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Leptin modulates innate and adaptive immune cell recruitment after cigarette smoke exposure in mice.
J Immunol. 2010 Jun 15; 184(12):7169-77.JI

Abstract

Leptin, a pleiotropic type I cytokine, was recently demonstrated to be expressed by resident lung cells in chronic obstructive pulmonary disease patients and asymptomatic smokers. To elucidate the functional role of leptin in the onset of chronic obstructive pulmonary disease, we tested leptin-deficient ob/ob mice (C57BL/6), leptin receptor-deficient db/db mice (C57BKS), and littermates in a model of cigarette smoke (CS)-induced pulmonary inflammation. Wild-type (WT) C57BL/6 mice were exposed for 4 or 24 wk to control air or CS. Pulmonary leptin expression was analyzed by immunohistochemistry and real-time PCR. Pulmonary inflammation upon 4 wk CS exposure was evaluated in bronchoalveolar lavage fluid (BALF) and lung tissue of WT, ob/ob, and db/db mice. Immunohistochemical analysis revealed leptin expression in bronchial epithelial cells, pneumocytes, alveolar macrophages, and bronchial/vascular smooth muscle cells. The 4 and 24 wk CS exposure increased leptin expression in bronchial epithelial cells and pneumocytes versus air-exposed WT mice (p<0.05). The 4 wk CS exposure resulted in increased accumulation of neutrophils, dendritic cells, macrophages, and lymphocytes in BALF and lung tissue of WT, ob/ob, and db/db mice. CS-exposed ob/ob and db/db mice showed in general higher numbers of neutrophils and lower numbers of CD4+, CD8+, and dendritic cells versus CS-exposed WT mice. Consistently, CXCL1 levels were enhanced in BALF of CS-exposed ob/ob and db/db mice versus WT mice (p<0.05). Exogenous leptin administration completely restored the skewed inflammatory profile in ob/ob mice. These data reveal an important role of leptin in modulating innate and adaptive immunity after CS inhalation in mice.

Authors+Show Affiliations

Department of Respiratory Medicine, NUTRIM School for Nutrition, Toxicology and Metabolism, Horn, The Netherlands. j.vernooy@pul.unimaas.nlNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

20488786

Citation

Vernooy, Juanita H J., et al. "Leptin Modulates Innate and Adaptive Immune Cell Recruitment After Cigarette Smoke Exposure in Mice." Journal of Immunology (Baltimore, Md. : 1950), vol. 184, no. 12, 2010, pp. 7169-77.
Vernooy JH, Bracke KR, Drummen NE, et al. Leptin modulates innate and adaptive immune cell recruitment after cigarette smoke exposure in mice. J Immunol. 2010;184(12):7169-77.
Vernooy, J. H., Bracke, K. R., Drummen, N. E., Pauwels, N. S., Zabeau, L., van Suylen, R. J., Tavernier, J., Joos, G. F., Wouters, E. F., & Brusselle, G. G. (2010). Leptin modulates innate and adaptive immune cell recruitment after cigarette smoke exposure in mice. Journal of Immunology (Baltimore, Md. : 1950), 184(12), 7169-77. https://doi.org/10.4049/jimmunol.0900963
Vernooy JH, et al. Leptin Modulates Innate and Adaptive Immune Cell Recruitment After Cigarette Smoke Exposure in Mice. J Immunol. 2010 Jun 15;184(12):7169-77. PubMed PMID: 20488786.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Leptin modulates innate and adaptive immune cell recruitment after cigarette smoke exposure in mice. AU - Vernooy,Juanita H J, AU - Bracke,Ken R, AU - Drummen,Nadja E A, AU - Pauwels,Nele S A, AU - Zabeau,Lennart, AU - van Suylen,Robert Jan, AU - Tavernier,Jan, AU - Joos,Guy F, AU - Wouters,Emiel F M, AU - Brusselle,Guy G, Y1 - 2010/05/19/ PY - 2010/5/22/entrez PY - 2010/5/22/pubmed PY - 2010/6/19/medline SP - 7169 EP - 77 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 184 IS - 12 N2 - Leptin, a pleiotropic type I cytokine, was recently demonstrated to be expressed by resident lung cells in chronic obstructive pulmonary disease patients and asymptomatic smokers. To elucidate the functional role of leptin in the onset of chronic obstructive pulmonary disease, we tested leptin-deficient ob/ob mice (C57BL/6), leptin receptor-deficient db/db mice (C57BKS), and littermates in a model of cigarette smoke (CS)-induced pulmonary inflammation. Wild-type (WT) C57BL/6 mice were exposed for 4 or 24 wk to control air or CS. Pulmonary leptin expression was analyzed by immunohistochemistry and real-time PCR. Pulmonary inflammation upon 4 wk CS exposure was evaluated in bronchoalveolar lavage fluid (BALF) and lung tissue of WT, ob/ob, and db/db mice. Immunohistochemical analysis revealed leptin expression in bronchial epithelial cells, pneumocytes, alveolar macrophages, and bronchial/vascular smooth muscle cells. The 4 and 24 wk CS exposure increased leptin expression in bronchial epithelial cells and pneumocytes versus air-exposed WT mice (p<0.05). The 4 wk CS exposure resulted in increased accumulation of neutrophils, dendritic cells, macrophages, and lymphocytes in BALF and lung tissue of WT, ob/ob, and db/db mice. CS-exposed ob/ob and db/db mice showed in general higher numbers of neutrophils and lower numbers of CD4+, CD8+, and dendritic cells versus CS-exposed WT mice. Consistently, CXCL1 levels were enhanced in BALF of CS-exposed ob/ob and db/db mice versus WT mice (p<0.05). Exogenous leptin administration completely restored the skewed inflammatory profile in ob/ob mice. These data reveal an important role of leptin in modulating innate and adaptive immunity after CS inhalation in mice. SN - 1550-6606 UR - https://www.unboundmedicine.com/medline/citation/20488786/Leptin_modulates_innate_and_adaptive_immune_cell_recruitment_after_cigarette_smoke_exposure_in_mice_ L2 - http://www.jimmunol.org/cgi/pmidlookup?view=long&amp;pmid=20488786 DB - PRIME DP - Unbound Medicine ER -