Journal of Occupational Medicine and Toxicology Lipopolysaccharide Induced Inflammation in the Perivascular Space in Lungs

Background: Lipopolysaccharide (LPS) contained in tobacco smoke and a variety of environmental and occupational dusts is a toxic agent causing lung inflammation characterized by migration of neutrophils and monocytes into alveoli. Although migration of inflammatory cells into alveoli of LPS-treated rats is well characterized, the dynamics of their accumulation in the perivascular space (PVS) leading to a perivascular inflammation (PVI) of pulmonary arteries is not well described.

[1]  E. Theogaraj,et al.  The long‐term effects of perinatal glucocorticoid exposure on the host defence system of the respiratory tract , 2006, The Journal of pathology.

[2]  K. Janardhan,et al.  Toll like receptor-4 expression in lipopolysaccharide induced lung inflammation. , 2006, Histology and histopathology.

[3]  C. Taube,et al.  Strain‐specific differences in perivascular inflammation in lungs in two murine models of allergic airway inflammation , 2005, Clinical and experimental immunology.

[4]  H. Townsend,et al.  Multiple exposures to swine barn air induce lung inflammation and airway hyper-responsiveness , 2005, Respiratory research.

[5]  C. Parkos,et al.  Neutrophil transepithelial migration: role of toll-like receptors in mucosal inflammation. , 2005, Memorias do Instituto Oswaldo Cruz.

[6]  R. Pabst The Periarterial Space in the Lung: Its Important Role in Lung Edema, Transplantation, and Microbial or Allergic Inflammation , 2004, Pathobiology.

[7]  T. Sandström,et al.  LPS-induced bronchoalveolar neutrophilia; effects of salmeterol treatment. , 2004, Respiratory medicine.

[8]  B. Szponar,et al.  Tobacco smoking increases dramatically air concentrations of endotoxin. , 2004, Indoor air.

[9]  J. Pearce,et al.  Toll-like receptor 4 in normal and inflamed lungs and other organs of pig, dog and cattle. , 2004, Histology and histopathology.

[10]  R. Pabst,et al.  Expression of vascular adhesion protein-1 in normal and inflamed mice lungs and normal human lungs , 2003, Virchows Archiv.

[11]  H. Hirata,et al.  Anti-interleukin-9 antibody treatment inhibits airway inflammation and hyperreactivity in mouse asthma model. , 2002, American journal of respiratory and critical care medicine.

[12]  R. Pabst,et al.  Perivascular capillaries in the lung: an important but neglected vascular bed in immune reactions? , 2002, The Journal of allergy and clinical immunology.

[13]  C. Doerschuk Mechanisms of Leukocyte Sequestration in Inflamed Lungs , 2001, Microcirculation.

[14]  R. Strieter,et al.  Role of tumor necrosis factor-alpha in lipopolysaccharide-induced pathologic alterations. , 1990, American Journal of Pathology.

[15]  D. Luchtel,et al.  Pulmonary microcirculation: tubules rather than sheet and post. , 1982, Journal of applied physiology: respiratory, environmental and exercise physiology.

[16]  G. Appleyard,et al.  Expression of integrin subunits alphav and beta3 in acute lung inflammation. , 2004, Histochemistry and cell biology.

[17]  Emiel F M Wouters,et al.  Long-term intratracheal lipopolysaccharide exposure in mice results in chronic lung inflammation and persistent pathology. , 2002, American journal of respiratory cell and molecular biology.