1. Inflammation, immunological reaction and role of infection in pulmonary hypertension 
S.S. Pullamsetti, R. Savai, W. Janssen, B.K. Dahal, W. Seeger, F. Grimminger, H.A. Ghofrani, N. Weissmann, R.T. Schermuly 
Clinical Microbiology and Infection 
Volume 17, Issue 1, Pages 7-14 (January 2011)
DOI: /j x
Copyright © 2011 European Society of Clinical Infectious Diseases Terms and Conditions

2. Fig. 1.1
Schematic illustration of infection-mediated and inflammation-mediated vascular remodelling: In response to infection and inflammatory events, lung vascular cells produce inflammatory mediators (chemokines and cytokines), thereby recruiting the inflammatory cells (macrophages, dendritic cells, mast cells, B-cells, T-cells and regulatory T-cells). With the coordination of inflammatory mediators, inflammatory cells may perpetuate the release of cytokines, chemokines and growth factors. Finally, these processes lead to vascular remodelling though matrix remodelling, collagen deposition, vascular cell proliferation, migration, and in situ thrombosis. CCL2, chemokine (C-C motif) ligand 2; CCL5, chemokine (C-C motif) ligand 5 or RANTES (regulated upon activation, normal T-cell expressed and secreted); CX3CL1, chemokine (C-X3-C motif) ligand 1 (fractalkine); CX3CR1, chemokine (C-X3-C motif) receptor 1; EC, endothelial cells; FB, fibroblasts; FGF, fibroblast growth factor; IL-1, interleukin-1; IL-6, interleukin 6; MCP-1, monocyte chemotactic protein-1; PDGF, platelet-derived growth factor; PAH, pulmonary arterial hypertension; SDF-1α, stromal cell-derived factor 1α; SMC, smooth muscle cells; TNF-α, tumour necrosis factor-α; Treg cell, regulatory T-cell; VEGF, vascular endothelial growth factor.
Clinical Microbiology and Infection  , 7-14DOI: ( /j x)
Copyright © 2011 European Society of Clinical Infectious Diseases Terms and Conditions