PubMed Health⌕ Search

Biomedical subjects

B Albini

Publications and source records attributed to B Albini.

At least 55 records · Page 3Linked to original sources
PubMed1986

Materno-embryonally transferred antibodies precipitate autoimmune thyroiditis in obese strain (OS) chickens.

In Obese strain (OS) chickens the role of maternal antibodies, passively transferred through the egg to the developing chick, was evaluated as a causative factor in the early development of spontaneous autoimmune thyroiditis (SAT). In the egg, passive antibody titers were highest in the yolk and lower in the allantoic fluid and sera of developing embryos. This passage of antibodies was documented by use of radiolabeled antibodies. In dams with high antibody titers, antibodies could be found in the sera of chicks at the time of hatch. Thyroglobulin was absent in the yolk of OS eggs during embryonal life, as compared with its detection in normal eggs. Immune complexes (thyroglobulin-autoantibody) detected in the thyroids of OS, but not CS, chicks at the time of hatch, or earlier, appear to reflect the presence of the maternally transferred antibodies. A pair of crosses between OS chickens, with thyroiditis, and the C strain (CS), without thyroiditis, was made to evaluate the role of transferred antibodies in the pathogenesis of autoimmune disease. When an OS chicken was the dam, maternal antibodies could be passively transferred; when a CS chicken was the dam, no maternal antibodies were present to be transferred. Nevertheless, both hybrids developed full-blown thyroiditis, demonstrating that binding of transferred maternal antibody to thyroglobulin is not a prerequisite for the induction of SAT. However, presence of maternal antibodies precipitated the onset of disease. Immune complexes formed in the embryonic thyroid are likely to participate in early autoimmune disease, although the development of full-blown thyroiditis may await the competency of the chick's immune system to provide the characteristic cellular infiltrate.

Animals↗
PubMed1986

Lack of circulating immune complexes in inflammatory bowel disease.

Multi-organ involvement and especially extraintestinal manifestations have suggested an immune complex-mediated pathogenesis of ulcerative colitis and Crohn's disease. Using various techniques controversial data have been reported on the incidence and levels of circulating immune complexes and their correlation to clinical presentation. Sera of 131 patients with inflammatory bowel disease (78 Crohn's disease, 53 ulcerative colitis) representing a wide spectrum of disease activity, treatment and presence or absence of extraintestinal manifestations were tested for circulating immune complexes using Raji cell indirect immunofluorescence assay, Raji cell radioimmunoassay, C1q solid phase assay and polyethylene glycol precipitation coupled with measurements of optical density and subsequent immunoelectrophoresis or radial immunodiffusion. Circulating immune complexes in low concentrations were observed in a small number of patients with inflammatory bowel disease, the frequency and concentrations being slightly higher in patients with Crohn's disease than in those with ulcerative colitis. No association of concentrations of circulating immune complexes with disease activity or presence of extraintestinal manifestations could be demonstrated. These data do not support the claim for a major role of circulating immune complexes in the pathogenesis of inflammatory bowel disease.

Adolescent↗
PubMed1986

Autoimmune disease induced by oral administration of mercuric chloride in Brown-Norway rats.

Only few reports are available on the consequences of chronic oral administration of low doses of mercuric chloride (HgCl2). Forty Brown-Norway rats received 150 micrograms HgCl2/100 g body weight 3 times a week by gavage or by i.m. injection with 100 micrograms twice per week. After 2 weeks of oral HgCl2 administration, the rats lost weight and hair. Phases of proteinuria were observed in weeks 5-8 and then continuously from week 12 until the end of the experiment at week 39. Antibodies binding to renal, intestinal, and vascular basement membrane developed after 2 weeks; circulating immune complexes were detectable in increasing titers starting at week 3. There were linear deposits of IgG, IgM, and IgA in the glomerular basement membrane and tubular basement membrane, and along the intestinal basement membrane. After week 11, the first granular immune deposits were observed in renal and intestinal basement membranes. Light microscopy showed thickening of glomerular basement membrane, mesangial matrix, and tubular basement membrane. In addition, interstitial nephritis was observed in some animals. Interestingly, kidney involvement was as severe in the orally as the i.m.-treated animals.

