100.177/qdio/handle/2XILL650/369744
作者单位	[Ren, Yahao] China Med Univ, Sch Publ Hlth, Dept Nutr & Food Hyg, Shenyang 110122, Peoples R China; [Ichinose, Takamichi; Youshida, Seiichi] Oita Univ Nursing & Hlth Sci, Dept Hlth Sci, Oita 8701201, Japan; [He, Miao; Sun, Guifan] China Med Univ, Sch Publ Hlth, Dept Environm Hlth, Shenyang 110122, Peoples R China; [Nishikawa, Masataka] Natl Inst Environm Studies, Environm Chem Div, Ibaraki 3058506, Japan
推荐引用方式 GB/T 7714	Ren, Yahao,Ichinose, Takamichi,He, Miao,et al. Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways[J],2019,15(1).
APA	Ren, Yahao,Ichinose, Takamichi,He, Miao,Youshida, Seiichi,Nishikawa, Masataka,&Sun, Guifan.(2019).Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways.ALLERGY ASTHMA AND CLINICAL IMMUNOLOGY,15(1).
MLA	Ren, Yahao,et al."Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways".ALLERGY ASTHMA AND CLINICAL IMMUNOLOGY 15.1(2019).