Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma fibronectin (PFN) is a high molecular weight adhesive glycoprotein. Following trauma or sepsis PFN is acutely depleted, with rapid restoration of normal or supranormal levels after 24 to 48 hours. Cecal ligation with perforation provides an animal model of surgical trauma combined with polymicrobial sepsis. The present study examines whether this PFN level restoration 6 to 24 hours postoperatively is associated with de novo PFN synthesis and how this response is altered by pre-existing protein-calorie deprivation. Thirty-six adult male rats were divided into four groups: I--Controls, II--Prefasted Controls, III--Ligated, IV--Prefasted and Ligated. Control and experimental groups received intracardiac 35S-methionine 2 hours postoperatively. Plasma fibronectin (PFN) levels, PFN specific activity, plasma total protein, and total protein specific activity were determined at 0, 6, 24, and 48 hours postoperatively. Ligated rats (Groups III & IV) demonstrated significant PFN level increases 24 to 48 hours postoperatively (p less than 0.01-0.05). Despite a significant preoperative PFN level depression in prefasted rats (Groups II & IV), the 24-48 hours response to cecal ligation was not significantly altered. PFN specific activity was significantly increased among the operative groups 6 hours postoperatively, demonstrating de novo PFN synthesis following cecal ligation and perforation.
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PMID:Plasma fibronectin response to sepsis: mobilization or synthesis? 648 33

Fibronectin is an essential opsonin for phagocytosis of nonbacterial particulate matter by the reticuloendothelial system (RES). Fibronectin deficiency causes RES phagocytic depression and repletion of fibronectin reverses RES depression. Fibronectin depletion has been linked with multiple organ failure after surgery and trauma in patients with intra-abdominal infection. The mechanisms for fibronectin depletion have not been established. Plasma fibronectin levels were measured in 29 patients requiring operation after trauma and 15 patients undergoing elective abdominal operations. Opsonic fibronectin fell in the immediate postoperative period and on the first postoperative day in both groups. Total fluid replacement, blood loss, and operative time did not correlate with depression in fibronectin levels after trauma, although a weak correlation may exist between total fluid administration and fibronectin concentration in postoperative patients. Total fluid replacement, blood loss, and operative time may be contributing factors, but are not the major determinants of fibronectin deficiency after trauma or operation.
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PMID:Opsonic fibronectin after operation or trauma: effect of hemodilution and duration of operation. 648 46

The nonspecific host defense system of 66 patients with thermal injuries was studied prospectively. Our goal was to correlate the magnitude of injury with changes in host defenses and to determine if the responses of patients with and without sepsis were different. Eighteen patients experienced one or more septic episodes. Synchronous serial measurements of circulating fibronectin levels, neutrophil locomotive activity and phagocytosis, and intracellular killing in all patients showed that multiple components of the nonspecific host defense system were impaired after thermal injury. The depression of random migration and chemotaxis and the magnitude of the initial depression in serum fibronectin levels were related to the severity of injury but did not predict sepsis. Only a decrease in neutrophil bactericidal activity or a secondary depression in the serum fibronectin level was associated with the onset of sepsis.
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PMID:Sequential prospective analysis of the nonspecific host defense system after thermal injury. 668 77

Plasma fibronectin is a nonspecific opsonin which mediates phagocytosis of particulate matter by macrophages. Fibronectin depletion results in depression of reticuloendothelial system phagocytic function. This may potentiate microvascular embolization and sludging in critical illness. It has been hypothesized that sepsis is a major cause of fibronectin depletion. To explore this hypothesis, plasma fibronectin concentrations were measured in rats with intraabdominal abscesses and in rabbits subjected to the generalized Shwartzman reaction (spaced doses of endotoxin). In both groups of animals there was a significant increase (P less than 0.05) rather than decrease in fibronectin concentrations at times when sepsis and disseminated intravascular coagulation were manifest. This study does not support the hypothesized relationship between sepsis and fibronectin depletion. Until the kinetics of fibronectin production and utilization are further delineated, caution must be exercised in the interpretation of immunoreactive plasma fibronectin levels.
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PMID:Plasma fibronectin concentration in animal models of sepsis and endotoxemia. 682 8

Previous studies have demonstrated that intravenous administration of erythrocyte stroma is followed by a depression of RES phagocytic function. The present study evaluated the possibility that depression of hepatic blood flow, activation of the coagulation system, or depletion of opsonic factors mediates the RES depression induced by erythrocyte stroma. Stroma was prepared from washed rat erythrocytes and injected into rats at doses of 0.3, 0.5, 0.75, and 1.0 ml/100 gm. RES depression increased progressively after stroma doses greater than 0.3 ml/100 gm. Hepatic blood flow was decreased only after the 1.0 ml/100 gm dose. Fibrinogen levels were decreased with the 1.0 ml/100 gm dose but were unchanged with the 0.5 ml/100 gm dose of stroma, and the RES depression induced by the 0.5 ml/100 gm dose was not modified by the administration of heparin. Circulating fibronectin levels were not consistently depressed after stroma injection, and in vitro incubation of stroma with serum did not affect fibronectin levels. Erythrocyte stroma decreased hemolytic complement levels but depletion of complement with purified cobra venom factor did not depress RES phagocytic function. Preopsonization of the RES test particle did not modify the stroma-induced RES depression. These results indicate that decreased hepatic blood flow, activation of the coagulation system, or depletion of opsonins did not contribute to the RES depression induced by the 0.5 ml/100 gm dose of stroma. These results suggest that impairment of phagocytic cell function may mediate the effect of erythrocyte debris on RES phagocytic function.
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PMID:Effect of erythrocyte stroma on reticuloendothelial system phagocytic function. 686 72

