Ventilator-induced injury augments interleukin-1beta production and neutrophil sequestration in lipopolysaccharide-treated lungs. 2007

Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
Department of Thoracic Medicine, Chang Gung Memorial Hospital, Chang Gung University, School of Medicine, Taipei, Taiwan.

Mechanical ventilators are commonly used to support critically ill patients; however, inappropriate ventilator settings might initiate or augment lung injury. To determine whether a large tidal volume (Vt) augments inflammatory responses and neutrophil sequestration in the lungs of rats receiving intratracheal lipopolysaccharides (LPS). Rats received intratracheal instillation of LPS (0.5 mg/kg) followed by 4 h of mechanical ventilation (MV) at 60 strokes per min with a Vt of 10 mL/kg as control MV, or 30 strokes per min with a Vt of 20 mL/kg of body weight as high-volume MV (HMV). In addition, monoclonal antibodies against rat intercellular adhesion molecule 1 (ICAM-1) or immunoglobulin G (50 mg/kg) were administered 30 min before LPS instillation and MV. Our study demonstrates that HMV enhances pulmonary permeability and induces neutrophil recruitment into the alveolar space and pulmonary edema. Intratracheal instillation of LPS caused marked lung injury, neutrophil recruitment, and production of cytokines and chemokines. Combining LPS instillation and HMV synergistically upregulated interleukin 1beta (IL-1beta) production and neutrophil sequestration in lung tissues. The ICAM-1 expression in lung tissues was responsible for the synergistic effects of neutrophil sequestration. Synergistic upregulation of IL-1beta production and neutrophil sequestration was attenuated by blocking ICAM-1 by neutralizing antibody pretreatment. High Vt MV in LPS-injured lung causes synergistic production of IL-1beta and sequestration of neutrophil via ICAM-1-dependent effects.

UI MeSH Term Description Entries
D008070 Lipopolysaccharides Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed) Lipopolysaccharide,Lipoglycans
D008168 Lung Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood. Lungs
D008171 Lung Diseases Pathological processes involving any part of the LUNG. Pulmonary Diseases,Disease, Pulmonary,Diseases, Pulmonary,Pulmonary Disease,Disease, Lung,Diseases, Lung,Lung Disease
D008297 Male Males
D009504 Neutrophils Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes. LE Cells,Leukocytes, Polymorphonuclear,Polymorphonuclear Leukocytes,Polymorphonuclear Neutrophils,Neutrophil Band Cells,Band Cell, Neutrophil,Cell, LE,LE Cell,Leukocyte, Polymorphonuclear,Neutrophil,Neutrophil Band Cell,Neutrophil, Polymorphonuclear,Polymorphonuclear Leukocyte,Polymorphonuclear Neutrophil
D012121 Respiration, Artificial Any method of artificial breathing that employs mechanical or non-mechanical means to force the air into and out of the lungs. Artificial respiration or ventilation is used in individuals who have stopped breathing or have RESPIRATORY INSUFFICIENCY to increase their intake of oxygen (O2) and excretion of carbon dioxide (CO2). Ventilation, Mechanical,Mechanical Ventilation,Artificial Respiration,Artificial Respirations,Mechanical Ventilations,Respirations, Artificial,Ventilations, Mechanical
D012122 Ventilators, Mechanical Mechanical devices used to produce or assist pulmonary ventilation. Mechanical Ventilator,Mechanical Ventilators,Respirators,Ventilators, Pulmonary,Pulmonary Ventilator,Pulmonary Ventilators,Ventilator, Pulmonary,Ventilators,Respirator,Ventilator,Ventilator, Mechanical
D001992 Bronchoalveolar Lavage Fluid Washing liquid obtained from irrigation of the lung, including the BRONCHI and the PULMONARY ALVEOLI. It is generally used to assess biochemical, inflammatory, or infection status of the lung. Alveolar Lavage Fluid,Bronchial Lavage Fluid,Lung Lavage Fluid,Bronchial Alveolar Lavage Fluid,Lavage Fluid, Bronchial,Lavage Fluid, Lung,Pulmonary Lavage Fluid,Alveolar Lavage Fluids,Bronchial Lavage Fluids,Bronchoalveolar Lavage Fluids,Lavage Fluid, Alveolar,Lavage Fluid, Bronchoalveolar,Lavage Fluid, Pulmonary,Lavage Fluids, Alveolar,Lavage Fluids, Bronchial,Lavage Fluids, Bronchoalveolar,Lavage Fluids, Lung,Lavage Fluids, Pulmonary,Lung Lavage Fluids,Pulmonary Lavage Fluids
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D014409 Tumor Necrosis Factor-alpha Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS. Cachectin,TNF-alpha,Tumor Necrosis Factor Ligand Superfamily Member 2,Cachectin-Tumor Necrosis Factor,TNF Superfamily, Member 2,TNFalpha,Tumor Necrosis Factor,Cachectin Tumor Necrosis Factor,Tumor Necrosis Factor alpha

Related Publications

Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
July 2008, American journal of respiratory cell and molecular biology,
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
November 2004, American journal of physiology. Lung cellular and molecular physiology,
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
August 2007, Chinese medical journal,
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
June 1995, Thorax,
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
January 1991, Annals of the New York Academy of Sciences,
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
July 2006, Shock (Augusta, Ga.),
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
November 2000, Toxicological sciences : an official journal of the Society of Toxicology,
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
February 1994, Journal of applied physiology (Bethesda, Md. : 1985),
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
December 1989, The American review of respiratory disease,
Shu-Min Lin, and Horng-Chyuan Lin, and Kang-Yun Lee, and Chien-Da Huang, and Chien-Ying Liu, and Chun-Hua Wang, and Han-Pin Kuo
December 2014, Journal of applied toxicology : JAT,
Copied contents to your clipboard!