Gerbitz, A and Ewing, P and Olkiewicz, K and Willmarth, NE and Williams, D and Hildebrandt, G and Wilke, A and Liu, C and Eissner, G and Andreesen, R and Holler, E and Guo, RF and Ward, PA and Cooke, KR (2005) A role for CD54 (intercellular adhesion molecule-1) in leukocyte recruitment to the lung during the development of experimental idiopathic pneumonia syndrome. TRANSPLANTATION, 79 (5). pp. 536-542. ISSN 0041-1337, 1534-6080
Full text not available from this repository. (Request a copy)Abstract
Background. Idiopathic pneumonia syndrome (IPS) is a frequently fatal complication of allogeneic bone marrow transplantation (BMT). IPS is associated with elevated bronchoalveolar lavage (BAL) fluid levels of tumor necrosis factor-alpha and lipopolysaccharide, both of which are potent activators of endothelial cells (ECs). EC expression of the adhesion molecule CD54 (intercellular adhesion molecule [ICAM]-1) has been shown to be a major regulator of pulmonary inflammation in various experimental models. Methods. Using a well-established murine BMT system in which lung injury and graft-versus-host disease (GvHD) are induced by minor histocompatibility antigenic differences between donor and host, the RNase Protection Assay, mice deficient in ICAM-1 expression, and a monoclonal blocking antibody to ICAM, we evaluated the role of the pulmonary vascular expression of CD54 in the development of IPS. Results. Enhanced pulmonary vascular expression of ICAM-1 coincided with the development of IPS. When ICAM-1 -/- mice were used as allogeneic BMT recipients, IPS severity (measured by lung histopathology, BAL cellularity, and cytokine expression) was significantly reduced compared with wild-type controls. Similar results were also observed when wild-type recipients were treated with a monoclonal blocking antibody to ICAM-1. Surprisingly, ICAM-1 had differential effects on leukocyte infiltration into GvHD target organs; ICAM-1 deficiency had no impact on intestinal histopathology, whereas ICAM-1-/- BMT recipients had significantly enhanced hepatic injury. Conclusions. These data demonstrate that although the expression of ICAM-1 is critical for the development of IPS, different mechanisms of leukocyte recruitment are operative in other GvHD target organs.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | BONE-MARROW-TRANSPLANTATION; TUMOR-NECROSIS-FACTOR; VERSUS-HOST-DISEASE; STEM-CELL TRANSPLANTATION; LIPOPOLYSACCHARIDE STIMULATION; INTERSTITIAL PNEUMONITIS; PULMONARY INFLAMMATION; MONOCLONAL-ANTIBODIES; MUTANT MICE; DONOR CELLS; bone marrow transplantation; endothelium; graft-versus-host disease; cytokines |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin III (Hämatologie und Internistische Onkologie) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 20 May 2021 13:57 |
| Last Modified: | 20 May 2021 13:57 |
| URI: | https://pred.uni-regensburg.de/id/eprint/36371 |
Actions (login required)
 |
View Item |
