Plasma Fn Levels Research Articles

Effects of vacuum sealing drainage on wound healing and plasma fibronectin

Objective To observe the changes in the levels of plasma fibronectin (Fn) before and after vacuum sealing drainage (VSD) in the treatment of wounds,and study the action mechanism of VSD.Methods The plasma samples were collected from 20 patients with soft tissue defect for determination of plasma Fn levels before and after the treatment with VSD.The growth of granulation tissue,the wound area and the wound healing were observed,and their correlation with plasma Fn level was analyzed.Results Before and after the treatment with VSD,the plasma Fn levels were (244.52 ± 27.02) and (277.69 ±28.34) mg/L (P ＜0.05),and wound granulation tissue score was (2.35 ± 0.89) and (4.73 ± 1.24)(P ＜ 0.05),respectively.The wound granulation tissue score was positively correlated with the plasma Fn level (r =0.883,P ＜ 0.05).The wound area after treatment [(165.58 ± 37.35) cm2] was significantly reduced as compared with that before treatment [(206.30 ± 43.40) em2,P ＜ 0.05],and negatively correlated with the plasma Fn level (r =-0.661,P ＜ 0.05).Conclusion VSD can increase the plasma Fn level,speed up wound granulation tissue growth,and promote wound healing. Key words: Vacuum sealing drainage; Fibronectin; Wound healing

Radiation-induced toxicity in cancer patients with low plasma fibronectin levels

AbstractThe present study was carried out to evaluate the levels of plasma fibronectin (Fn) in cancer patients undergoing radiation therapy (RT) in correlation with outcomes in terms of radiation toxicity. A total of 26 patients with lung and gastrointestinal (GI) cancer, treated with RT were enrolled in this study. Plasma Fn levels were determined before and following a course of RT. The Radiation Therapy Oncology Group (RTOG) criteria were used to determine the grade of RT toxicity. Statistical analysis utilised the nonparametric Mann–WhitneyU-test as well as bivariate linear regression. Pre-RT Fn levels were significantly higher in cancer patients without toxicity (median ± SE) (485.0 ± 87 μg/ml) as compared with the levels of plasma Fn in patients with grade I–II RTOG acute toxicity (354.0 ± 74 μg/ml,p= 0.01). No significant difference in Fn levels was found in patients with grade I toxicity compared with patients with grade II toxicity. In addition, low baseline Fn levels (148 and 299 μg/ml) were observed in two lung cancer patients who developed symptomatic pneumonitis during the first 2 months after RT. These preliminary results suggest that low baseline Fn may have potential as a predictive marker for development of RT-induced toxicity.

Plasma fibronectin as a marker of sepsis

Objectives: To evaluate the value of plasma fibronectin (pFN) as a diagnostic marker of sepsis. Subjects and methods: Plasma FN was determined in patients showing sepsis-related symptoms who had blood cultures performed. These patients were assigned to one of two groups according to their clinical situation: (1) Clinical Septic Group: patients with sepsis according to American College of Chest Physicians/Society of Critical Care Medicine (ACCP/SCCM) criteria; (2) Fever Peak Group: patients who did not fulfil sufficient ACCP/SCCM criteria for sepsis. Two additional control groups were also established: (3) Non-infectious Diseases Control Group and (4) Healthy Control Group. Results: Plasma FN levels, microbiological and clinical data were compared among the different patient groups. For each group, the number of patients, median and mean pFN levels and the 95% confidence interval of the mean were: (1) n=43, 102 mg/l, 122 mg/l (100–144); (2) n=70, 185 mg/l, 207 mg/l (184–231); (3) n=22, 175 mg/l, 181 mg/l (151–211); and (4) n=22, 256 mg/l, 261 mg/l (229–292). Bonferroni’s test of multiple comparisons was able to detect a significant difference between pFN concentrations corresponding to the septic group, compared to the remaining groups ( p ANOVA<0.001). Conclusion: Plasma FN appears to act as a marker of sepsis in that patients showed diminished pFN levels. Along with other clinical and laboratory variables, the use of this marker would allow a rapid diagnosis of sepsis and limit the number of blood cultures to be processed and the number of antibiotic prescriptions, particularly when symptoms are insidious and diagnosis is doubtful. We propose further and more complex studies using a higher number of patients.

Plasma fibronectin levels during acute rejection and acute tubular necrosis in renal transplant patients.

