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Early posttransplant inflammation promotes the development of alloimmunity and chronic human lung allograft rejection.
Transplantation. 2007 Jan 27; 83(2):150-8.T

Abstract

BACKGROUND

Chronic human lung allograft rejection, represented by bronchiolitis obliterans syndrome (BOS), is the single most important factor that limits the long-term survival following lung transplantation (LT). However, the pathogenesis of BOS remains unclear. We hypothesized that the early posttransplant inflammation would promote the development of donor anti-human leukocyte antigen (HLA) alloimmunity and predispose to BOS.

METHODS

Serum levels of interleukin (IL)-1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-15, IL-17, Eotaxin, IP-10, MIG, MCP-1, MIP-1alpha, MIP-1beta, RANTES, tumor necrosis factor (TNF)-alpha, interferon (IFN)-alpha, IFN-gamma, granulocyte-macrophage colony-stimulating factor, IL-1Ralpha, and IL-2R were serially analyzed in 31 BOS+ and matched 31 BOS- patients using quantitative multiplex bead immunoassays. Donor-specific HLA class II cellular immunity was analyzed using enzyme-linked immunospot (ELISPOT) by testing recipient peripheral blood mononuclear cells against mismatched donor HLA-DR peptides. Anti-HLA class II antibodies were monitored using flow panel reactive antibodies.

RESULTS

There was early posttransplant elevation in basal serum levels of proinflammatory chemokines IP-10 and MCP-1 and Th1-cytokines IL-1beta, IL-2, IL-12, and IL-15 in BOS+ patients, compared to BOS- and normal subjects. In addition, a threefold decline in IL-10 levels was found during BOS development. BOS+ patients revealed increased development of HLA class II alloantibodies and Th1-predominant donor-specific cellular immunity with high frequency of IFN-gamma and low IL-5 producing T-cells.

CONCLUSION

Early posttransplant elevation of proinflammatory mediators is associated with alloimmunity and chronic human lung allograft rejection.

Authors+Show Affiliations

Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17264811

Citation

Bharat, Ankit, et al. "Early Posttransplant Inflammation Promotes the Development of Alloimmunity and Chronic Human Lung Allograft Rejection." Transplantation, vol. 83, no. 2, 2007, pp. 150-8.
Bharat A, Narayanan K, Street T, et al. Early posttransplant inflammation promotes the development of alloimmunity and chronic human lung allograft rejection. Transplantation. 2007;83(2):150-8.
Bharat, A., Narayanan, K., Street, T., Fields, R. C., Steward, N., Aloush, A., Meyers, B., Schuessler, R., Trulock, E. P., Patterson, G. A., & Mohanakumar, T. (2007). Early posttransplant inflammation promotes the development of alloimmunity and chronic human lung allograft rejection. Transplantation, 83(2), 150-8.
Bharat A, et al. Early Posttransplant Inflammation Promotes the Development of Alloimmunity and Chronic Human Lung Allograft Rejection. Transplantation. 2007 Jan 27;83(2):150-8. PubMed PMID: 17264811.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early posttransplant inflammation promotes the development of alloimmunity and chronic human lung allograft rejection. AU - Bharat,Ankit, AU - Narayanan,Kishore, AU - Street,Tyler, AU - Fields,Ryan C, AU - Steward,Nancy, AU - Aloush,Aviva, AU - Meyers,Brian, AU - Schuessler,Richard, AU - Trulock,Elbert P, AU - Patterson,G Alexander, AU - Mohanakumar,Thalachallour, PY - 2007/2/1/pubmed PY - 2007/3/7/medline PY - 2007/2/1/entrez SP - 150 EP - 8 JF - Transplantation JO - Transplantation VL - 83 IS - 2 N2 - BACKGROUND: Chronic human lung allograft rejection, represented by bronchiolitis obliterans syndrome (BOS), is the single most important factor that limits the long-term survival following lung transplantation (LT). However, the pathogenesis of BOS remains unclear. We hypothesized that the early posttransplant inflammation would promote the development of donor anti-human leukocyte antigen (HLA) alloimmunity and predispose to BOS. METHODS: Serum levels of interleukin (IL)-1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-15, IL-17, Eotaxin, IP-10, MIG, MCP-1, MIP-1alpha, MIP-1beta, RANTES, tumor necrosis factor (TNF)-alpha, interferon (IFN)-alpha, IFN-gamma, granulocyte-macrophage colony-stimulating factor, IL-1Ralpha, and IL-2R were serially analyzed in 31 BOS+ and matched 31 BOS- patients using quantitative multiplex bead immunoassays. Donor-specific HLA class II cellular immunity was analyzed using enzyme-linked immunospot (ELISPOT) by testing recipient peripheral blood mononuclear cells against mismatched donor HLA-DR peptides. Anti-HLA class II antibodies were monitored using flow panel reactive antibodies. RESULTS: There was early posttransplant elevation in basal serum levels of proinflammatory chemokines IP-10 and MCP-1 and Th1-cytokines IL-1beta, IL-2, IL-12, and IL-15 in BOS+ patients, compared to BOS- and normal subjects. In addition, a threefold decline in IL-10 levels was found during BOS development. BOS+ patients revealed increased development of HLA class II alloantibodies and Th1-predominant donor-specific cellular immunity with high frequency of IFN-gamma and low IL-5 producing T-cells. CONCLUSION: Early posttransplant elevation of proinflammatory mediators is associated with alloimmunity and chronic human lung allograft rejection. SN - 0041-1337 UR - https://www.unboundmedicine.com/medline/citation/17264811/Early_posttransplant_inflammation_promotes_the_development_of_alloimmunity_and_chronic_human_lung_allograft_rejection_ L2 - http://dx.doi.org/10.1097/01.tp.0000250579.08042.b6 DB - PRIME DP - Unbound Medicine ER -