Adenosine signaling via the adenosine 2B receptor is involved in bronchiolitis obliterans development.
Adenosine signaling via the adenosine 2B receptor is involved in bronchiolitis obliterans development.
复制标题
通过腺苷2B受体通过腺苷信号传导参与闭塞性的支气管炎。
DOI:
10.1016/j.healun.2010.07.005
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发表时间:
2010-12
期刊:
影响因子:
--
通讯作者:
Lau CL
中科院分区:
文献类型:
--
作者:
Zhao Y;LaPar DJ;Steidle J;Emaminia A;Kron IL;Ailawadi G;Linden J;Lau CL
Adenosine is produced in response to ischemia or inflammation and protects tissues from injury. There are four adenosine receptors, which play a critical role in the physiological negative-feedback mechanism for limitation and termination of tissue-specific and systemic inflammatory responses. Accumulating evidence has focused on the anti-inflammatory and immunosuppressive role of the adenosine 2A receptor (A2AR), and we have previously reported on its’ role in the development of bronchiolitis obliterans (BO) following lung transplantation. However, few studies have reported on the role of the adenosine 2B receptor (A2BR) in BO. Data suggests that the A2BR has pro-inflammatory and profibrotic roles. We hypothesized that adenosine signaling through the A2BR is involved in the development of BO. A murine heterotopic tracheal model across a total alloantigeneic mismatch was used to study A2BR signaling in BO. Tracheal transplants consisted of Balb/c donor tracheas transplanted into wild-type or A2BR knockout C57BL/6 recipients. Transplanted tracheas were removed 3, 7, 12, and 21 days after transplantation. The luminal obliteration was evaluated through hematoxylin and eosin staining and the cellular infiltration (macrophage, neutrophil, CD3+ and Foxp3+ regulatory T cell) was detected by immunohistochemical staining. In comparison to allografts in wild type recipients, tracheas transplanted into A2BR knockout mice displayed less BO development on day 21. A2BR knockout mice had an increase in CD3+ T cells and CD4+/CD25+/Foxp3+ regulatory T cells when compared to wild type on day 7. By day 12, more CD3+ T cells were present in the wild-type trachea compared to the A2BR KO, but the percentage of CD4+/CD25+/Foxp3+ regulatory T cells remained higher in the tracheas of A2BR KO mice. A2BR stimulation may promote the development of BO via inhibiting CD4+/CD25+/Foxp3+ regulatory T cell infiltration.
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DOI:
10.1084/jem.20061097
发表时间:
2006-11-27
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Lappas CM;Day YJ;Marshall MA;Engelhard VH;Linden J
通讯作者:
Linden J
DOI:
10.1016/j.jtcvs.2007.08.041
发表时间:
2008-01-01
影响因子:
6
作者:
Gazoni, Leo M.;Laubach, Victor E.;Kron, Irving L.
通讯作者:
Kron, Irving L.
影响因子:
4.6
作者:
Fiser, SM;Tribble, CG;Kron, IL
通讯作者:
Kron, IL
DOI:
10.1165/rcmb.2007-0450oc
发表时间:
2008-08-01
影响因子:
6.4
作者:
Rollins, Brett M.;Burn, Mellisa;Tarran, Robert
通讯作者:
Tarran, Robert
影响因子:
56.9
作者:
Hori, S;Nomura, T;Sakaguchi, S
通讯作者:
Sakaguchi, S