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Oxidized phospholipids protect against lung injury and endothelial barrier dysfunction caused by heat-inactivated Staphylococcus aureus.
Am J Physiol Lung Cell Mol Physiol. 2015 Mar 15; 308(6):L550-62.AJ

Abstract

Increased endothelial cell (EC) permeability and vascular inflammation along with alveolar epithelial damage are key features of acute lung injury (ALI). Products of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine oxidation (OxPAPC) showed protective effects against inflammatory signaling and vascular EC barrier dysfunction induced by gram-negative bacterial wall lipopolysaccharide (LPS). We explored the more general protective effects of OxPAPC and investigated whether delayed posttreatment with OxPAPC boosts the recovery of lung inflammatory injury and EC barrier dysfunction triggered by intratracheal injection of heat-killed gram-positive Staphylococcus aureus (HKSA) bacteria. HKSA-induced pulmonary EC permeability, activation of p38 MAP kinase and NF-κB inflammatory cascades, secretion of IL-8 and soluble ICAM1, fibronectin deposition, and expression of adhesion molecules ICAM1 and VCAM1 by activated EC were significantly attenuated by cotreatment as well as posttreatment with OxPAPC up to 16 h after HKSA addition. Remarkably, posttreatment with OxPAPC up to 24 h post-HKSA challenge dramatically accelerated lung recovery by restoring lung barrier properties monitored by Evans blue extravasation and protein content in bronchoalveolar lavage (BAL) fluid and reducing inflammation reflected by decreased MIP-1, KC, TNF-α, IL-13 levels and neutrophil count in BAL samples. These studies demonstrate potent in vivo and in vitro protective effects of posttreatment with anti-inflammatory oxidized phospholipids in the model of ALI caused by HKSA. These results warrant further investigations into the potential use of OxPAPC compounds combined with antibiotic therapies as a treatment of sepsis and ALI induced by gram-positive bacterial pathogens.

Authors+Show Affiliations

Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, University of Chicago, Chicago, Illinois.Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, University of Chicago, Chicago, Illinois.Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, University of Chicago, Chicago, Illinois.Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, University of Chicago, Chicago, Illinois.Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, University of Chicago, Chicago, Illinois.Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, University of Chicago, Chicago, Illinois kbirukov@medicine.bsd.uchicago.edu.Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, University of Chicago, Chicago, Illinois.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

25575515

Citation

Meliton, Angelo Y., et al. "Oxidized Phospholipids Protect Against Lung Injury and Endothelial Barrier Dysfunction Caused By Heat-inactivated Staphylococcus Aureus." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 308, no. 6, 2015, pp. L550-62.
Meliton AY, Meng F, Tian Y, et al. Oxidized phospholipids protect against lung injury and endothelial barrier dysfunction caused by heat-inactivated Staphylococcus aureus. Am J Physiol Lung Cell Mol Physiol. 2015;308(6):L550-62.
Meliton, A. Y., Meng, F., Tian, Y., Sarich, N., Mutlu, G. M., Birukova, A. A., & Birukov, K. G. (2015). Oxidized phospholipids protect against lung injury and endothelial barrier dysfunction caused by heat-inactivated Staphylococcus aureus. American Journal of Physiology. Lung Cellular and Molecular Physiology, 308(6), L550-62. https://doi.org/10.1152/ajplung.00248.2014
Meliton AY, et al. Oxidized Phospholipids Protect Against Lung Injury and Endothelial Barrier Dysfunction Caused By Heat-inactivated Staphylococcus Aureus. Am J Physiol Lung Cell Mol Physiol. 2015 Mar 15;308(6):L550-62. PubMed PMID: 25575515.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidized phospholipids protect against lung injury and endothelial barrier dysfunction caused by heat-inactivated Staphylococcus aureus. AU - Meliton,Angelo Y, AU - Meng,Fanyong, AU - Tian,Yufeng, AU - Sarich,Nicolene, AU - Mutlu,Gokhan M, AU - Birukova,Anna A, AU - Birukov,Konstantin G, Y1 - 2015/01/09/ PY - 2015/1/11/entrez PY - 2015/1/13/pubmed PY - 2015/5/12/medline KW - cytoskeleton KW - inflammation KW - oxidized phospholipids KW - pulmonary endothelium KW - vascular leak SP - L550 EP - 62 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am J Physiol Lung Cell Mol Physiol VL - 308 IS - 6 N2 - Increased endothelial cell (EC) permeability and vascular inflammation along with alveolar epithelial damage are key features of acute lung injury (ALI). Products of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine oxidation (OxPAPC) showed protective effects against inflammatory signaling and vascular EC barrier dysfunction induced by gram-negative bacterial wall lipopolysaccharide (LPS). We explored the more general protective effects of OxPAPC and investigated whether delayed posttreatment with OxPAPC boosts the recovery of lung inflammatory injury and EC barrier dysfunction triggered by intratracheal injection of heat-killed gram-positive Staphylococcus aureus (HKSA) bacteria. HKSA-induced pulmonary EC permeability, activation of p38 MAP kinase and NF-κB inflammatory cascades, secretion of IL-8 and soluble ICAM1, fibronectin deposition, and expression of adhesion molecules ICAM1 and VCAM1 by activated EC were significantly attenuated by cotreatment as well as posttreatment with OxPAPC up to 16 h after HKSA addition. Remarkably, posttreatment with OxPAPC up to 24 h post-HKSA challenge dramatically accelerated lung recovery by restoring lung barrier properties monitored by Evans blue extravasation and protein content in bronchoalveolar lavage (BAL) fluid and reducing inflammation reflected by decreased MIP-1, KC, TNF-α, IL-13 levels and neutrophil count in BAL samples. These studies demonstrate potent in vivo and in vitro protective effects of posttreatment with anti-inflammatory oxidized phospholipids in the model of ALI caused by HKSA. These results warrant further investigations into the potential use of OxPAPC compounds combined with antibiotic therapies as a treatment of sepsis and ALI induced by gram-positive bacterial pathogens. SN - 1522-1504 UR - https://www.unboundmedicine.com/medline/citation/25575515/Oxidized_phospholipids_protect_against_lung_injury_and_endothelial_barrier_dysfunction_caused_by_heat_inactivated_Staphylococcus_aureus_ L2 - https://journals.physiology.org/doi/10.1152/ajplung.00248.2014?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -