PubMed Health⌕ Search

Biomedical subjects

B Albini

Publications and source records attributed to B Albini.

At least 37 records · Page 2Linked to original sources

Tissue distribution of mucosal antibody-producing cells specific for respiratory syncytial virus in severe combined immune deficiency (SCID) mice engrafted with human tonsils.

Groups of C.B-17 SCID mice were reconstituted intraperitoneally with human tonsillar mononuclear cells (hu-TMC) from children seropositive for antibody to respiratory syncytial virus (RSV) and subsequently challenged intraperitoneally with inactivated RSV or sham-immunized. The synthesis and the distribution characteristics of human antibody to RSV in various murine tissues were studied using an enzyme-linked immunospot assay (ELISPOT). No specific antibody was observed in sham-immunized animals. In contrast, mice engrafted with hu-TMC exhibited the appearance of specific human antibody secreting cells (hu-ASC) after i.p. immunization with inactivated RSV. RSV-specific hu-ASC were detected only in animals engrafted with cells from donors seropositive for antibodies to Epstein-Barr virus. Hu-TMC engrafted mice showed RSV-specific IgM and, in lower numbers, IgG hu-ASC in several tissues including the lungs. Numbers of RSV-specific IgA hu-ASC were low, however, and detected only in the lung. No RSV-specific hu-ASC were detected in the intestine. These data demonstrate for the first time that hu-TMC-SCID chimeras respond to immunization with viral antigen. Furthermore, the results suggest that hu-TMC engraft in lungs but not in the intestinal tissue.

Adolescent↗

Distribution and engraftment patterns of human tonsillar mononuclear cells and immunoglobulin-secreting cells in mice with severe combined immunodeficiency: role of the Epstein-Barr virus.

Tonsils seem to be the ideal source of lymphocytes seeding to the mucosa of the respiratory tract. The distribution and engraftment of human lymphocytes injected into mice with severe combined immunodeficiency (SCID) are not well understood. C.B-17 SCID mice were injected intraperitoneally with human tonsillar mononuclear cells (hu-TMC). The hu-TMC-SCID mouse chimeras were subsequently tested for the appearance and distribution of human lymphocytes tagged with H33342 and immunoglobulin-secreting cells in various systemic and mucosal immunocompetent tissues. This was done by fluorescence microscopy of tissue sections for cells supravitally stained before transfer and by an enzyme-linked immunospot assay using cells isolated from murine organs. Most importantly, engraftment of hu-TMC proved to be dependent on the presence of anti-Epstein-Barr virus (EBV) antibody in the donor. hu-TMC engrafted, in decreasing numbers, in the following systemic organs: peritoneal cavity, liver, spleen and bone marrow. Among mucosal tissues tested, hu-TMC were seen in lungs, but not in the intestines. The engraftment of hu-TMC in the lung was more extensive than that in the spleen. These studies demonstrate that hu-TMC engraft in a variety of murine tissues. The striking preference of hu-TMC for the lungs when compared to intestines suggests selective engraftment among distinct mucosal tissues. The hu-TMC-SCID mouse chimera promises to be a unique animal model to study human-mucosa-associated lymphoid cells and EBV-related lymphomagenesis and B cell tumor progression.

Adult↗

Humoral transplantation antibodies play a role in protracted rejection of murine renal allografts.

Murine renal allografts were studied using (C57BL/6J x A/J)F1 mice as recipients and DBA/2 mice as donors. In this strain combination, protracted rejection was noted in that the circulation was maintained in the graft for over 10 weeks. In all grafts examined after 3 weeks, mononuclear cell infiltrates were noted; in addition, all grafts had immune deposits, apparently containing transplantation antibodies, in glomeruli, tubuli and vessels. These results stressed the role of humoral immunity in protracted renal allograft rejection.

Animals↗

Glomerulonephritis in NZW kidneys grafted into NZB/W mice.