Fibronectin is a cell surface glycoprotein and belongs to the opsonic system. It can be easily determined in human plasma by laser nephelometry. Patients in shock or with septicemia have extremely low concentrations of fibronectin in plasma which seems to correlate with a depression of the reticuloendothelial system (RES). Determination of fibronectin in human plasma may be a useful parameter for monitoring RES function. Severe intoxication with Paraquat causes a reduction of fibronectin and possibly influences RES function as well.
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PMID:Plasma fibronectin in man after a severe paraquat intoxication. 695 13

Comparison of three different lines of bovine aortal endothelial cells provides a clear demonstration of reversible morphologic phenotype coincidental with change in expression and growth mode. These phenotypic forms can be externally controlled so that cells may exist either in an epithelioid contact-inhibitable state or as a fibroblastoid non-contact-inhibitable state. Clonal cell line N (normal) shows a strong tendency to maintain the epithelioid phenotype. Clonal cell line Sp (sprout) can readily and reversibly adopt the epithelioid or fibroblastoid phenotype. A factor in normal serum is responsible for maintaining the cells in the epithelioid phenotype. This factor could be a growth factor since several polypeptide growth factors are shown to drive cells from the fibroblastoid phenotype to the epithelioid phenotype within 11 hours. This growth factor-induced change is not mediated through induced DNA synthesis. Clonal cell line V (variant) normally maintains the fibroblastoid phenotype but can be directed to the epithelioid phenotype provided cells are on an appropriate collagenous matrix. Associated with these changes in morphological phenotype are depression of the expression of the pro alpha 2 chain of collagen type I which may be characteristic of the contact-inhibited state and of an 80,000 mol wt polypeptide synthesized only by cells in the fibroblastoid phenotype. An endothelial cell collagen EC1 (mol wt 177,000) was synthesized by all cell lines regardless of phenotype whereas a suspected breakdown product EC3 (mol wt 100,000) was found only in the epithelioid phenotype. Other differences and similarities between cell lines include expression of a 135,000 mol wt glycoprotein GP (V and N), the procollagen of collagen type III (N) of fibronectin (N, V, Sp), and of the pro alpha 1 chain of collagen type I (Sp, V). The characteristic expression of each line and its response to signals controlling morphologic phenotype impinges on the question of whether there exist several distinct types of vascular endothelial cells with different functional potentials controlled by extracellular signals.
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PMID:Signals causing change in morphological phenotype, growth mode, and gene expression of vascular endothelial cells. 710 19

Fibronectin (Fn), a normal serum protein which appears to have important roles in wound healing and in reticuloendothelial system function, is depressed by most types of trauma. Fn is released into the tissue at the site of an injury which suggests the depression is the result of Fn sequestration at the wound site. A competitive inhibition assay for Fn was used to measure the concentration of Fn in fluid draining the site of a radical mastectomy and the level in concurrently obtained plasma. Plasma levels of Fn were significantly depressed following surgery but were returning toward normal by 24 hours postsurgery. The concentration of Fn in drainage fluid collected two hours postop was slightly but significantly lower than the plasma collected simultaneously. By 8 hours after surgery, drainage fluid levels were significantly higher than that in concurrently obtained plasma, and the difference was even more pronounced at 24 hours postop. Fn in the drainage fluid retained opsonic activity but at a lower level than the opsonic activity in plasma. The higher concentration of Fn in drainage fluid than in plasma appears to be due to binding of the Fn to tissue debris in the exudate, which prevents the reentry of Fn into the vascular compartment.
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PMID:Sequestration of fibronectin at the site of an injury. 713 38

Previous research has shown that disseminated intravascular coagulation causes a depression in RE function. Fibronectin, a high-molecular-weight surface-binding glycoprotein, is known to modulate RE function by facilitating opsonic activity and is sensitive to proteolytic cleavage by plasmin, yielding FNDP. The present investigation suggests that isolated FNDP, generated in vitro by incubation with plasmin, can depress phagocytosis in vivo as well as in vitro. Phagocytosis in rats was determined by a clearance technique employing CR51-RBCs and in vitro by employing a monolayer of peritoneal exudate macrophages. The in vivo studies demonstrated significantly reduced hepatic phagocytosis after the injection of FNDP an delayed clearance of injected test particles. Macrophage uptake in vitro, supported by either normal rat serum or purified fibronectin, was significantly reduced when incubated with FNDP. These results suggest that depression of the RE system and phagocytosis during intravascular coagulation may be mediated in part by the formation of plasmin degradation products of plasma fibronectin.
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PMID:Depression of phagocytosis by plasmin degradation products of plasma fibronectin. 725 34

Plasma fibronectin has a high affinity for denatured collagen (gelatin) and exerts an opsonic influence on phagocytosis of test colloids and clearance of tissue debris by macrophages. This study evaluated the effect of in vitro and in vivo interaction of gelatin with plasma on measurable bioassayable opsonic activity and immunoreactive fibronectin. Incubation of human, dog, sheep, and rat plasma with gelatin prior to in vitro assay decreased (P less than 0.05) the ability of plasma to augment particle uptake in the liver slice bioassay. Incubation of plasma with gelatin also decreased the concentration of fibronectin that could be detected by electroimmunoassay. Intravenous infusion of gelatin into rats, dogs, and sheep resulted in an acute depression in both bioassayable and immunoreactive opsonic observations suggest that deficits of opsonic fibronectin as documented in injured patients by bioassay and electroimmunoassay may not be exclusively related to actual depletion of fibronectin from blood but may be, in part, due to binding of fibronectin to blood-borne material post-trauma, i.e., collagenous tissue debris, whose presence in plasma may limit its detection by both assays.
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PMID:Influence of gelatin on bioassayable and immunoreactive opsonic fibronectin. 732 64


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