Fibronectin (Fn), an acute phase glycoprotein synthesized by the liver, has an important immunomodulatory role. We have investigated the changes in plasma Fn in patients after renal transplantation in order to determine whether these changes predict graft injury or rejection episodes. Besides normal healthy controls, healthy pregnant controls, and a trauma control group, we used two groups of chronic renal failure patients as controls: group I, patients with end-stage renal failure (ESRF) on peritoneal dialysis; group II, patients with ESRF on hemodialysis. These were compared with two groups of renal transplant patients: group III, patients 3 months after successful renal transplantation; group IV, patients studied sequentially 10 days immediately posttransplantation. The renal transplant patients were treated with low-dose cyclosporine, azathioprine, and steroids. Citrated plasma samples were collected for Fn assay by a sandwich-type ELISA and for SDS-PAGE analysis and Western blotting. The mean plasma Fn levels were as follows: healthy controls 311.6 SEM, 13.5 micrograms/ml; healthy pregnant controls 357 SEM, 5.9 micrograms/ml; trauma controls 262.3 SEM 31.7, micrograms/ml; group I 169 SEM, 25.1 micrograms/ml; group II 199 SEM, 27.2 micrograms/ml; group III 272 SEM, 21.7 micrograms/ml; group IV 212 SEM, 27.4 micrograms/ml (day 3 postop). There was a significant difference in the plasma Fn levels on day 3 posttransplant between the patients with delayed and immediate renal function (P less than 0.03) (group IV). A significant decrease in plasma Fn levels occurred immediately after steroid therapy was stopped (P less than 0.03) in patients treated for acute rejection. Plasma Fn levels were significantly decreased in the presence of delayed graft function but did not predict rejection.

Rabbit Plasma Fibronectin Levels Associated withStaphylococcusaureusEnterotoxin B: An Acute-Phase Reaction

Variation in fibronectin (Fn) levels and white blood cell counts (WBC) following staphylococcal enterotoxin B (SEB) or SEB + cryoprecipitate containing Fn challenge was studied in New Zealand white rabbits. Increased plasma Fn levels were observed 2 h after the intravenous injection of SEB and peaked at 48-72 h (from a mean level 194.6 +/- 4.5 micrograms/ml prechallenge Fn level to a 72-hour postchallenge mean level of 407.9 +/- 25.4 micrograms/ml). Fn levels then decreased over the succeeding 5 days to approximately prechallenge levels. The total WBC count decreased by 88% within 2 h after the SEB injection. A slow increase in circulatory WBC was observed over the next 24 h. SEB caused an increase in plasma Fn levels and decreased WBC counts with lymphopenia that was followed by a normal lymphocyte count within 5 days. These data suggest that an acute-phase reaction was induced by interleukin-1. Fn prophylaxis provided no change in clinical signs when given at the time of SEB injection.

Lymphocyte activating factor (LAF) and the acute-phase response in adjuvant arthritic rats

The purpose of the study was to determine the temporal relationship between lymphocyte activating factor (LAF) activity and the acute-phase response, as measured by plasma fibronectin (Fn), C-reactive protein (CRP), and albumin levels in adjuvant arthritic rats. LAF activity as measured in the thymocyte costimulator assay, and plasma Fn, CRP, and albumin levels were measured during the acute (Day 3), intermediate (Day 10), and systemic (Day 17) phases of arthritic disease. On Day 3, supernatants from whole spleen cells of adjuvant-injected rats did not exhibit abnormal LAF activity. By Day 10, LAF activity in splenic supernatants from arthritics was significantly ( P ⩽ 0.05) higher than normal, although the increase was no greater than 60%. On Day 17 the LAF activity from arthritic rats had increased an average 300% compared to normals. In contrast to the time course of IL-1 activity, Fn and CRP levels in the arthritic rat were significantly higher than normal at all three time points, although there was a transient fall in Fn and CRP concentrations on Day 10. Plasma albumin levels in arthritic rats were subnormal ( P ⩽ 0.01) on Days 3, 10, and 17, although the concentration of plasma albumin on Day 10 was significantly higher than that measured on Day 3. The acute, intermediate, and systemic phases of adjuvant arthritic paw inflammation paralleled the abnormal profile of Fn, CRP, and albumin concentrations over time. However, LAF activity from arthritic rat spleen cells increased gradually and more closely coincided with the systemic appearance of the disease. Since the appearance of abnormal plasma protein levels in arthritic rats preceded the appearance of increased splenic LAF activity, it appears that there is no causal relationship between enhanced splenic LAF activity and early alteration of plasma Fn, CRP, and albumin levels.

