Adrenaline attenuates the acute lung injury after intratracheal lipopolysaccharide instillation: An experimental study

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3006806 19 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Adrenaline attenuates the acute lung injury after intratracheal lipopolysaccharide instillation: An experimental study
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Endotoxin is a major cause of endotoxinemia, sepsis, and pneumonia due to gram-negative bacteria. Experimental endotoxin administration via the tracheal route has been extensively used to study the biological and pathophysiologic pathways of inflammation. In particular, experimental endotoxin instillation in the respiratory tree has allowed an extended research with regard to the local response of the lungs to the pathogenic stimulus. This study aims (a) to define early events in the inflammatory cascade and (b) to evaluate the efficacy of adrenaline to ameliorate the acute pulmonary inflammation in vivo after administration of intratracheal lipopolysaccharide (LPS) in an in vivo animal model. Two groups of animals were used for that purpose, a control group (single LPS administration) and a study group (subcutaneous adrenaline infusion following LPS administration). We found that mononuclear recruitment, along with an increased population of CD4+ T lymphocytes, is an early event during the course of LPS-challenged inflammation. In the study group, we determined that adrenaline mediated the lung inflammation in a statistically significant degree. By the use of immunohistochemistry, we identified (1) an increased population of CD4+ T lymphocytes in the inflammatory infiltrate, further endorsing the hypothesis that T-helper lymphocytes, along with macrophages, secrete cytokines which amplify the inflammatory response, and (2) an upregulation of ICAM-1 expression, suggesting an important role in the early pathogenesis of LPS-induced acute lung injury. Our study establishes that systemic adrenaline administration after LPS instillation may ameliorate the inflammatory lung response in vivo. Copyright © Informa Healthcare USA, Inc.
Έτος δημοσίευσης:
2008
Συγγραφείς:
Philippakis, G.E.
Lazaris, A.C.
Papathomas, T.G.
Zissis, C.
Agrogiannis, G.
Thomopoulou, G.
Nonni, A.
Xiromeritis, K.
Nikolopoulou-Stamati, P.
Bramis, J.
Patsouris, E.
Perrea, D.
Bellenis, I.
Περιοδικό:
Inhalation Toxicology
Τόμος:
20
Αριθμός / τεύχος:
4
Σελίδες:
445-453
Λέξεις-κλειδιά:
adrenalin; cytokine; intercellular adhesion molecule 1; lipopolysaccharide, acute lung injury; animal experiment; animal model; animal tissue; antigen expression; antiinflammatory activity; article; CD4+ T lymphocyte; controlled study; cytokine release; drug efficacy; experimental study; helper cell; immunohistochemistry; immunoreactivity; in vivo study; inflammatory infiltrate; macrophage; male; mononuclear cell; nonhuman; pathogenesis; priority journal; rat; systemic therapy; T lymphocyte subpopulation; treatment outcome; upregulation, Acute Disease; Animals; Bronchodilator Agents; CD4-Positive T-Lymphocytes; Cell Count; Disease Models, Animal; Drug Antagonism; Drug Therapy, Combination; Epinephrine; Intercellular Adhesion Molecule-1; Intubation, Intratracheal; Leukocytes, Mononuclear; Lipopolysaccharides; Macrophages, Alveolar; Male; Pneumonia; Rats; Up-Regulation, Animalia; Negibacteria
Επίσημο URL (Εκδότης):
DOI:
10.1080/08958370801903891
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