After left nephrectomy, 3 10-week old NZB/W mice received orthotopic grafts of kidneys from parental NZW mice of the same age. At autopsy conducted at the age of 33-38 weeks, glomerulonephritis of similar extent was noted in the recipients' own and in the grafted kidneys. Also, very similar granular deposits of immunoglobulins and complement were demonstrated in these kidneys. It was concluded that the absence of glomerulonephritis in NZW mice cannot be attributed to the refractoriness of their kidney to this disease.

Animals↗

Studies on immunological tolerance induced in mice by kidney allografts.

(C57BL/6 x A/J)F1 murine recipients of DBA/2 kidney allografts developed tolerance to DBA/2 tissues, which was measured by observation of growth of a DBA/2 tumor. Eleven, 14 and 18 days after inoculation, the size of the tumor was considerably larger in kidney-grafted than in nongrafted animals. Still, the susceptibility of grafted animals to the tumor did not equal the susceptibility of the DBA/2 mice syngeneic with the tumor. Removal of the renal graft left the recipients with significant tolerance which, however, was weaker than that of the mice in which the kidney graft was left undisturbed. In parabiosis experiments, it was noted that the size of the DBA/2 tumor was equal in the partner which received the DBA/2 kidney graft and in the partner which was not grafted. These experiments rather clearly showed that the tolerance studied was of an 'infectious' type and that it was apparently transferred by some suppressing factor(s) present in the circulation.

Animals↗

In vitro proliferation of murine spleen cells: genetic control of proliferative responses induced by phorbol ester and calcium ionophore A23187.

Proliferative responses of normal (not immunized intentionally) spleen cells from inbred strains of mice to co-stimulation with phorbol ester (PMA) and calcium ionophore A23187 were studied. Striking differences in the magnitude of the responses of spleen cells and splenic T cells from various strains were observed. It appeared that these differences reflected mainly differences in the inducibility of the expression of the gene for the alpha chain of the IL2 receptor (IL2R) by phorbol ester. Formal genetic analysis suggested that the differences in response to phorbol ester and calcium ionophore are controlled by two independent genes with the alleles controlling good response being dominant. The differences in the inducibility of the IL2R gene seemed to be controlled by alleles of a single gene. At least one of the putative genes may be a regulatory element affecting the gene for the alpha chain of IL 2R. The results may have a practical significance for devising more efficient procedure(s) to generate LAK cells used for tumor immunotherapy.

Animals↗

Serum antibodies to cow's milk proteins in pediatric inflammatory bowel disease: Crohn's disease vs. ulcerative colitis.

Serum antibodies to five cow's milk proteins, alpha-casein, bovine serum albumin (BSA), beta-lactoglobulin A and B (BLG-a, BLG-b) and alpha-lactalbumin (ALA) were investigated in young patients with inflammatory bowel disease, 56 with Crohn's disease (CD), 24 with ulcerative colitis (UC). IgG antibodies against BSA and BLG-a and -b were higher in Crohn's disease patients as compared to those with ulcerative colitis and controls. The IgG anti-BSA were higher in the group of CD patients with higher score of disease activity. Additionally, IgA antibodies to alpha-casein were higher in CD and UC compared to control. These findings may be due to increased uptake of dietary antigens or enhanced immunological response occurring in CD patients.

Adolescent↗

Serum antibodies to cow's milk proteins in pediatric inflammatory bowel disease. Crohn's disease versus ulcerative colitis.

Serum antibodies to five cow's milk proteins (alpha-casein, bovine serum albumin, beta-lactoglobulin A and B, and alpha-lactalbumin) were investigated in young patients with inflammatory bowel disease (56 Crohn's disease, 24 ulcerative colitis). IgG antibodies against bovine serum albumin, beta-lactoglobulin A and beta-lactoglobulin B were higher in Crohn's disease patients than in those with ulcerative colitis or the controls. IgG anti-bovine serum albumin antibodies were higher in those Crohn's disease patients who had higher scores of disease activity. Finally, IgA antibodies to alpha-casein were higher in patients with Crohn's disease and ulcerative colitis when compared to controls. These findings may be due to increased uptake of dietary antigens or enhanced immunological response occurring in Crohn's disease patients.

