The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Immune and Inflammatory Cell Involvement in the Pathology of Idiopathic Pulmonary Arterial Hypertension
Abstract
RATIONALE: Pulmonary arterial hypertension (PAH) is characterized by vasoconstriction and vascular remodeling. Recent studies have revealed that immune and inflammatory responses play a crucial role in pathogenesis of idiopathic PAH. OBJECTIVES: To systematically evaluate the number and cross-sectional distribution of inflammatory cells in different sizes of pulmonary arteries from explanted lungs of patients with idiopathic PAH versus healthy donor lungs and to demonstrate functional relevance by blocking stromal-derived factor-1 by the Spiegelmer NOX-A12 in monocrotaline-induced pulmonary hypertension in rats. METHODS: Immunohistochemistry was performed on lung tissue sections from patients with idiopathic PAH and healthy donors. All positively stained cells in whole-lung tissue sections, surrounding the vessels, and in the different compartments of the vessels were counted. To study the effects of blocking SDF-1, rats with monocrotaline-induced pulmonary hypertension were treated with NOX-A12 from Day 21 to Day 35 after monocrotaline administration. MEASUREMENTS AND MAIN RESULTS: We found a significant increase of the perivascular number of macrophages (CD68(+)), macrophages/monocytes (CD14(+)), mast cells (toluidine blue(+)), dendritic cells (CD209(+)), T cells (CD3(+)), cytotoxic T cells (CD8(+)), and helper T cells (CD4(+)) in vessels of idiopathic PAH lungs compared with control subjects. FoxP3(+) mononuclear cells were significantly decreased. In the monocrotaline model, the NOX-A12-induced reduction of mast cells, CD68(+) macrophages, and CD3(+) T cells was associated with improvement of hemodynamics and pulmonary vascular remodeling. CONCLUSIONS: Our findings reveal altered perivascular inflammatory cell infiltration in pulmonary vascular lesions of patients with idiopathic pulmonary arterial hypertension. Targeting attraction of inflammatory cells by blocking stromal-derived factor-1 may be a novel approach for treatment of PAH.
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Cites
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Foxp3+CD25+CD4+ natural regulatory T cells in dominant self‐tolerance and autoimmune disease
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Inflammation, Growth Factors, and Pulmonary Vascular Remodeling
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Self-citationModern Age Pathology of Pulmonary Arterial Hypertension
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CXCL12 (SDF1α)-CXCR4/CXCR7 Pathway Inhibition: An Emerging Sensitizer for Anticancer Therapies?
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Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension
Rabinovitch, M., Guignabert, C., Humbert, M., & Nicolls, M. R. (2014) · Circulation Research · doi:10.1161/circresaha.113.301141 · Cited by 1,029
Relevant Issues in the Pathology and Pathobiology of Pulmonary Hypertension
Tuder, R. M., Archer, S. L., Dorfmüller, P., Erzurum, S. C., Guignabert, C., Michelakis, E., Rabinovitch, M., Schermuly, R., Stenmark, K. R., & Morrell, N. W. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.10.025 · Cited by 585
Self-citationGood, R. B., Gilbane, A. J., Trinder, S. L., Denton, C. P., Coghlan, G., Abraham, D. J., & Holmes, A. M. (2015) · The American Journal of Pathology · doi:10.1016/j.ajpath.2015.03.019 · Cited by 349
The Metabolic Basis of Pulmonary Arterial Hypertension
Sutendra, G., & Michelakis, E. D. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.01.004 · Cited by 268
Obesity, estrogens and adipose tissue dysfunction - implications for pulmonary arterial hypertension
Mair, K. M., Gaw, R., & MacLean, M. R. (2020) · Pulmonary Circulation · doi:10.1177/2045894020952023 · Cited by 129
Metadata
- Authors
- Savai, R., Pullamsetti, S. S., Kolbe, J., Bieniek, E., Voswinckel, R., Fink, L., Scheed, A., Ritter, C., Dahal, B. K., Vater, A., Klussmann, S., Ghofrani, H. A., Weissmann, N., Klepetko, W., Banat, G. A., Seeger, W., Grimminger, F., & Schermuly, R. T.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-11-01
- Volume
- 186
- Issue
- 9
- Pages
- 897-908
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2162698108
- Cited by
- 408
- References
- 37
- FWCI
- 15.89
- Type
- journal article
- Language
- en
- Open access
- closed
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- Savai, R., Pullamsetti, S. S., Kolbe, J., Bieniek, E., Voswinckel, R., Fink, L., Scheed, A., Ritter, C., Dahal, B. K., Vater, A., Klussmann, S., Ghofrani, H. A., Weissmann, N., Klepetko, W., Banat, G. A., Seeger, W., Grimminger, F., & Schermuly, R. T. (2012). Immune and Inflammatory Cell Involvement in the Pathology of Idiopathic Pulmonary Arterial Hypertension. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.201202-0335oc
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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