Intercellular adhesion molecule-I (ICAM-I, CD54) deficiency segregates the unique pathophysiological requirements for generating idiopathic pneumonia syndrome (IPS) versus graft-versus-host disease following allogeneic murine bone marrow transplantation - PubMed (original) (raw)

Comparative Study

Intercellular adhesion molecule-I (ICAM-I, CD54) deficiency segregates the unique pathophysiological requirements for generating idiopathic pneumonia syndrome (IPS) versus graft-versus-host disease following allogeneic murine bone marrow transplantation

A Panoskaltsis-Mortari et al. Biol Blood Marrow Transplant. 2001.

Free article

Abstract

Following allogeneic bone marrow transplantation (alloBMT), idiopathic pneumonia syndrome (IPS) and graft-versus-host disease (GVHD) caused by donor cell alloreactivity remain major obstacles to a successful outcome. Intercellular adhesion molecule-1 (ICAM-1) is an adhesion molecule that is involved in regulating lymphohematopoietic cell migration and facilitating T-cell responses. To determine whether ICAM-1 expression in the host would affect IPS or GVHD tissue injury responses, ICAM-1(-/-) mice were compared with ICAM-1(+/+) controls. ICAM-1(-/-) recipients did not exhibit the manifestations of IPS injury such as an increase in lung weights nor decreased lung function. The influx of T cells, macrophages, and neutrophils was dramatically dampened as was the production of the inflammatory cytokines interferon-gamma and tumor necrosis factor alpha and the chemokines monocyte chemotactic protein 1, macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, and lymphotactin, normally upregulated in the lung during IPS. In contrast, systemic levels of these mediators were unaffected and GVHD-induced lesions in the liver and colon did not differ in severity regardless of ICAM-1 expression. GVHD-mediated mortality was accelerated in ICAM-1(-/-) recipients at doses of allogeneic spleen cells that are otherwise not uniformally lethal. These data implicate ICAM-1 as playing a critical role in the generation of IPS; therefore, ICAM-1 may be a discerning element, segregating IPS from GVHD injury post-alloBMT.

PubMed Disclaimer

Cited by

Pulmonary Toxicity After Total Body Irradiation - Critical Review of the Literature and Recommendations for Toxicity Reporting.
Vogel J, Hui S, Hua CH, Dusenbery K, Rassiah P, Kalapurakal J, Constine L, Esiashvili N. Vogel J, et al. Front Oncol. 2021 Aug 26;11:708906. doi: 10.3389/fonc.2021.708906. eCollection 2021. Front Oncol. 2021. PMID: 34513689 Free PMC article. Review.
Targeting the Canonical Nuclear Factor-κB Pathway with a High-Potency IKK2 Inhibitor Improves Outcomes in a Mouse Model of Idiopathic Pneumonia Syndrome.
Fowler KA, Jania CM, Tilley SL, Panoskaltsis-Mortari A, Baldwin AS, Serody JS, Coghill JM. Fowler KA, et al. Biol Blood Marrow Transplant. 2017 Apr;23(4):569-580. doi: 10.1016/j.bbmt.2017.01.083. Epub 2017 Feb 1. Biol Blood Marrow Transplant. 2017. PMID: 28161607 Free PMC article.
A call to arms: a critical need for interventions to limit pulmonary toxicity in the stem cell transplantation patient population.
Radhakrishnan SV, Hildebrandt GC. Radhakrishnan SV, et al. Curr Hematol Malig Rep. 2015 Mar;10(1):8-17. doi: 10.1007/s11899-014-0244-z. Curr Hematol Malig Rep. 2015. PMID: 25662904
An official American Thoracic Society research statement: noninfectious lung injury after hematopoietic stem cell transplantation: idiopathic pneumonia syndrome.
Panoskaltsis-Mortari A, Griese M, Madtes DK, Belperio JA, Haddad IY, Folz RJ, Cooke KR; American Thoracic Society Committee on Idiopathic Pneumonia Syndrome. Panoskaltsis-Mortari A, et al. Am J Respir Crit Care Med. 2011 May 1;183(9):1262-79. doi: 10.1164/rccm.2007-413ST. Am J Respir Crit Care Med. 2011. PMID: 21531955 Free PMC article. Review.
Gas6 deficiency in recipient mice of allogeneic transplantation alleviates hepatic graft-versus-host disease.
Burnier L, Saller F, Kadi L, Brisset AC, Sugamele R, Baudino L, Bono F, Herbert JM, Carmeliet P, Schapira M, Izui S, Angelillo-Scherrer A. Burnier L, et al. Blood. 2010 Apr 22;115(16):3390-7. doi: 10.1182/blood-2009-02-206920. Epub 2010 Feb 4. Blood. 2010. PMID: 20139094 Free PMC article.

Intercellular adhesion molecule-I (ICAM-I, CD54) deficiency segregates the unique pathophysiological requirements for generating idiopathic pneumonia syndrome (IPS) versus graft-versus-host disease following allogeneic murine bone marrow transplantation - PubMed (original) (raw)