Administration, Oral↗
PubMed1985

[Immune complexes: studies on animal models].

A review is presented of some selected experiments conducted on animal models of immune complex-mediated diseases. The immune response and kinetics of antigen deposition are analysed in the model of systemic chronic serum sickness of rabbits and chickens. Experimental nephritis, induced by mercuric chloride, illustrates a pathogenesis in which autoantibodies to basement membranes become components of immune complexes. A recently developed Streptococcus mutans-induced nephritis in rabbits should make it possible to obtain some understanding of early pathogenetic mechanisms. These could very well be analogous to aspects of the pathogenesis of streptococcus-associated nephritides of man.

Animals↗
PubMed1985

Streptococcus mutans-induced nephritis in rabbits.

Intravenous administration of disrupted Streptococcus mutans into rabbits over 23-76 weeks led to severe nephritis involving glomeruli, tubules, and interstitium. Light-microscopic observation of glomeruli documented diffuse endocapillary proliferative glomerulonephritis accompanied often (65%) by epithelial crescents. Electron-microscopic observation revealed humps in glomeruli of 70% of kidney specimens. In the glomeruli of some rabbits, extensive fibrin deposits and sclerosis were evident. Immunofluorescence showed linear, granular, often ribbonlike or patchy immune deposits encompassing, in order of decreasing frequency, C3, IgG, streptococcal antigen, IgA, and IgM. The histopathologic and immunohistologic features of the nephritis seen in rabbits given S mutans thus shows many features of Streptococcus-associated nephritides in man, in particular, the diffuse glomerular nephritis encountered in subacute bacterial endocarditis. Further, analysis of nephritis induced by administration of S mutans may have implications for the evaluation and purification of dental caries vaccines.

Animals↗
PubMed1984

Binding of Streptococcus mutans antigens to heart and kidney basement membranes.

Using indirect immunofluorescence, alkali-extracted components of Streptococcus mutans were found to bind in vitro to capillary walls and sarcolemmal sheaths of monkey cardiac muscle and to glomerular and tubular basement membranes of monkey kidney. Adsorption of S. mutans components to tissue fragments was also detected by indirect radioimmunoassay and immunoblotting on nitrocellulose paper. Antibodies did not bind to untreated, control tissues in these experiments, proving that antigens shared by S. mutans and tissue components were not involved. Rabbit and monkey heart and kidney components bound S. mutans antigens of 24,000, 35,000, and 65,000 Mr. Monkey heart also bound molecules of 90,000 and 120,000 Mr. Rabbits immunized by intravenous injection of disrupted S. mutans cells developed severe nephritis that was characterized by the deposition of immunoglobulins, complement component C3, and S. mutans antigens in the glomeruli. Immunoglobulin G eluted from nephritic kidneys reacted in immunoblots with the 24,000, 35,000, and 65,000 Mr components of S. mutans extract, indicating that the antigens that bound to tissue in vitro also bound in vivo and reacted with antibodies in situ. Antibodies to other S. mutans antigens were not detected in the kidney eluate, although they were present in the serum of the same rabbit.

Animals↗
PubMed1984

Preliminary analysis of primary and secondary anti-Thy-1 responses elicited by immunization with cell-bound and cell-free antigen.

Primary and secondary anti-Thy-1 responses were elicited in C57BL/6Kh and (C57BL/6Kh X BALB/cKh)F1 mice by injection of either intact or sonicated Thy-1 disparate thymocytes as the source of the two forms of Thy-1 antigen--cell bound and cell free, respectively. The primary response was characterized by a high number of anti-Thy-1 plaque-forming cells in the spleen and a high titer of serum antibodies that belonged predominantly to the IgM class. The secondary response consisted of a moderate number of plaque-forming cells and a high titer of serum antibodies that belonged to the IgG and IgM classes. Only secondary responses ensued in mice primed and boosted with the same form of antigen, whereas primary and secondary responses developed concomitantly in animals primed with one form and boosted with both forms simultaneously. These data suggested that the two forms of Thy-1 antigen activate in a given responder two discrete subsets of T cells.

