Lung Inflammation Induced by Lipoteichoic Acid or Lipopolysaccharide in Humans


Dateien zu dieser Ressource

Dateien Größe Format Anzeige

Zu diesem Dokument gibt es keine Dateien.

HOOGERWERF, Jacobien J., Alex F. DE VOS, Paul BRESSER, Jaring S. VAN DER ZEE, Jennie M. PATER, Anita de BOER, Michael TANCK, Daniel L. LUNDELL, Chung HER-JENH, Christian DRAING, Sonja von AULOCK, Tom van der POLL, 2008. Lung Inflammation Induced by Lipoteichoic Acid or Lipopolysaccharide in Humans. In: American Journal of Respiratory and Critical Care Medicine. 178(1), pp. 34-41. ISSN 1073-449X. eISSN 1535-4970. Available under: doi: 10.1164/rccm.200708-1261OC

@article{Hoogerwerf2008Infla-1183, title={Lung Inflammation Induced by Lipoteichoic Acid or Lipopolysaccharide in Humans}, year={2008}, doi={10.1164/rccm.200708-1261OC}, number={1}, volume={178}, issn={1073-449X}, journal={American Journal of Respiratory and Critical Care Medicine}, pages={34--41}, author={Hoogerwerf, Jacobien J. and De Vos, Alex F. and Bresser, Paul and Van der Zee, Jaring S. and Pater, Jennie M. and Boer, Anita de and Tanck, Michael and Lundell, Daniel L. and Her-Jenh, Chung and Draing, Christian and Aulock, Sonja von and Poll, Tom van der} }

Hoogerwerf, Jacobien J. terms-of-use Lung Inflammation Induced by Lipoteichoic Acid or Lipopolysaccharide in Humans Lundell, Daniel L. Bresser, Paul De Vos, Alex F. Van der Zee, Jaring S. Draing, Christian Rationale: Recognition of pathogen-associated molecular patterns by Toll-like receptors (TLRs) is considered to be important for an appropriate immune response against pathogens that enter the lower airways.<br />Objectives: We studied the effects of two different TLR agonists relevant for respiratory infections in the human lung: lipoteichoic acid (LTA; TLR2 agonist, component of gram-positive bacteria) and lipopolysaccharide (LPS; TLR4-agonist, component of gram-negative bacteria).<br />Methods: Fifteen healthy subjects were given LPS or LTA: by bronchoscope, sterile saline was instilled into a lung segment followed by instillation of LTA or LPS into the contralateral lung. After 6 hours, a bronchoalveolar lavage was performed and inflammatory parameters were determined. Isolated RNA from purified alveolar macrophages was analyzed by multiplex ligation dependent probe amplification. In addition, spontaneous cytokine release by alveolar macrophages was measured.<br />Measurements and Main Results: Marked differences were detected between LTA- and LPS-induced lung inflammation. Whereas both elicited neutrophil recruitment, only LPS instillation was associated with activation of neutrophils (CD11b surface expression, degranulation product levels) and consistent rises of chemo-/cytokine levels. Moreover, LPS but not LTA activated alveolar macrophages, as reflected by enhanced expression of 10 different mRNAs encoding proinflammatory mediators and increased spontaneous cytokine release upon incubation ex vivo. Remarkably, only LTA induced C5a release.<br />Conclusions: This is the first study to report the in vivo effects of LTA in men and to compare inflammation induced by LTA and LPS in the human lung. Our data suggest that stimulation of TLR2 or TLR4 results in differential pulmonary inflammation, which may be of relevance for understanding pathogenic mechanisms at play during gram-positive and gram-negative respiratory tract infection. Aulock, Sonja von Pater, Jennie M. Publ. In: American Journal of Respiratory and Critical Care Medicine 178 (2008), 1, pp. 34-41 De Vos, Alex F. 2011-03-23T09:06:41Z Bresser, Paul Hoogerwerf, Jacobien J. Lundell, Daniel L. Pater, Jennie M. Aulock, Sonja von Tanck, Michael Her-Jenh, Chung Tanck, Michael 2011-03-23T09:06:41Z Van der Zee, Jaring S. Her-Jenh, Chung Boer, Anita de eng Poll, Tom van der 2008 Poll, Tom van der Boer, Anita de Draing, Christian

Das Dokument erscheint in:

KOPS Suche


Mein Benutzerkonto