Abstract
Background: The pathogenesis driving the formation of abdominal aortic aneurysms continues to be poorly understood. Therefore, we systemically define the cytokine and circulating immune cell environment observed in human abdominal aortic aneurysm compared with risk-factor matched controls. Methods: From 2015 to 2017, a total of 274 patients donated blood to the Indiana University Center for Aortic Disease. Absolute concentrations of circulating cytokines were determined, using enzyme-linked immunosorbent assays while the expression of circulating immune cell phenotypes were assayed via flow cytometric analysis. Results: Human abdominal aortic aneurysm is characterized by a significant depletion of the antigen-specific, CD4+ Tr1 regulatory lymphocyte that corresponds to an upregulation of the antigen-specific, inflammatory Th17 cell. We found no differences in the incidence of Treg, B10, and myeloid-derived suppressor regulatory cells. Similarly, no disparities were noted in the following inflammatory cytokines: IL-1β C-reactive protein, tumor necrosis factor α interferon γ and IL-23. However, significant upregulation of the inflammatory cytokines osteopontin, IL-6, and IL-17 were noted. Additionally, no changes were observed in the regulatory cytokines IL-2, IL-4, IL-13, TNF-stimulated gene 6 protein, and prostaglandin E2, but we did observe a significant decrease in the essential regulatory cytokine IL-10. Conclusion: In this investigation, we systematically characterize the abdominal aortic aneurysm–immune environment and present preliminary evidence that faulty immune regulation may also contribute to aneurysm formation and growth.
| Original language | English (US) |
|---|---|
| Journal | Surgery (United States) |
| DOIs | |
| State | Accepted/In press - Jan 1 2018 |
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ASJC Scopus subject areas
- Surgery
Cite this
Description of human AAA by cytokine and immune cell aberrations compared to risk-factor matched controls. / Wang, S. Keisin; Green, Linden A.; Gutwein, Ashley R.; Drucker, Natalie A.; Motaganahalli, Raghu; Gupta, Alok K.; Fajardo, Andres; Murphy, Michael.
In: Surgery (United States), 01.01.2018.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Description of human AAA by cytokine and immune cell aberrations compared to risk-factor matched controls
AU - Wang, S. Keisin
AU - Green, Linden A.
AU - Gutwein, Ashley R.
AU - Drucker, Natalie A.
AU - Motaganahalli, Raghu
AU - Gupta, Alok K.
AU - Fajardo, Andres
AU - Murphy, Michael
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Background: The pathogenesis driving the formation of abdominal aortic aneurysms continues to be poorly understood. Therefore, we systemically define the cytokine and circulating immune cell environment observed in human abdominal aortic aneurysm compared with risk-factor matched controls. Methods: From 2015 to 2017, a total of 274 patients donated blood to the Indiana University Center for Aortic Disease. Absolute concentrations of circulating cytokines were determined, using enzyme-linked immunosorbent assays while the expression of circulating immune cell phenotypes were assayed via flow cytometric analysis. Results: Human abdominal aortic aneurysm is characterized by a significant depletion of the antigen-specific, CD4+ Tr1 regulatory lymphocyte that corresponds to an upregulation of the antigen-specific, inflammatory Th17 cell. We found no differences in the incidence of Treg, B10, and myeloid-derived suppressor regulatory cells. Similarly, no disparities were noted in the following inflammatory cytokines: IL-1β C-reactive protein, tumor necrosis factor α interferon γ and IL-23. However, significant upregulation of the inflammatory cytokines osteopontin, IL-6, and IL-17 were noted. Additionally, no changes were observed in the regulatory cytokines IL-2, IL-4, IL-13, TNF-stimulated gene 6 protein, and prostaglandin E2, but we did observe a significant decrease in the essential regulatory cytokine IL-10. Conclusion: In this investigation, we systematically characterize the abdominal aortic aneurysm–immune environment and present preliminary evidence that faulty immune regulation may also contribute to aneurysm formation and growth.
AB - Background: The pathogenesis driving the formation of abdominal aortic aneurysms continues to be poorly understood. Therefore, we systemically define the cytokine and circulating immune cell environment observed in human abdominal aortic aneurysm compared with risk-factor matched controls. Methods: From 2015 to 2017, a total of 274 patients donated blood to the Indiana University Center for Aortic Disease. Absolute concentrations of circulating cytokines were determined, using enzyme-linked immunosorbent assays while the expression of circulating immune cell phenotypes were assayed via flow cytometric analysis. Results: Human abdominal aortic aneurysm is characterized by a significant depletion of the antigen-specific, CD4+ Tr1 regulatory lymphocyte that corresponds to an upregulation of the antigen-specific, inflammatory Th17 cell. We found no differences in the incidence of Treg, B10, and myeloid-derived suppressor regulatory cells. Similarly, no disparities were noted in the following inflammatory cytokines: IL-1β C-reactive protein, tumor necrosis factor α interferon γ and IL-23. However, significant upregulation of the inflammatory cytokines osteopontin, IL-6, and IL-17 were noted. Additionally, no changes were observed in the regulatory cytokines IL-2, IL-4, IL-13, TNF-stimulated gene 6 protein, and prostaglandin E2, but we did observe a significant decrease in the essential regulatory cytokine IL-10. Conclusion: In this investigation, we systematically characterize the abdominal aortic aneurysm–immune environment and present preliminary evidence that faulty immune regulation may also contribute to aneurysm formation and growth.
UR - http://www.scopus.com/inward/record.url?scp=85046143507&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85046143507&partnerID=8YFLogxK
U2 - 10.1016/j.surg.2018.03.002
DO - 10.1016/j.surg.2018.03.002
M3 - Article
C2 - 29716755
AN - SCOPUS:85046143507
JO - Surgery
JF - Surgery
SN - 0039-6060
ER -