Animals↗
PubMed1984

Transplacental transmission of antibodies to tubular basement membrane in guinea-pigs with autoimmune tubulointerstitial nephritis.

The offspring of female guinea-pigs with tubulo-interstitial nephritis were studied for possible passive transfer of disease. Whereas no immune deposits were seen on or before day 30 of gestation, IgG was detected in the tubular basement membrane (TBM) of fetuses at and after day 44. Serum of offspring contained antibodies to TBM, albeit in much lower titres than found in circulation of the mother guinea-pigs. No histopathological changes were seen in fetal kidneys. Thus, autoantibodies induced by heteroimmunization of pregnant guinea-pigs may be transmitted to offspring in the last third of the gestation period and can bind to fetal TBM. However, this transfer of antibodies does not cause disease.

Animals↗
PubMed1983

Splenomegaly and immune complex splenitis in rabbits with experimentally induced chronic serum sickness: immunopathological findings.

This study describes the morphological and immunocytochemical aspects of the spleen in rabbits with experimentally induced chronic serum sickness. Thirty-seven rabbits were immunized with daily injections of bovine serum albumin (BSA) and six served as non-immunized controls. The most significant lesions were found in rabbits with chronic serum sickness induced by high doses of BSA. The spleens were increased in size and in weight. Granular deposits of BSA, rabbit IgG and C3, presumably immune complexes (IC), were found in the basement membranes of the venous sinuses and of the capillaries in the marginal zone, in the walls of splenic arterioles and, occasionally, between the macrophages in the splenic cords and lymphoid cells in lymphatic follicles. An increased number of degranulated polymorphonuclear leukocytes, macrophages and giant cells, degenerative changes of dendritic cells and, in some instances, splenic fibrosis were also seen. These splenic lesions developed when the concentration of BSA-antibodies in the sera decreased. The spleens of rabbits receiving high doses of BSA in a stage between acute and chronic serum sickness were also increased in size and in weight. The red pulp was enlarged, and immune deposits were observed within macrophages but not in splenic structures. The spleens of non-responder rabbits had a slight decrease in number of lymphatic follicles and germinal centers only. The spleens of non-immunized rabbits were consistently normal. The results indicate that in rabbits receiving multiple injections of high doses of BSA, chronic serum sickness is associated with splenomegaly and IC-splenitis and that these lesions occur when the level of circulating BSA antibody declines. IC-splenitis could impair the clearance of IC and influence the immune function of the spleen. These findings could have implications in the pathogenesis of splenomegaly and of defective splenic function in human IC-mediated diseases.

Animals↗
PubMed1983

Serology and tissue lesions in rabbits immunized with Streptococcus mutans.

Rabbits were immunized i.v. or i.d. with sterile suspensions of disrupted Streptococcus mutans strain MT703 or K1R. Indirect immunofluorescence assays indicated that sera from four of 10 rabbits immunized i.d. contained antibodies reactive with monkey and human heart and kidney components; 19 of 24 rabbits immunized i.v. had antibodies reactive with these tissues. Heart-reactive antibodies were also detected by immunoelectrophoresis and indirect radioimmunoassay. These antibodies were absorbed well by cytoplasmic membranes, a whole cell extract, and an alkali extract of S. mutans but only weakly by intact bacteria. Between 6 and 8 weeks after the first i.v. administration of S. mutans vaccines, rabbits developed proteinuria and hematuria with subsequent weight loss and lethargy. Approximately 25% of the animals died from illness between the fifth and sixth month of immunization. In 13 of 15 rabbits, immune deposits of C3 and IgG, IgM, or IgA and fibrinogen were seen in kidneys within the glomeruli, basement membranes of the peritubular capillaries, and in the interstitium. In the heart, deposits were seen along the capillaries of the myocardium. In 8 of 14 rabbits, focal deposits of S. mutans antigen were detected in glomeruli and in the kidney interstitium. The kidneys showed gross pathologic and histopathologic changes. Most kidneys were pale and enlarged. Microscopic examination revealed hypercellularity of the glomeruli, presence of neutrophils, thickening of glomerular and tubular basement membranes, tubular atrophy, edema, and fibrosis of the interstitium. The kidney disease presented features of poststreptococcal glomerulonephritis. Microscopic examination of heart sections revealed mild perivascular infiltration by polymorphonuclear leukocytes and plasma cells in some of the rabbits.

