Table 1 Signaling through complement mediators and immune cells in airway tissue remodeling
From: Complement mediators: key regulators of airway tissue remodeling in asthma
Complement | Immune cells | Signaling molecule | Remodeling |
|---|---|---|---|
C3a, C5a | M2 macrophages | TGF-β | Expression and secretion of ECM proteins |
C3a, C5a | M1 macrophages | ↑iNOS, ROS, NO, IL-12, IL-1β and TNF-α | AHR, airway fibrosis, attraction of eosinophils and neutrophils |
C3a, C5a | Eosinophil | MBP and ECP granules, RANTES, IL-13, LTC4, LTC4 and LTE4, TGF-β | Vascular permeability, mucus secretion, and ASM contraction, modulation of cellular trafficking |
C3a, C5a | Basophils | Histamine, LTC4, IL-4, IL-13 | ASM contraction, vascular permeability, promotes Th2 and IgE production |
C3a, C5a | PMNs | TXA2, MPOs, MMP-9, ROS | Bronchoconstriction, stimulate release of serotonin and histamine through platelets and mast cells respectively. Vascular permeability, mucus hypersecretion |
C3a, C5a | Mast cells | Histamine, TNF-α, GM-CSF, IL-4, IL-13 LTC4, LTB4 and PGD2 | Stimulates ASM contraction, vasodilatation and release of IL-16 production by CD8+ cells and airway epithelial cells |
C5b and MAC | Th2/CD4+ | IL-4, IL-5 and IL-13 | IL-13 suppress activation of NF-kB, and concomitant IL-5 induced eosinophilic inflammation in an IL-4- independent manner |