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Biomedical subjects

R B Colvin

Publications and source records attributed to R B Colvin.

At least 217 records · Page 12Linked to original sources
PubMed1981

Fibronectin in healing rabbit corneal wounds.

Fibronectin, a glycoprotein present in plasma and extracellular matrix, is believed to be involved in cell-cell and cell-matrix interactions. Using immunofluorescence techniques, we studied the time course of appearance and distribution of fibronectin in healing rabbit corneal epithelial wounds and compared fibronectin to other selected proteins in the cornea. In the normal cornea, fibronectin was detected only in Descemet's membrane and not in the epithelial basement membrane. Shortly after wounding, fibronectin deposited on the denuded corneal surface and was a continuous prominent layer by 8 hours. The epithelium had begun to migrate over the deposited fibronectin by 22 hours and by 52 hours had completely covered the denuded surface. Fibrinogen/fibrin was also detected on the initial bare wound surface. Once the wound was reepithelialized, the subepithelial fibronectin and fibrin layer then progressively disappeared, so that by 2 weeks only a small amount was detected. Fibronectin also appeared in the deep stroma of corneas after wounding in elongated patches, a pattern suggestive of keratocyte association. Fibronectin had an inverse relationship to bullous pemphigoid antigen which was used as a marker for the lamina lucida of the epithelial basement membrane. The bullous pemphigoid antigen, which was found in the normal corneal epithelial basement membrane, was removed with the epithelium and reappeared during the wound healing when fibronectin was diminishing. IgG and albumin did not localize on the wound surface, and the diffuse staining seen in the stroma did not change during healing. These findings are compatible with the hypothesis that fibronectin and fibrin play a role in epithelial migration and temporary adhesion to the surface during corneal wound healing, at a time when the normal anchoring mechanism is lost.

Albumins↗
PubMed1979

Delayed-type hypersensitivity skin reactions in congenital afibrinogenemia lack fibrin deposition and induration.

Induration is a characteristic feature of delayed-type hypersensitivity skin reactions and is the usual measure of their intensity. The precise basis of induration has not been established, although activation of the clotting system with consequent fibrin deposition has been clearly implicated. In this study, two subjects with congenital afibrinogenemia, a genetic defect in fibrinogen synthesis, were skin tested with standard microbial antigens: streptokinase-streptodornase, monilia, mumps, and tuberculin purified protein derivative. One positive delayed reaction from each subject was biopsied at 40-48 h and compared with 23 biopsies of similar skin tests in normal volunteers. The eight skin tests in the afibrinogenic subjects lacked induration, although the erythema was similar in size (10-34 mm in diameter), intensity, and time-course to those in normals. Biopsies from the two strongest reactions from the afibrinogenemic subjects showed a typical perivascular mononuclear infiltrate. No more than traces of fibrin/fibrinogen were detected by immunofluorescence, in striking contrast to the abundant fibrin/fibrinogen deposition in 23 positive, indurated reactions in normal subjects. These findings indicate that fibrinogen itself is essential for the development of induration in delayed-type skin reactions in man. As judged by 1-mum sections and fluorescence, this is probably a result of the formation of an extravascular fibrin gel.

Adult↗
PubMed1979

Transplantation in miniature swine. VI. Factors influencing survival of renal allografts.

Renal allografts were performed between and among animals from three herds of miniature swine that were selectively inbred to homozygosity at the major histocompatibility complex, MSLA. The results suggest several genetic factors which influence the survival of renal allografts in these animals. As expected, the major histocompatibility complex (MHC) was of dominant importance, and all MSLA-mismatched grafts were rejected promptly (12 +/- 3.7 days). Some MSLA-matched grafts were also rejected (30 +/- 15.0 days), indicating that non-MSLA loci also determine antigens which can lead to kidney rejection. Other MSLA-matched grafts were accepted indefinitely. At least one immune response gene that determined ability to reject kidneys across non-MSLA differences seemed to be segregating in our swine population. Animals that had accepted MSLA-matched renal grafts for extended periods demonstrated markedly prolonged survival of subsequent donor skin grafts compared to skin graft survival across the same non-MSLA difference in normal animals. This finding suggests that failure to reject kidneys across non-MSLA differences indicates systemic tolerance, and that there may be a relationship between the induction of such tolerance and the proposed immune response gene controlling rejection.

Animals↗
PubMed1979

Transplantation in miniature swine. VII. Evidence for cellular immune mechanisms in hyperacute rejection of renal alografts.

Renal allografts were performed in miniature swine that were identical at their major histocompatibility locus and were presensitized by skin grafts from their prospective renal donors. All of these renal grafts were rejected in a hyperacute or markedly accelerated manner compared to the survival of comparable grafts in nonsensitized animals. Studies directed at the mechanism of this rejection revealed no circulating recipient antidonor antibodies by several serological assays. In contrast, mixed lymphocyte cultures (MLCs) and cell-mediated lympholysis (CML) assays demonstrated marked recipient antidonor lymphocyte reactivity that appeared after skin grafts, diminished during the tenure of the renal graft in the host circulation, and reappeared after removal of the rejected kidney. These results suggest that cellular immune mechanisms may plan a role in the accelerated rejection of major histocompatibility complex (MHC)-identical renal allografts.

