Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We adopted whole blood flow cytometry and direct labeling of the CD11b/CD18 and CD62L antigens to study the relationship between their expression and leukocytosis in patients with infection/inflammation, acute stress and healthy volunteers. Mean +/- S.D. channel fluorescence intensity of CD11b/CD18 antigen on peripheral blood polymorphonuclears did not differ between patients with infection/ inflammation (173+/-78) and controls (167+/-72), but was significantly (p = 0.04) reduced in stress (135+/-60). No correlation was found between CD11b/CD18 antigen level and either polymorphonuclears absolute number or serum C-reactive protein. A significant negative correlation was noted between CD62L antigen expression on polymorphonuclears and their absolute number. We assume that cells with increased CD11b/CD18 surface concentrations are retained in the capillaries and that part of the leukocytes in the peripheral blood are stressed leukocytes with reduced CD11b/CD18. Thus, leukocytes detected in peripheral blood are not necessarily the most "inflamed" ones.
 ...
PMID:Neutrophilia of infection/inflammation: are we really dealing with "inflamed" leukocytes? 986 59

We adopted whole blood flow cytometry and direct labeling of the CD11b/CD18 and the CD62L antigens to study the relationship between their expression on the surface of peripheral leukocytes and the state of leukocyte adhesiveness/aggregation (LAA) as revealed by the leukergy test. We examined patients with infection/inflammation, acute stress and controls. The mean +/- S.D. channel fluorescence intensity of CD11b/CD18 antigen did not differ between patients with infection/inflammation (173 +/- 78) and controls (167 +/- 72). However, a significant (p < 0.0001) difference between these groups was noted regarding LAA state. There was a significant (p = 0.04) reduction in CD11b/CD18 in stress (135 +/- 60) and a significant (p < 0.001) increment in LAA. In both study groups, there was a significant reduction in CD62L. Patients were divided into those with CD11b/CD18 above and below the control's average. No correlation was found between the antigens and LAA. We assume that LAA in patients with stress state is CD11b/CD18 and CD62L independent.
 ...
PMID:Dissociation between the state of leukocyte adhesiveness/aggregation in the peripheral blood and the availability of the CD11B/CD18 and CD62L antigens on the surface of the cells in patients with stress. 1050 70

Using a nonhuman primate model, we examined the mechanisms by which acute social stress inhibits the ability of NK cells to form conjugates with, and lyse target cells. We examined the expression and role of the primary NK cell adhesion molecules, CD2 and LFA-1, in mediating conjugation to target cells. Acute stress induced a decrease in NK cell expression of CD2 (17+/-3%); and to a lesser degree induced a decrease in expression of LFA-1 (CD11a: 8+/-3%; CD18: 7+/-3%). Antibody blocking studies indicated that anti-LFA-1 significantly inhibited NK cell conjugate formation and cytotoxicity in both control (approximately 40% and approximately 50%, respectively) and stressed (approximately 20% and approximately 45%, respectively) conditions. However, anti-CD2 blocked conjugation and cytotoxicity in the control condition by approximately 50%, but had no capacity to further affect the inhibition of conjugation or cytotoxicity of NK cells induced by acute stress. These data indicate that there are differential effects of acute stress on the expression and function of LFA-1 and CD2, and that the stress-induced inhibition of NK cell adhesion and cytotoxicity is dependent upon modulation of adhesion and/or signalling through CD2.
 ...
PMID:Acute stress impairs NK cell adhesion and cytotoxicity through CD2, but not LFA-1. 1050 80

Hemodialysis patients exhibit a defective immune response leading to an increased susceptibility of infections and neoplasms. Far from being helpful, dialytic therapy per se also may be responsible for this acquired immunodeficiency. Dialysis membranes and bacterial products present in dialysis water may trigger and even perpetuate an abnormal mononuclear cell activation. Upon contact with cellulosic dialysis membranes, monocytes display an increased expression of surface markers of cell activation, such as adhesion molecules CD18, CD49, CD54 and the lipopolysaccharide (LPS) ligand (CD14). Moreover, proinflammatory cytokines as IL-1beta and TNF-alpha are released both in vivo and in vitro when monocytes are exposed to cellulosic membranes. Of special interest is the fact that end-stage renal disease patients undergoing hemodialysis exhibit an increased mononuclear cell apoptosis. This apoptosis is directly related to the degree of biocompatibility of the dialysis membrane. Apoptosis is activated when monocytes enter in contact with the cellulosic dialysis membrane through cell surface receptors linked to G-proteins. In early steps of apoptosis signaling, pertussis toxin-sensitive G proteins are coupled to protein kinase C (PKC)-dependent phosphorylative mechanisms. Furthermore, recent evidence support that the execution phase of apoptosis is mediated by a caspase-3 dependent pathway. Finally, very recent available data support that monocytes subjected to repeated activation suffer a process of accelerated senescence, as demonstrated by the senescent phenotype (CD14 and CD32) expressed and their shortened telomeric length. This senescent profile may generage a defective cellular response in acute stress situations, explaining (at least in part) the altered immune response observed in hemodialysis patients.
 ...
PMID:Cell apoptosis and hemodialysis-induced inflammation. 1198 20