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Elevated CXCL10 (IP-10) in bronchoalveolar lavage fluid is associated with acute cellular rejection after human lung transplantation.
| Title | Elevated CXCL10 (IP-10) in bronchoalveolar lavage fluid is associated with acute cellular rejection after human lung transplantation. |
| Publication Type | Journal Article |
| Year of Publication | 2014 |
| Authors | Husain, S, Resende, MR, Rajwans, N, Zamel, R, Pilewski, JM, Crespo, MM, Singer, LG, McCurry, KR, Kolls, JK, Keshavjee, S, Liles, CW |
| Journal | Transplantation |
| Volume | 97 |
| Issue | 1 |
| Pagination | 90-7 |
| Date Published | 2014 Jan 15 |
| ISSN | 1534-6080 |
| Keywords | Acute Disease, Biological Markers, Bronchoalveolar Lavage Fluid, Case-Control Studies, Chemokine CXCL10, Female, Graft Rejection, Humans, Immunity, Cellular, Linear Models, Lung Transplantation, Male, Middle Aged, Odds Ratio, Ontario, Pennsylvania, Prospective Studies, Risk Factors, Up-Regulation |
| Abstract | BACKGROUND: CXCL10 (IP-10) is a potent chemoattractant for T cells that has been postulated to play a role in infection and acute cellular rejection (ACR) in animal models. We measured CXCL10 (IP-10) (and other cytokines previously implicated in the pathogenesis of ACR) in the bronchoalveolar lavage (BAL) of lung transplant recipients (LTRs) to determine the association between CXCL10 (IP-10) and ACR in LTRs. METHODS: In a prospective study of 85 LTRs, expression of cytokines (tumor necrosis factor, interferon-γ, interleukin [IL]-6, IL-8, IL-15, IL-16, IL-17, CXCL10 [IP-10], and MCP-1 [CCL2]) in BAL samples (n=233) from patients with episodes of ACR (n=44), infection ("Infect"; n=25), concomitant "Infect+ACR" (n=10), and "No Infect and No ACR" (n=154) were analyzed. RESULTS: The levels of both CXCL10 (IP-10) and IL-16 were significantly increased in histologically proven ACR compared with the "No Infect and No ACR" group (CXCL10 [IP-10]: 107.0 vs. 31.9 pg/mL [P=0.001] and IL-16: 472.1 vs. 283.01 pg/mL [P=0.01]). However, in a linear mixed-effects model, significant association was found only between CXCL10 (IP-10) and ACR. A one-log increase of CXCL10 (IP-10) was associated with a 40% higher risk of ACR (odds ratio, 1.4; 95% confidence interval, 1.12-1.84). CONCLUSION: Higher values of CXCL10 (IP-10) in BAL fluid are associated with ACR in LTRs, suggesting a potential mechanistic role in the pathogenesis of ACR in LTRs. These results suggest that therapeutic strategies to inhibit CXCL10 (IP-10) and or its cognate receptor, CXCR3, warrant investigation to prevent and/or treat ACR in clinical lung transplantation. |
| DOI | 10.1097/TP.0b013e3182a6ee0a |
| Alternate Journal | Transplantation |
| PubMed ID | 24025324 |