Animals↗
PubMed1982

Dissociation of immune complexes in tissue sections by excess of antigen.

Immune complexes (IC) present in the glomeruli of rabbits with chronic serum sickness (CSS) and in patients with systemic lupus erythematosus (SLE), idiopathic membranous nephropathy (IMN), and acute poststreptococcal glomerulonephritis (PSGN) were analyzed by incubation with antigenic preparations. The efficacy of these preparations to dissolve IC was assayed by comparison of results of direct immunofluorescence tests performed with the kidney tissues before and after incubation with antigenic preparations. The FITC-conjugated antisera used in these tests were specific for IgG, C3, and-in the case of CSS-for the eliciting antigen, bovine serum albumin (BSA). During the acute proteinuric phase of CSS in rabbits, incubation of tissue sections with BSA alone led to complete dissolution of IC. In many rabbits with late phase proteinuria, however, tissues had to be incubated with both BSA and aggregated fraction II of rabbit serum. In all biopsy specimens from patients with IMN, and in some specimens from patients with PSGN and SLE, aggregated fraction II of human serum resulted in complete or incomplete dissolution of IC. On the other hand, incubation of tissues with excess DNA in SLE or with streptococcal antigens PSGN did not lead to dissolution of IC. These studies suggest significant participation of antibodies to aggregated immunoglobulins (i.e., rheumatoid factors or rheumatoid-like factors) in IC found in the above-mentioned diseases. Other antigen -antibody systems, however, may also contribute to the deposits in the glomerulonephritides studied.

Animals↗
PubMed1981

Serological and immunohistological studies on lepromatous leprosy.

Sera of patients with lepromatous leprosy were studied for the presence of a variety of antibodies and immune complexes (IC). The frequencies of heterophile, Hanganutziu-Deicher and Forssman antibodies were 61 and 43%, respectively, which were significantly higher than those in other diseases. The frequency of antibodies to cardiolipin was 89% and the frequency of rheumatoid factor was 34%. Circulating IC were demonstrated in 54% of the patients' sera by Raji-cell test and in 43% by anti-antibody inhibition test. Analyses of immunoglobulin classes of IC revealed that IgG was predominant in IC of patients with lepra reaction (LR) and IgM in patients without LR. Immune deposits were found in and between cells of dermis in skin biopsy specimens of patients with LR.

Animals↗
PubMed1981

Immune complexes in tissues of obese strain (OS) chickens.

Obese strain (OS) chickens develop spontaneous autoimmune thyroiditis (SAT) comparable in many aspects to human Hashimoto's thyroiditis. In a chronologic study on chickens of the Obese strain with B1B1 and B4B4 genotypes, immune and electron dense deposits suggesting immune complexes (IC) were found in the basal lamina of thyroid follicles (BLTF) as early as the time of hatching. The incidence of IC deposition in BLTF increased with age. In some of the chickens studied, thyroglobulin could also be demonstrated in the immune deposits. In addition, IC were also detected in the glomerular basement membrane of kidneys and in basement membranes of cecal tonsils. The early occurrence of IC in tissues of OS chickens suggests a possible primary role of these immune reactants in the pathogenesis of SAT.

Aging↗