Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Adhesion of neutrophils (PMNs) to vascular endothelial cells (EC) is a critical step in recruitment and infiltration of leukocytes into tissues during inflammation. Substance P (SP), a neuropeptide released from sensory nerves, evoked PMN adhesion to EC. The NK receptor subtype(s) and the cell type(s) involved were investigated. 2. SP was coincubated with human PMNs and EC from the human umbilical vein (HUVEC); adhesion was quantitated by computerised microimaging fluorescence analysis. 3. The proadhesive effects of SP (range 10(-18)-10(-6) M) were illustrated in a biphasic dose-response curve, with a maximum at 10(-15) M (276+/-16% adhesion vs control; P<0.01) and another one at 10(-10) M (200+/-18% adhesion vs control; P<0.01). Neurokinin A was less active and neurokinin B was inactive. The adhesion molecules LFA-1 and OKM-1, but not selectins, were involved according to results with selective mAbs. 4. The NK(1) agonist [Sar(9),Met(O(2))(11)]SP reproduced the effects of SP, whereas the NK(2) agonist [betaAla(8)]-neurokininA (4-10) acted at 10(-13)-10(-8) M only. The NK(3) agonist, senktide, was ineffective. 5. The NK(1) antagonists, CP 96,345 and L 703,606 (both 10(-6) M), abolished the effect of 10(-15) M SP and inhibited that of 10(-10) M SP by 56+/-5% (P<0.01). By comparison, the NK(2) antagonist, SR 48,968 (10(-7) M), partially antagonised the adhesion evoked by 10(-10) M SP (% inhibition: 61+/-6; P<0.05). 6. Since preincubation of PMNs and HUVEC with SP gave the same results it is clear that both cell types contributed to its proadhesive effects. 7. These results indicate that SP induced a proadhesive effect during inflammatory processes, which was mediated by NK(1) and NK(2) receptors.
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PMID:Substance P increases neutrophil adhesion to human umbilical vein endothelial cells. 1287 28

Accumulating evidence has so far indicated that cross-talk between the nervous and immune systems plays a pivotal role in the pathophysiology of various diseases. As a prototypic demonstration of neuro-immune systems, the interaction between nerves and mast cells has been examined intensively. Anatomically, mast cells are often located in close proximity to nerves. Functionally, both cells communicate with each other in a bi-directional manner. Substance P released from nerves and proteases and cytokines from mast cells have proved to be important mediators in such communication. On the other hand, the molecules involved in membrane-membrane contacts between nerves and mast cells were largely unknown. In 2003, both cells were found to express the identical adhesion molecule, named SynCAM (synaptic cell adhesion molecule) or SgIGSF (spermatogenic immunoglobulin superfamily). Since SgIGSF/SynCAM binds homophilically, its involvement in nerve-mast cell interaction was examined in vitro. Superior cervical ganglia expressed SgIGSF/SynCAM along their neurites. Adhesion to these neurites of mast cells lacking SgIGSF/SynCAM was poor, and this was normalized by ectopic expression of SgIGSF/SynCAM. Moreover, SgIGSF/SynCAM-expressing mast cells were more competent in communicating with the neurites. Further understanding of the adhesion molecule-dependent interaction will be expected to open a new avenue in the field of neuro-immune cross-talk.
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PMID:Direct interaction between nerves and mast cells mediated by the SgIGSF/SynCAM adhesion molecule. 1693 56

Oxidative stress has been implicated in intra-abdominal adhesion formation. Substance P, a neurokinin-1 receptor (NK-1R) ligand, facilitates leukocyte recruitment and reactive oxygen species (ROS) generation. We have shown in a rat model of adhesion formation that intraperitoneal administration of a NK-1R antagonist at the time of abdominal operation reduces postoperative adhesion formation. Thus we determined the effects of NK-1R antagonist administration on peritoneal leukocyte recruitment and oxidative stress within 24 h of surgery. Adhesions were induced in Wistar rats randomly assigned to receive the antagonist or vehicle intraperitoneally. Peritoneal tissue was isolated at 2, 4, 6, and 24 h after surgery for analysis of the oxidative stress biomarkers 8-isoprostane (8-IP), protein carbonyl, NADPH oxidase, myeloperoxidase (MPO), and ICAM-1 and VCAM-1 mRNAs. Total antioxidant capacity of peritoneal fluid was also determined. MPO, NADPH oxidase, 8-IP, and protein carbonyl were elevated (P < 0.05) by 6 h. ICAM-1 mRNA was elevated (P < 0.05) by 2 h, whereas VCAM-1 levels decreased (P < 0.05) at 24 h. The NK-1R antagonist delayed the MPO rise and reduced (P < 0.05) 8-IP levels by 6 h and ICAM-1 mRNA, VCAM-1 mRNA, and protein carbonyl at 2 h. The antagonist also increased (P < 0.05) the antioxidant capacity of peritoneal fluid at all time points. These data further support a role for oxidative stress in adhesion formation and suggest that the NK-1R antagonist may limit adhesions, in part, by reducing postoperative oxidative stress through an inhibition of neutrophil recruitment and an increase in peritoneal fluid antioxidant capacity.
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PMID:A neurokinin-1 receptor antagonist that reduces intra-abdominal adhesion formation decreases oxidative stress in the peritoneum. 1762 72