Animals↗
PubMed1978

Kidney transplants in mice. An analysis of the immune status of mice bearing long-term, H-2 incompatible transplants.

Kidney transplants between strains of mice which are incompatible at either the K or the D end of the H-2 complex usually function for prolonged periods supporting the lives of nephrectomized recipients. This occurs with no recipient treatment. With multiple H-2 and non-H-2 determined incompatibilities, transplants may be rejected but more slowly than skin grafts. In the strain combination studied most extensively in these experiments (B10.D2 to B6AF(1)) in which the incompatibility was confined to the K end of the H-2 region, about 70 percent of recipients survived for many weeks with normal blood urea nitrogen levels. Skin grafts between untreated members of these strains were rejected promptly (mean survival time of 13.5 +/- 1.1 days) as were kidney transplants to recipients of prior skin grafts. Donor strain skin grafts to recipients of kidney transplants after kidney transplantation enjoyed greatly prolonged survival whereas skin grafts from a third party (A.SW) were rejected normally. If kidney tissue was transferred in the form of free grafts without primary vascular union, it was rejected promptly leaving its recipient highly immunized. Cellular and humoral immunity to donor antigens declined over the first few weeks after transplantation, and the spleens of long-term recipients contained no "killer cells." Recipient lymphoid cells could mount active graft versus host reactions to donor strain antigens on transfer to neonatal mice. Nevertheless, they were distinctly less able to respond specifically by the production of killer cells to donor strain antigens after sensitization in vitro. No evidence that this defect was associated with the presence of suppressor cells was forthcoming from several types of in vivo and in vitro tests.

Animals↗
PubMed1978

Immune complex mediated diseases.

Immune complexes formed in the circulation are believed to be the principal pathogenetic agents in certain human diseases, notably in various forms of glomerulonephritis and arteritis. Criteria for the recognition of immune complex deposits in tissue are discussed and recently developed sensitive methods that detect circulating immune complexes are reviewed. In addition, the evidence implicating certain antigens and causative agents in human immune complex mediated glomerulonephritis and arteritis is evaluated.

Animals↗
PubMed1978

Glomerular C3 receptors in human renal disease.

The relationship between glomerular C3 receptor activity and intraglomerular C3 deposition was studied in 73 cases of various forms of renal disease. C3 receptor activity was measured by enumeration of complement-coated sheep red blood cells (IgM EAC) that adhered to glomeruli in frozen sections and expressed as a percentage of the mean number present in control kidneys. Adjacent sections were studied for the presence and distribution of C3 deposits. The precise location of corresponding dense deposits was determined through 1-mu sections or electron micrographs. Marked depression of C3 receptor activity was found in most cases in which there was accumulation of C3 along the glomerular basement membrane, irrespective of whether the deposits were in a subepithelial, intramembranous, or subendothelial location. In contrast, when C3 was not detectable or was found exclusively in the mesangium, C3 receptor activity was affected only moderately, if at all. These data are consistent with the hypothesis that the interaction of C3 with podocytes is a major determinant in the loss of C3 receptor activity in glomerular disease, but do not exclude the possibility that interaction with mesangial or endothelial cells may also influence C3 receptor activity.

Adenocarcinoma↗
PubMed1978

IGA nephropathy in HLA-identical siblings.

This report describes a patient with end stage IgA nephropathy who received a renal transplant from his asymptomatic HLA-identical brother. A biopsy of the donor kidney performed at the time of transplantation showed evidence of widespread electron-dense mesangial deposits. On immunofluorescence these deposits stained with IgA, documenting clinically occult IgA nephropathy in this otherwise healthy donor. These findings are of particular interest in view of the association of IgA nephropathy with the HLA-Bw35 alloantigen, and raise the possibility that asymptomatic disease, already present in a donor kidney, may have accounted for what has previously been called "recurrence" of this disease in renal allograft recipients.

Adult↗
PubMed1978

Plasminogen activator of guinea pig basophilic leukocytes: probable localization to the plasma membrane.

The plasminogen activator (PA) activity of guinea pig basophil-enriched leukocyte preparations was localized to basophils, and not to contaminating lymphocytes and eosinophils, by correlating PA activity with basophil frequency and, more directly, by means of an improved cytochemical method here described. PA activity was fully expressed in living cells in the absence of immunologic stimuli and was suppressed/lost to a variable extent by different techniques of cell disruption. Conversely, killed, but not living, basophils expressed significant plasminogen-independent fibrinolytic activity, presumably reflecting access of cytoplasmic proteases of broken basophils to fibrin substrate. The PA activity of intact cells was destroyed by gentle trypsinization under conditions that did not impair cell viability. When disrupted cells were ultracentrifuged on a sucrose density gradient, PA activity was absent from purified granules and was confined to fractions containing cell membranes. The simplest explanation of these data is that guinea pig basophils have PA activity associated with their plasma membranes. This conclusion has several important implications for basophil functions in cell-mediated and other immunologic reactions in vivo.

Animals↗