Adolescent↗

IgG rheumatoid factor in human and rabbit transplantation sera.

Sera of human recipients of kidney allografts and rabbit recipients of skin allografts were tested by means of enzyme immunoassays (EIA) for IgG rheumatoid factor (RF) combining with human IgG (RF-H) or rabbit IgG (RF-R). In humans, the mean OD value in EIA for RF-H was significantly higher in 185 sera of allograft recipients than in 46 pretransplantation sera and 100 sera of normal subjects. Furthermore, the mean OD in patients who rejected their grafts was higher than in patients with satisfactory graft function. Interestingly, there was no difference in OD values for RF-R between sera of graft recipients and sera of normal subjects. Of 52 rabbit recipients of skin allografts, 24 were positive for both RF-R and RF-H, 4 were positive only for RF-R, another 4 only for RF-H, and 20 were negative for both. Renal allografts originating from the previous donors of skin grafts resulted, in most instances, in a significant decrease in the strength of the reaction for both RF-R and RF-H. The possible role of graft rejection in stimulation of RF formation as well as the possible role of RF in graft rejection should be considered.

Animals↗

Heart-reactive antibodies in rabbit anti-Streptococcus mutans sera fail to cross-react with Streptococcus mutans.

Immunization of rabbits with Streptococcus mutans antigens results in the production of serum antibodies that bind in vitro to human, rabbit, and monkey cardiac muscle. Antibodies to heart, however, have also been reported to occur at lower titers in the sera of unimmunized rabbits. In this study, the specificities of heart-reactive antibodies (HRA) in sera of unimmunized and S. mutans-immunized rabbits were compared using indirect immunofluorescence, Western blot, and Bio-Dot immunoassays. Both groups of sera gave striational indirect immunofluorescence-staining patterns on thin sections of native human and monkey cardiac muscle. Western blot analyses revealed that antibodies in normal sera bound 9 to 20 components of human, rabbit, and monkey heart. The major bands had Mr of 205,000, 160,000, 135,000, and 70,000. Several of the normal sera did not have antibody activity to S. mutans antigens, indicating that these HRA do not cross-react with these bacteria. Although immunization of rabbits with S. mutans caused increased titers of HRA (two to three doubling dilutions), Western blot assays using anti-S. mutans sera showed banding patterns qualitatively similar to those of normal sera on heart extracts. Antibodies to skeletal muscle myosin were detected in both serum groups. Of eighteen normal rabbit sera sixteen had antimyosin titers of 10 to 40, whereas all eighteen anti-S. mutans sera had titers of 10 to 160. Affinity-purified antimyosin antibodies isolated from anti-S. mutans serum did not bind to S. mutans components. Conversely, affinity-purified antibodies to S. mutans antigens did not bind to myosin or to other cardiac muscle components. Among these were antibodies to the 185-kDa cell wall protein (also known as B, I/II, IF, Spa A, and P1) previously believed to possess antigenic mimicry. HRA were removed from anti-S. mutans sera by absorption with S. mutans but this effect was not specific, because a non-cross-reactive internal standard antibody was also absorbed to the same extent. Because previous evidence for antigenic mimicry between S. mutans and cardiac muscle was based on serum cross-absorption experiments, this immunologic relationship is not substantiated. These results indicated that naturally occurring antibodies to cardiac muscle components are present in the sera of unimmunized rabbits and that immunization with S. mutans does not stimulate production of new heart-reactive antibody, but rather serves to boost antibody production by preexisting clones of self-reactive B-lymphocytes.

Animals↗

The distribution of immunocompetent cells in the compartments of the palatine tonsils in bacterial and viral infections of the upper respiratory tract.

