High-volume ventilation induces pentraxin 3 expression in multiple acute lung injury models in rats

• Published in: American journal of physiology. Lung cellular and molecular physiology Vol. 292; no. 1; pp. L144 - L153
• Main Authors: Okutani, Daisuke, Han, Bing, Mura, Marco, Waddell, Thomas K, Keshavjee, Shaf, Liu, Mingyao
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.01.2007
• Subjects: Acute Disease; Animals; Base Sequence; C-Reactive Protein - genetics; Disease Models, Animal; DNA Primers - genetics; Gene expression; Hemorrhage - metabolism; Lipopolysaccharides - toxicity; Lung - metabolism; Lung - pathology; Lung Injury; Lungs; Male; Positive-Pressure Respiration - adverse effects; Positive-Pressure Respiration - methods; Proteins; Rats; Rats, Sprague-Dawley; Respiration, Artificial - adverse effects; Respiration, Artificial - methods; Respiratory diseases; Rodents; Serum Amyloid P-Component - genetics; Up-Regulation
• ISSN: 1040-0605; 1522-1504
• DOI: 10.1152/ajplung.00002.2006

Thoracic Surgery Research Laboratory, University Health Network Toronto General Hospital, and Department of Surgery, University of Toronto, Toronto, Ontario, Canada Submitted 3 January 2006 ; accepted in final form 8 August 2006 Pentraxin 3 (PTX3) is an acute-phase protein, which can be produced by a variety of tissue cells at the site of infection or inflammation. It plays an important role in innate immunity in the lung and in mediating acute lung injury. The aim of this study was to determine the effect of mechanical ventilation on PTX3 expression in multiple lung injury models. Male Sprague-Dawley rats were challenged with intravenous injection of lipopolysaccharide (LPS) or hemorrhage followed by resuscitation (HS). The animals were then subjected to either relatively higher (12 ml/kg) or lower (6 ml/kg, positive end-expiratory pressure of 5 cmH 2 O) volume ventilation for 4 h. High-volume ventilation significantly enhanced PTX3 expression in the lung, either alone or in combination with LPS or hemorrhage. A significant increase of PTX3 immunohistochemistry staining in the lung was seen in all injury groups. The PTX3 expression was highly correlated with the severity of lung injury determined by blood gas, lung elastance, and wet-to-dry ratio. To determine the effects of HS, LPS, or injurious ventilation (25 ml/kg) alone on PTX3 expression, another group of rats was studied. Injurious ventilation significantly damaged the lung and increased PTX3 expression. A local expression of PTX3 induced by high-volume ventilation, either alone or in combination with other pathological conditions, suggests that it may be an important mediator in ventilator-induced lung injury. pentraxin; inflammation; ventilator-induced lung injury; sepsis; hemorrhagic shock Address for reprint requests and other correspondence: M. Liu, Professor of Surgery, Toronto General Hospital, Room: TMDT 2–814, 200 Elizabeth St., Toronto, Ontario, Canada M5G 2C4 (e-mail: mingyao.liu{at}utoronto.ca )