alexa Sepsis by using Cecal Ligation and Single Puncture Causes Alveolar Space Enlargement in LPA2 Knockout Mice | OMICS International | Abstract
ISSN: 2155-6121

Journal of Allergy & Therapy
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Research Article

Sepsis by using Cecal Ligation and Single Puncture Causes Alveolar Space Enlargement in LPA2 Knockout Mice

Yutong Zhao1*, Panfeng Fu2, Jing Zhao1, Rachel K. Mialki1, Jianxin Wei1, Longshuang Huang2, Jerold Chun3, Adriana S. Leme1, Steven D. Shapiro1 and Viswanathan Natarajan2,4

1Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA

2Department of Pharmacology, University of Illinois at Chicago, Chicago, IL, USA

3Department of Molecular Biology, The Scripps Research Institutes, San Diego, CA, USA

4Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA

*Corresponding Author:
Yutong Zhao
Department of Medicine, University of Pittsburgh
3459 Fifth avenue, MUH NW628
Pittsburgh, PA, 15213, USA
Tel: 4126489488
E-mail: [email protected]

Received Date: May 22, 2011; Accepted Date: June 25, 2012; Published Date: June 30, 2012

Citation: Zhao Y, Fu P, Zhao J, Mialki RK, Wei J, et al. (2012) Sepsis by using Cecal Ligation and Single Puncture Causes Alveolar Space Enlargement in LPA2 Knockout Mice. J Aller Ther S4:005 doi: 10.4172/2155-6121.S4-005

Copyright: © 2012 Zhao Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Lysophosphatidic acid (LPA) plays a dual-function in lung inflammatory diseases. LPA receptors contribute to the pathogenesis of asthma, acute lung injury, and fibrosis. Here, we investigate the role of LPA receptor type 2 (LPA2) in sepsis-induced lung inflammation and injury. Sepsis was induced using cecal ligation and single puncture (CLP) with 27 gauge needle. Plasma interleukin-6 (IL-6) and KC levels were elevated in septic wild type and LPA2-/- mice, while septic LPA2-/- mice reduces plasma KC, not IL-6 levels, compared to septic wild type mice. Bronchoalveolar lavage (BAL) KC levels increased in septic wild type and LPA2-/- mice, while the sepsis had no effect on BAL IL-6 levels, protein leak, and inflammatory cell infiltration in the lungs in wild type and LPA2-/- mice. Hematoxylin and eosin (H&E) staining revealed that septic LPA2-/- mice aggravated alveolar space enlargement. Western blotting analysis of lung tissues demonstrate that the level of cortactin, an F-actin binding protein, was decreased in septic LPA2-/- mice, when compared to wild type mice. The level of immunoglobulin G (IgG) in BAL fluids significantly increased in septic LPA2-/- mice, when compared to septic wild type mice and sham mice. Furthermore, we found that sham and septic LPA2-/- mice increased surfactant proteins B, C, and D (SP-B, SP-C, and SP-D) expression in lungs, while SP-A levels in lungs was decreased in sham and septic LPA2-/- mice. These results suggest LPA2 may regulate cortactin and surfactant protein expression in the lung. LPA2 and its downstream signaling may play a protective role against sepsis induced emphysema like disease.

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