Employing a series of monoclonal antibodies directed against T cell subsets using the avidin-biotin complex method as the immunoperoxidase technique and using fluorescein-conjugated antisera directed against the major immunoglobulins, we have studied the distribution of immunocompetent cells in sections of tonsils from 21 patients with various inflammatory diseases of the tonsils, including Streptococcal tonsillitis, recurrent tonsillitis and tonsillitis associated with infectious mononucleosis. The following conclusions can be made in regard to our study. The percentage of T cells decreases in all compartments of the tonsils with increasing episodes of tonsillitis as well as with infectious mononucleosis and Streptococcal tonsillitis. Similarly, the percentage of HLA-DR positive cells decreases with increasing episodes of tonsillitis and is statistically significant in the mantle zone. The percentage of IgM B cells and IgD B cells tends to increase in the extrafollicular zone and decrease in the mantle zone with increasing episodes of tonsillitis as well as with increasing age. The percentage of IgG and IgA plasma cells is highest in children who have had 3-5 episodes of tonsillitis, but markedly decreases in the follicle and extrafollicular compartments in patients who have had more than 5 episodes of tonsillitis. FACS analysis of B cells in the tonsils and peripheral blood show a marked decrease in IgD in both the tonsil and the peripheral blood and a significant increase of IgG in the peripheral blood. These findings may suggest late clonal expansion of B cells in recurrent tonsillitis and Streptococcal tonsillitis. Finally, the distribution of immunocompetent cells in recurrent tonsillitis, Streptococcal tonsillitis and tonsillitis associated with infectious mononucleosis appears to be independent of age.

Adolescent↗

Distribution of rotavirus antigen in intestinal lymphoid tissues: potential role in development of the mucosal immune response to rotavirus.

Groups of suckling BALB/c mice were inoculated with murine rotavirus (MRV) at 5 days of age and sequentially tested for the presence of MRV antigen (Ag) in intestinal villus epithelium (VE), Peyer's patch (PP), mesenteric lymph node (MLN), spleen, liver and lung, using indirect immunofluorescence techniques (IF). MRV Ag was first detected in VE 24 h after oral administration of the virus and remained in VE for as long as 10 days post-inoculation (pi). MRV Ag was observed in the epithelium overlying PP at 3-7 days pi and in subepithelial and interfollicular areas in the PP between 3 and 20 days pi. MRV Ag was also detected in MLN during the same period of time. Small numbers of MRV-Ag-containing cells were detected in the lamina propria (LP) of intestinal villi at 10 days pi. Most MRV-Ag-containing cells in PP and MLN were Ia-positive but negative for Lyt-1, Lyt-2 and MAC-1 cell surface markers. MRV-Ag-containing cells were negative for surface or cytoplasmic immunoglobulin. Intestinal antibody response to MRV indicated by the presence of MRV-specific IgA plasma cells in LP was first detectable 10 days pi. Highest density of MRV-specific plasma cells was observed in the duodenum, with a similar distribution to that of MRV-Ag-containing cells in PP. These observations suggest that MRV-Ag uptake is largely limited to the PP associated epithelium and the virus Ag is subsequently transported to the underlying lymphoid follicles and MLN. These findings suggest a close relationship between the availability of MRV Ag in the lymphoid follicles at different locations and the subsequent development of local antibody responses in different segments of small intestine.

Animals↗

Serum antibodies to cow's milk proteins in ulcerative colitis and Crohn's disease.

