see also:

• CRP - science and pathophysiology

• PTX3 is a member of the Pentraxin family of proteins which also includes CRP
  • Short and long pentraxins share a 200-amino-acid-long C-terminal domain that contains a motif known as the pentraxin signature (HxCxS/TWxS)
  • PTX3 is a “long penthraxin” and also has an unrelated N-terminal domain which mediates some of its binding activities (eg. Aspergillus)
• acts as a bridge between the soluble and the cellular arms of innate immunity and its binding capabilities means it acts as a functional evolutionary predecessor of antibodies
• it is involved in vascular inflammation and endothelial dysfunction through various mechanisms
• it modulates inflammatory cells, thus stimulating vascular inflammation
• PTX3 levels positively correlate with arterial hypertension, flow mediated dilation and, with intima media thickness.
• circulating PTX3 level is a strong marker of disease severity in coronary artery disease and is predictive of cardiovascular and all-cause mortality independent of CRP
• PTX3 may be associated with the severity of cardiovascular disease in rheumatoid arthritis, ankylosing spondylitis, and primary vasculitides but not in systemic lupus erythematosus (SLE)
• elevated serum or plasma levels of PTX3 are found in rheumatoid arthritis, small- and large-vessel vasculitides, other autoimmune diseases, infections, and degenerative disorders.
• immune deposits of PTX3 have been found in the renal glomeruli and tubulointerstitial areas in lupus nephritis suggesting a pathophysiologic role in renal injury
• appears to be protective against invasive aspergillosis

• rapidly produced at local sites of inflammation by macrophages, neutrophils, endothelial cells, dendritic cells, fibroblasts, and other cell types in response to IL-1 and TNF-α
• in neutrophils, PTX3 is constitutively stored in the specific granules and is released by several stimuli, including TLR agonists
• gene can be induced by the EGF-like factor AREG
• polymorphisms in the PTX3 gene are associated with risk for pulmonary tuberculosis and P. aeruginosa infections in cystic fibrosis

• opsonisation actions by binding to:
  • selected fungi, bacteria, and viruses
  • several complement components (e.g., C1q and factor H) to help regulate complement activation
    • NB. all pentraxins are involved in complement regulation through interactions with C1q (CRP, SAP, PTX3), ficolins (CRP, PTX3), and factor H (CRP, PTX)
  • apoptotic cells
  • cell-adhesion molecules (P-selectin) and thus inhibit the rolling of leukocytes on the endothelium.
    • neutrophil-released PTX3 can regulate local inflammation by suppressing P-selectin-dependent recruitment of neutrophils to peripheral tissues
• antiviral activity esp. for influenza and CMV
  • inhibition of virus-induced hemagglutination and viral neuramidase activity
  • neutralization of virus infectivity
• within endothelial cells:
  • decreases nitric oxide (NO) synthesis
  • inhibits cell proliferation and alters their functions
  • blocks the effect of fibroblast growth factor 2 (FGF2) by making a molecular complex with these molecules inactivating them
  • interacting with P-selectin, it promotes vascular inflammatory response and endothelial dysfunction
  • increases the matrix metalloproteinases synthesis directly or by blocking NO synthesis
• as an acute phase reactant in inflammation
• developmental neural actions:
  • secreted by astrocytes mainly during late embryonic and early postnatal development
  • specifically enhances formation and function of developing excitatory synapses via the recruitment of AMPAR subunits

• tumor necrosis factor-inducible gene 6 protein (TSG-6) block the PTX3-FGF2 interaction