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Different doses of lipopolysaccharides regulate the lung inflammation of asthmatic mice via TLR4 pathway in alveolar macrophages.
J Asthma 2009; 46(3):229-33JA

Abstract

Allergic asthma is a complicated genetic disorder caused by interaction of the acquired and innate immune responses. Acquired immune responses to protein antigens could induce type 2 T lymphocyte-driven responses and result in atopic asthma. Recent studies demonstrated that endotoxin, LPS and air pollution-induced innate immunity induce asthma through Toll-like receptors (TLR). However, the definite mechanism of LPS-induced asthma is still not known. Here, we investigated the effects of different doses of LPS in a mouse model of allergic asthma to define the molecular mechanism of LPS-induced asthma. We found that low doses of LPS in OVA induced significant inflammatory infiltration in lung tissue of asthmatic mice. Histologic studies demonstrated that lungs of these asthmatic mice were characterized by the recruitment of both eosinophils and neutrophils, increased airway mucus secretion and the elevated levels of Th2 cytokines. A high dose of LPS in OVA can induce a Th1 associated response, histologically characterized by neutrophil recruitment, the absence of airway mucus secretion and an increase of IFN-gamma production. Regardless of high or low dose of LPS, TLR4 in alveolar macrophages (AM) was up-regulated in lungs of asthmatic mice. Our data demonstrated that the dose of LPS exposure determines the type of inflammatory response and a low dose of LPS together with OVA augments the antigen-induced lung inflammation in asthma. This study demonstrates that the TLR4 signaling pathway plays a vital role in the development of asthma and indicates the tight connection between endotoxin exposure and asthma prevalence in the clinic.

Authors+Show Affiliations

Department of Pulmonary Medicine, Qilu Hospital of Shandong University, Jinan, Shandong, China. dl5506@yahoo.com.cnNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19373628

Citation

Dong, Liang, et al. "Different Doses of Lipopolysaccharides Regulate the Lung Inflammation of Asthmatic Mice Via TLR4 Pathway in Alveolar Macrophages." The Journal of Asthma : Official Journal of the Association for the Care of Asthma, vol. 46, no. 3, 2009, pp. 229-33.
Dong L, Li H, Wang S, et al. Different doses of lipopolysaccharides regulate the lung inflammation of asthmatic mice via TLR4 pathway in alveolar macrophages. J Asthma. 2009;46(3):229-33.
Dong, L., Li, H., Wang, S., & Li, Y. (2009). Different doses of lipopolysaccharides regulate the lung inflammation of asthmatic mice via TLR4 pathway in alveolar macrophages. The Journal of Asthma : Official Journal of the Association for the Care of Asthma, 46(3), pp. 229-33. doi:10.1080/02770900802610050.
Dong L, et al. Different Doses of Lipopolysaccharides Regulate the Lung Inflammation of Asthmatic Mice Via TLR4 Pathway in Alveolar Macrophages. J Asthma. 2009;46(3):229-33. PubMed PMID: 19373628.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Different doses of lipopolysaccharides regulate the lung inflammation of asthmatic mice via TLR4 pathway in alveolar macrophages. AU - Dong,Liang, AU - Li,Hongjia, AU - Wang,Shujuan, AU - Li,Yanli, PY - 2009/4/18/entrez PY - 2009/4/18/pubmed PY - 2009/5/8/medline SP - 229 EP - 33 JF - The Journal of asthma : official journal of the Association for the Care of Asthma JO - J Asthma VL - 46 IS - 3 N2 - Allergic asthma is a complicated genetic disorder caused by interaction of the acquired and innate immune responses. Acquired immune responses to protein antigens could induce type 2 T lymphocyte-driven responses and result in atopic asthma. Recent studies demonstrated that endotoxin, LPS and air pollution-induced innate immunity induce asthma through Toll-like receptors (TLR). However, the definite mechanism of LPS-induced asthma is still not known. Here, we investigated the effects of different doses of LPS in a mouse model of allergic asthma to define the molecular mechanism of LPS-induced asthma. We found that low doses of LPS in OVA induced significant inflammatory infiltration in lung tissue of asthmatic mice. Histologic studies demonstrated that lungs of these asthmatic mice were characterized by the recruitment of both eosinophils and neutrophils, increased airway mucus secretion and the elevated levels of Th2 cytokines. A high dose of LPS in OVA can induce a Th1 associated response, histologically characterized by neutrophil recruitment, the absence of airway mucus secretion and an increase of IFN-gamma production. Regardless of high or low dose of LPS, TLR4 in alveolar macrophages (AM) was up-regulated in lungs of asthmatic mice. Our data demonstrated that the dose of LPS exposure determines the type of inflammatory response and a low dose of LPS together with OVA augments the antigen-induced lung inflammation in asthma. This study demonstrates that the TLR4 signaling pathway plays a vital role in the development of asthma and indicates the tight connection between endotoxin exposure and asthma prevalence in the clinic. SN - 1532-4303 UR - https://www.unboundmedicine.com/medline/citation/19373628/Different_doses_of_lipopolysaccharides_regulate_the_lung_inflammation_of_asthmatic_mice_via_TLR4_pathway_in_alveolar_macrophages_ L2 - http://www.tandfonline.com/doi/full/10.1080/02770900802610050 DB - PRIME DP - Unbound Medicine ER -