Elevation of plasma fibronectin and serum amyloid P in autoimmune NZB, [formula omitted], and [formula omitted] mice

The acute-phase proteins, fibronectin (Fn) and serum amyloid P (SAP), are opsonins which by virtue of their adhesive properties may be involved in the glomerular nephritis associated with splenic lupus erythematosus (SLE). Because of their possible involvement in the pathophysiology of lupus, plasma Fn and SAP levels from three strains of autoimmune mice were measured over time to determine if Fn and SAP rose as the mice sickened and renal function degenerated. Baseline levels of Fn and SAP were measured when the mice were between 1.5 and 3 months of age. The characteristic rapid onset of autoimmune disease in MRL 1pr mice was accompanied by a two- to threefold increase in plasma Fn and SAP by Day 100. The B W mice, which develop autoimmune diseas more slowly, did not have a significant increase in plasma Fn and SAP until Day 240. The NZB mice, with the most delayed onset of disease, exhibited a modest but significant elevation of plasma Fn and SAP by Day 360. Histologic examination of the kidneys of B W and NZB mice indicated that pathological abnormality of the glomeruli and tubules coincided with the elevation of plasma Fn and SAP levels. In contrast, blood samples taken over time from normal BALB c mice did not possess abnormal levels of Fn or SAP. It appears that elevation of plasma Fn and SAP in the MRL 1pr , B W , and NZB mice is related to the onset and severity of autoimmune disease and the subsequent loss of renal function.

Tissue Debris at the Injury Site Is Coated by Plasma Fibronectin and Subsequently Removed by Tissue Macrophages

Fibronectin (Fn) is a normal plasma and extracellular matrix glycoprotein that is thought to be important in reticuloendothelial system function as well as in promoting adhesion of various cell types to basement membranes and to each other. Plasma Fn levels are depressed following almost any type of trauma. It opsonizes circulating tissue debris for removal by the fixed cells of the reticuloendothelial system. It has been assumed but not proven that Fn also opsonizes tissue debris at the site of the injury for subsequent phagocytosis by tissue macrophages. In this study, rats were given intracardiac injections of Fn coupled with fluorescence isothiocyanate (Fn-FITC) and human serum albumin-rhodamine isothiocyanate (HSA-RITC). Abdominal Rebuck skin windows were then prepared. Within 24 hours, debris at the sites of injury were observed to be coated with Fn-FITC but not HSA-RITC. This Fn-labeled debris was subsequently ingested by macrophages at the site. No macrophages were found that had taken up HSA-RITC. Thus, Fn is seen to coat tissue debris and effete cells within the wound, and the coated material is subsequently removed by tissue macrophages.

Alteration of interleukin-1 production and the acute phase response following medication of adjuvant arthritic rats with cyclosporin-A or methotrexate

The purpose of the paper was to determine whether two clinically active antirheumatic compounds, cyclosporin-A (CS-A) and methotrexate (MTX) were efficacious in the treatment of adjuvant arthritis (AA) in rats, as measured by reduction of paw inflammation, lymphocyte activating factor (LAF) activity and the acute phase response. Parameters of the acute phase response consisted of plasma fibronectin (Fn), C-reactive protein (CRP), albumin and iron. Rats injected with Freund's complete adjuvant on day 1, developed systemic arthritis, which was quantitated by measuring non-injected paw swelling on day 17. When compared to normal animals, AA rats had significantly ( P⩽0.01) increased: (1) splenic LAF activity (100% increase), (2) plasma Fn (58%), and (3) CRP (122%), as well as abnormally reduced levels of: (1) plasma albumin (53% reduction), and (2) iron (54%). Orally dosing AA rats from days 3 to 17 with the immunoregulatory drugs, CS-A (3 and 5 mg/kg) or MTX (0.5 and 1 mg/kg), significantly ( P⩽0.01) reduced paw inflammation (100% reduction), increased final body wt 40 – 50 g over arthritic controls and decreased LAF activity from splenic leukocytes. The acute phase response, often associated with a high degree of LAF activity, was significantly ( P⩽0.01) decreased by dosing with CS-A (3 and 5 mg/kg) and MTX (0.5 and 1 mg/kg). The inhibition of the acute phase response was measured by reduction of high plasma Fn levels (42 – 79% decrease) and CRP levels (57 – 100% decrease) as well as elevation of subnormal levels of plasma albumin (57 – 101% increase) and iron (40 – 114% increase). Dosing with the nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin (50 and 100 mg/kg) or phenylbutazone (10 and 30 mg/kg), significantly inhibited paw inflammation (29 – 85%), but did not decrease the high rate of splenic LAF activity, nor did aspirin (55, 100 and 200 mg/kg) or phenylbutazone (1, 10 and 30 mg/kg) alter the acute phase response in AA rats, as measured by levels of plasma Fn, CRP, albumin and iron. Since CS-A and MTX have been reported to be effective in the treatment of RA, their activity in the LAF, Fn, CRP, albumin and iron assays of the AA rat suggests that these immunological and serological parameters may be useful in identifying potential antirheumatic drugs and distinguishing them from standard NSAIDs.

Plasma levels of fibronectin in polymyalgia rheumatica giant cell arteritis.

