Table 4.
Roles of PARs in allergic diseases.
| Disease | PAR involved | Response of cell or molecule |
|---|---|---|
| Rhinitis | PAR-1 | VEGF secretion from CHAEC [98]; |
| PAR-2 | Higher secretion rate and numbers of responding glands [122]; fluid hypersecretion of airway mucosa [123]; suppression of Cx26 production in human NEC [124]; IL-6 and IL-8 production in NECs [125]; tachykinin-mediated neurogenic inflammation [126]; | |
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| ||
| Asthma | PAR-1 | Bronchial inflammation is worsened [118]; expression of TGF-β1 to promote airway remodeling [119]; susceptible to AHR [120] |
| PAR-2 | Contractions of human airways [128]; bronchial SMC proliferation and migration [129]; increased anion secretion [130]; eosinophil infiltration, AHR, IgE levels to OVA sensitization [131] influx of eosinophils in BALF, protein leak in the bronchoalveolar space, increase BALF levels of the anaphylatoxins C3a and C5a [132]; increase IL-6 expression and induce the proliferation of asthmatic bronchial SMC [134]; augment TNF-α-induced MMP-9 expression [135]; generate Ca(2+) in HAECs [136, 138]; AHR, Th2, and Th17 cytokine release, serum IgE levels, and cellular infiltration [137]; CCL20 and GM-CSF production, increase recruitment and/or differentiation of mDC populations [139]; beta-adrenergic desensitization [140]; increase chemotactic activity for the HMC-1 mast cell line [141]; exaggerate cough [142]; chitinase-mediated [Ca(2+)] increase [13]; inhibit the development of airway eosinophilia and hyperresponsiveness in allergic mice through COX-2-mediated generation of the anti-inflammatory mediator PGE2 [143]; inhibit bronchoconstriction and airway hyperresponsiveness [144] | |
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| ||
| Skin disorders | PAR-2 | Production of the TSLP and TNF-α [146]; modulation of the calcium ions in skin [147]; scratching behavior in mice [148, 149]; ear edema and infiltration of inflammatory cells [150] |
|
| ||
| Colitis | PAR-2 | Inflammatory process in the intestinal mucosa [25]; impaired epithelial barrier [151]; somatic and visceral hyperalgesia and allodynia [152]; relaxation in colonic smooth muscle [153]; cytoskeleton contraction with subsequent changes in tight junction permeability [154]; visceral hypersensitivity [155] |
| PAR-4 | Contraction of the longitudinal muscle of colon [156]; antinociceptive [158]; increase paracellular permeability and myeloperoxidase activity [159, 160]; colonic hyposensitivity [157, 161] | |
VEGF: vascular endothelial growth factor; CHAEC: cultured human airway epithelial cell; Cx: connexin; NEC: nasal epithelial cell; TGF: transforming growth factor; AHR: airway hyperresponsiveness; SMC: smooth muscle cell; BALF: bronchoalveolar lavage fluid; TNF: tumor necrosis factor; HAEC: human airway epithelial cells; GM-CSF: granulocyte-macrophage colony-stimulating factor; mDC: myeloid DC; TSLP: thymic stromal lymphopoietin; CCL20: chemokine C-C motif ligand 20; PGE2: prostaglandin E2.