Human | JAM3 | 83700 | junctional adhesion molecule 3 | Junctional adhesion molecule-C participates in the later steps of the leukoendothelial adhesion and transmigration cascade in an acute pulmonary inflammation model using transgenic mouse tissue overexpressing JAM-C |
Human | TREM1 | 54210 | triggering receptor expressed on myeloid cells 1 | Results show that sTREM-1 and procalcitonin are not specific for infection and can increase markedly in acute inflammation without infection A new regulatory role is described for TREM-1-mediated signals in the resolution of acute inflammation and the control of neutrophil activity |
Human | SFTPD | 6441 | surfactant protein D | In vitro interactions during the early phase of host defense against influenza A virus suggest a complex interplay between SP-D and human neutrophil defensins at sites of active inflammation |
Human | SELE | 6401 | selectin E | Hepatocyte growth factor ameliorates acute renal inflammation in part by downregulating E-selectin mediated macrophage adhesion to the inflamed endothelium |
Human | CX3CL1 | 6376 | chemokine (C-X3-C motif) ligand 1 | CX3CR1/fractalkine interactions accounted for 26% of THP-1 cell and 17% of peripheral blood NK cell adhesion to renal tubular epithelial cells, suggesting a functional role in leucocyte adhesion/retention in acute renal inflammation |
Human | PTGS2 | 5743 | prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase) | upregulation of cytosolic phospholipase A2 and cox-2 in peripheral polymorphonuclear leukocytes during childhood bacterial infection increases thromboxane synthesis, which may contribute to acute inflammatory reaction |
Human | PLAUR | 5329 | plasminogen activator, urokinase receptor | essential role in acute inflammation as well as in chronic degenerative vascular processes such as atherosclerosis |
Human | ORM2 | 5005 | orosomucoid 2 | the sera of patients with acute inflammation demonstrated increased numbers of bi-antennary and alpha1,3-fucosylated N-glycan structures at each glycosylation site |
Human | NPPC | 4880 | natriuretic peptide C | CNP is a modulator of acute inflammation in the blood vessel wall characterized by leukocyte and platelet activation, mediated, at least in part, via suppression of P-selectin expression |
Human | NOS2 | 4843 | nitric oxide synthase 2, inducible | Healthy human dental pulp tissue failed to exhibit any iNOS; however, acute inflammation enhanced the mRNA and protein levels of iNOS, mainly in the leukocytes |
Human | MPO | 4353 | myeloperoxidase | MPO was observed to modulate the vascular signaling and vasodilatory functions of nitric oxide (NO) during acute inflammation |
Human | MAZ | 4150 | MYC-associated zinc finger protein (purine-binding transcription factor) | SAF-1 controls cell cycle progression via p21 induction, and pathophysiological conditions that favor overexpression of SAF-1, such as an acute inflammatory condition, can trigger cellular growth arrest |
Human | IL15 | 3600 | interleukin 15 | Decreased IL-15 may contribute to elevated IgE and acute inflammation in atopic dermatitis |
Human | IL10 | 3586 | interleukin 10 | In mice, expression of the human anti-inflammatory protein IL-10 in a recombinant adenoviral vector drug-delivery system was used prophylactically in acute experimental inflammatory syndromes to suppress the underlying inflammatory process |
Human | IL8 | 3576 | interleukin 8 | Neutrophilic infiltration around reactive bile ductules may be related to the IL-8 expressed in bile ductular epithelia circulating neutrophils are susceptible to augmentation by IL-8 through the reinforcement of IL-8 receptors in acute inflammatory conditions |
Human | IL6 | 3569 | interleukin 6 (interferon, beta 2) | IGF-1, IGFBP-2 levels were related to IL levels, disease activity and anatomical distribution, consistent with active inflammation modifying the IGF-IGFBP system, possibly relevant to disturbance of growth IL6 -6331T is associated with increased IL-6 concentrations in an acute inflammatory state via a mechanism involving binding of the Oct-1 transcription factor |
Human | F3 | 2152 | coagulation factor III (thromboplastin, tissue factor) | The results suggest that estrogens may modulate T F expression and cytokine production by monocytes and may thus be involved, at least in part, in the pathophysiology of acute inflammatory processes associated with high estrogen levels |
Human | ELANE | 1991 | elastase, neutrophil expressed | Release of human leukocyte elastase from neutrophils specifically down-regulates the responsiveness of neutrophils to C5a, and this effect may play a role in the down-regulation of acute inflammation |
Human | DEFB4A | 1673 | defensin, beta 4A | in the intrahepatic biliary tree, hBD-2 is expressed in response to local infection and/or active inflammation, whereas hBD-1 may constitute a preexisting component of the biliary antimicrobial defense system |
Human | CTSK | 1513 | cathepsin K | incomplete inactivation may partially explain why active cysteine cathepsins are still found during acute lung inflammation |
Human | CTSG | 1511 | cathepsin G | Release of cathepsin G from neutrophils specifically down-regulates the responsiveness of neutrophils to C5a, and this effect may play a role in the down-regulation of acute inflammation |
Human | CASP8 | 841 | caspase 8, apoptosis-related cysteine peptidase | Lower gene expression of caspase-8 correlates with detectable blood-brain barrier leakage and active inflammation in the brain as reflected by gadolinium-enhancing lesions on MRI |
Human | CALCA | 796 | calcitonin-related polypeptide alpha | Results show that procalcitonin and sTREM-1 are not specific for infection and can increase markedly in acute inflammation without infection |
Human | FAS | 355 | Fas cell surface death receptor | Lower gene expression of CD95 correlates with detectable blood-brain barrier leakage and active inflammation in the brain as reflected by gadolinium-enhancing lesions on MRI |
Human | ADAR | 103 | adenosine deaminase, RNA-specific | ADAR1 variants are differentially regulated during acute inflammation: the localization of these variants and of A-to-I RNA editing in the cytoplasm, nucleus, and nucleolus is intracellularly reorganized in response to inflammatory stimulation |