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Elevated CXCL10 (IP-10) in bronchoalveolar lavage fluid is associated with acute cellular rejection after human lung transplantation.

https://arctichealth.org/en/permalink/ahliterature107338
Source
Transplantation. 2014 Jan 15;97(1):90-7
Publication Type
Article
Date
Jan-15-2014
Author
Shahid Husain
Mariangela R Resende
Nimerta Rajwans
Ricardo Zamel
Joseph M Pilewski
Maria M Crespo
Lianne G Singer
Kenneth R McCurry
Jay K Kolls
Shaf Keshavjee
W Conrad Liles
Author Affiliation
1 Division of Infectious Diseases, Department of Medicine, Multi-Organ Transplant Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada. 2 Division of Infectious Diseases, Department of Medicine, Toronto General Research Institute, McLaughlin-Rotman Centre for Global Health, McLaughlin Centre for Molecular Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada. 3 The Toronto Lung Transplant Program, McEwen Centre for Regenerative Medicine, Toronto General Research Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada. 4 Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA. 5 Division of Respirology, Department of Medicine, The Toronto Lung Transplant Program, University Health Network, University of Toronto, Toronto, Ontario, Canada. 6 Department of Cardiothoracic Surgery, Cleveland Clinic, Cleveland, OH. 7 Departments of Pediatrics and Immunology, University of Pittsburgh, Pittsburgh, PA. 8 Department of Medicine, University of Washington, Seattle, WA. 9 Address correspondence to: Shahid Husain, M.D., M.S., Division of Infectious Diseases, Department of Medicine, Multi-Organ Transplant Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada.
Source
Transplantation. 2014 Jan 15;97(1):90-7
Date
Jan-15-2014
Language
English
Publication Type
Article
Keywords
Acute Disease
Biological Markers - analysis
Bronchoalveolar Lavage Fluid - immunology
Case-Control Studies
Chemokine CXCL10 - analysis
Female
Graft Rejection - immunology
Humans
Immunity, Cellular
Linear Models
Lung Transplantation - adverse effects
Male
Middle Aged
Odds Ratio
Ontario
Pennsylvania
Prospective Studies
Risk factors
Up-Regulation
Abstract
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.
In a prospective study of 85 LTRs, expression of cytokines (tumor necrosis factor, interferon-?, 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.
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).
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.
PubMed ID
24025324 View in PubMed
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Expansion of CD4+CD25+ helper T cells without regulatory function in smoking and COPD.

https://arctichealth.org/en/permalink/ahliterature133886
Source
Respir Res. 2011;12:74
Publication Type
Article
Date
2011
Author
Ester Roos-Engstrand
Jamshid Pourazar
Annelie F Behndig
Anders Bucht
Anders Blomberg
Author Affiliation
Dept. of Public Health and Clinical Medicine, Division of Medicine, Umeå University, Sweden. ester.roos-engstrand@lung.umu.se
Source
Respir Res. 2011;12:74
Date
2011
Language
English
Publication Type
Article
Keywords
Aged
Bronchoalveolar Lavage Fluid - immunology
Case-Control Studies
Cell Proliferation
Female
Flow Cytometry
Forced expiratory volume
Forkhead Transcription Factors - analysis
Humans
Interleukin-2 Receptor alpha Subunit - analysis
Interleukin-7 Receptor alpha Subunit - analysis
Lung - physiopathology
Lymphocyte Activation
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive - immunology - physiopathology
Smoking - adverse effects - immunology
Spirometry
Sweden
T-Lymphocyte Subsets - immunology
T-Lymphocytes, Helper-Inducer - immunology
Vital Capacity
Abstract
Regulatory T cells have been implicated in the pathogenesis of COPD by the increased expression of CD25 on helper T cells along with enhanced intracellular expression of FoxP3 and low/absent CD127 expression on the cell surface.
Regulatory T cells were investigated in BALF from nine COPD subjects and compared to fourteen smokers with normal lung function and nine never-smokers.
In smokers with normal lung function, the expression of CD25+CD4+ was increased, whereas the proportions of FoxP3+ and CD127+ were unchanged compared to never-smokers. Among CD4+ cells expressing high levels of CD25, the proportion of FoxP3+ cells was decreased and the percentage of CD127+ was increased in smokers with normal lung function. CD4+CD25+ cells with low/absent CD127 expression were increased in smokers with normal lung function, but not in COPD, when compared to never smokers.
The reduction of FoxP3 expression in BALF from smokers with normal lung function indicates that the increase in CD25 expression is not associated with the expansion of regulatory T cells. Instead, the high CD127 and low FoxP3 expressions implicate a predominantly non-regulatory CD25+ helper T-cell population in smokers and stable COPD. Therefore, we suggest a smoking-induced expansion of predominantly activated airway helper T cells that seem to persist after COPD development.
Notes
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PubMed ID
21651772 View in PubMed
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