In order to verify whether measurement of plasma fibronectin (Fn) could represent a useful tool in acute-phase-response assessment, Fn was measured in 16 previously untreated patients (group A) affected by polymyalgia rheumatica giant cell arteritis (PMR-GCA), both before, during, and after 45 days of steroid therapy, and its course was compared with the behavior of some acute-phase reactants such as erythrocyte sedimentation rate (ESR), fibrinogen (Fng), and prealbumin (Preal). No difference was detected between the baseline Fn levels found in patients and those registered in a control group composed of 15 sex- and age-matched healthy subjects; no correlation was found with the other acute-phase parameters considered, and no significant variation of plasma Fn levels was registered as a result of the steroid therapy administered. On the contrary, all the other parameters revealed a good degree of correlation and tended progressively and homogeneously towards normalization as a result of the therapy administered. Plasma Fn was also measured in another group of 16 PMR-GCA patients (group B), all of whom had pathological retinal fluoroangiographic findings, and its levels were compared with those of the von Willebrand factor antigen (vWfAg), a biochemical index of vascular damage. While the levels of Fn continued to be the same as those detected in the control group, the values of vWfAg registered in group B proved to be significantly different from those found in another homogeneous control group of 25 healthy subjects. Finally, no correlation could be detected between Fn and vWfAg, and neither of them showed any significant correlation with the ESR.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of glucocorticoids on plasma fibronectin levels in normal and arthritic rats.

In vivo studies with normal and adjuvant-induced arthritic rats were undertaken in order to measure the effects of glucocorticoids on paw inflammation and plasma fibronectin (Fn) levels. Dexamethasone, methylprednisolone, and corticosterone all enhanced plasma Fn levels in normal animals. All drugs also significantly decreased inflammation in arthritic rats as measured by paw swelling. Of the three glucocorticoids, only corticosterone did not significantly enhance Fn levels in arthritic rats, possibly due to its lesser potency and narrow therapeutic window.

Changes in plasma fibronectin levels in thyroid diseases.

The plasma levels of fibronectin (Fn) have been measured in normal subjects and in patients with thyroid diseases. The mean plasma Fn levels in 62 normal adults was 32.0 +/- 6.0 mg/dl, whereas it was elevated to 62.6 +/- 16.1 mg/dl (mean +/- SD) in 25 patients with hyperthyroidism and decreased to 19.2 +/- 8.0 mg/dl in 9 patients with hypothyroidism. The 9 patients with simple goiter have normal values of 29.1 +/- 8.0 mg/dl. With the administration of anti-thyroid drugs, plasma Fn levels normalized, with a time lag, in parallel with normalization of the thyroid function. Positive correlation was obtained between Fn levels and serum levels of triiodothyronine (T3) and thyroxine (T4). The present findings indicate that measurement of plasma Fn both in the basal state and during treatment provides evidence of altered Fn metabolism in thyroid diseases and serves to follow up the effect of treatment.

Fibronectin in acute and chronic inflammation.

Recent evidence suggests that fibronectin (Fn), a high molecular weight glycoprotein, may be used as an indicator protein in rats with adjuvant-induced arthritis. Rocket immunoelectrophoresis, using purified goat anti-rat Fn, provided a specific and sensitive means of measuring plasma Fn in rats during the development of various inflammatory disease states. It was shown that normal rat plasma Fn levels of approximately 400 micrograms/ml double within 24 hours after injection of adjuvant. Plasma Fn levels in this model of chronic systemic inflammatory joint disease were tracked for more than 4 months and remained significantly higher than normal. On the other hand, a carrageenan-induced inflammatory response in the pleural cavity of rats resulted in a large local accumulation of leukocytes, but no change in plasma Fn levels. A carrageenan-induced model of acute inflammation resulted in increased paw swelling within 6 hours and enhanced plasma Fn levels within 24 hours; plasma Fn levels returned to normal within 1 week. Quantitation of plasma Fn levels in the rat may provide a useful biochemical parameter for the study of chronic systemic inflammatory diseases.

The relationship between plasma fibronectin levels and autoimmune disease activity in MRL/l mice.

Plasma fibronectin levels increased significantly over time in MRL/l mice with progressive autoimmune disease. At 100 and 120 days of age both male and female MRL/l mice exhibited significantly higher fibronectin (Fn) levels than the more resistant MRL/l controls. Male mice at early time points had Fn levels no greater than controls due perhaps to the later onset of disease in MRL/l males. In contrast, female MRL/l mice, when compared with MRL/n controls, had higher Fn levels from 40 days of age. The proteinuria in these animals was also above MRL/n controls from the first time point taken (Day 40). In a temporal study with female MRL/l mice, Fn levels peaked at age 120 days and reflected the pattern of the survival curve, indicating that plasma Fn levels have an association with disease activity.