Serum antibodies of immunoglobulin G, immunoglobulin M, and immunoglobulin A isotypes to five major proteins of cow's milk, casein, bovine serum albumin, alpha-lactalbumin, beta-lactoglobulin A, and beta-lactoglobulin B, were measured using enzyme-linked immunosorbent assay in 51 patients with ulcerative colitis, 49 with Crohn's disease, and 20 age-matched controls. Immunoglobulin G and immunoglobulin M antibodies to cow's milk proteins were significantly elevated in patients with inflammatory bowel disease as compared to controls. In contrast, no significant increase in immunoglobulin A antibodies to 3 of 5 proteins was noted. The increased titers of antibodies to milk proteins seem to be specific and not due to a polyclonal immunoglobulin activation, as naturally occurring blood group antibodies were not elevated in patients with ulcerative colitis and Crohn's disease. A good correlation of disease activity, as measured by serum alpha 1-acid glycoprotein concentrations, and immunoglobulin G and immunoglobulin A antibody titers against certain cow's milk proteins could be demonstrated in Crohn's disease, but not ulcerative colitis. These findings suggest that production of antibodies to cow's milk proteins reflects specific immunization with these antigens. The study of antibody isotypes and correlation with disease activity may provide better insight into the immune response to dietary antigens and its possible role in the pathogenesis of inflammatory bowel diseases.

Adult↗

Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. I. Light, immunofluorescence and electron microscopic studies.

Invasion of periodontal tissues by different bacterial morphotypes has been reported in human periodontitis; however, limited information is available as to prevalence, localization and the bacterial species involved. The present study determined prevalence and gingival localization of Actinobacillus (Haemophilus) actinomycetemcomitans in periodontal lesions of juvenile periodontitis patients. Thirty-five gingival biopsies were obtained from 12 juvenile periodontitis patients at the time of periodontal therapy. One additional control biopsy was obtained from each of two adult periodontally healthy subjects, one adult periodontitis patient and one periodontally healthy monkey (Macaca fosibolius). The biopsies were carefully processed to avoid mechanical introduction of bacteria into the tissues and were examined using light and electron microscopy. Rabbit antisera specific for the three A. actinomycetemcomitans serotypes were used for immunofluorescence microscopic localization of A. actinomycetemcomitans antigens in the gingival sections. Immunofluorescence microscopy showed A. actinomycetemcomitans specific antigens in the gingival tissues of 11 of the 12 juvenile patients examined. None of the control specimens showed evidence of A. actinomycetemcomitans antigens in the gingival connective tissue. One specimen from a periodontally healthy subject and the monkey biopsy, however, showed A. actinomycetemcomitans antigens in bacterial plaque on the surface of the crevicular epithelium. Transmission electron microscopic examination showed microcolonies of small gram-negative rods in the connective tissue, as well as single bacterial cells between collagen fibers and in areas of cell debris. In addition to these extracellular bacterial cells, evidence of bacterial cells was also found within gingival connective tissue phagocytic cells. The data from the present study suggest that the gingival tissue in juvenile periodontitis lesions harbors A. actinomycetemcomitans.

Actinobacillus↗

Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. II. Correlation between immunofluorescence and culture techniques.

Recent immunohistological studies have suggested that Actinobacillus actinomycetemcomitans is present in the gingival tissues in juvenile periodontitis lesions. The present study examined tissue bound A. actinomycetemcomitans by bacterial culture and immunohistological demonstration of antigen in tissue. A total of 14 periodontitis lesions were examined. Eleven biopsies were obtained from gingiva adjacent to A. actinomycetemcomitans infected pockets, while the remaining three control biopsies were obtained from gingiva adjacent to pockets where subgingival A. actinomycetemcomitans infection could not be detected. Each biopsy was hemisected, one half was used for immunofluorescence microscopic examination while the other half was processed for culture of A. actinomycetemcomitans. The latter section was surface-disinfected, repeatedly washed and then minced to release bacteria from within the tissues. Aliquots from the serial washings and the minced tissue suspension were cultured on medium selective for A. actinomycetemcomitans. Surface disinfection and serial washings gradually decreased cultivable A. actinomycetemcomitans in the washings aliquots. Following tissue disruption, an increase in colony-forming units of A. actinomycetemcomitans was seen from eight of the 11 test biopsies. This bacterium could not be detected in washings or minced tissue suspensions from the control biopsies obtained from lesions in which subgingival A. actinomycetemcomitans was previously not detected. A positive correlation was seen between the presence of A. actinomycetemcomitans antigens in the gingival biopsies and; (1) A. actinomycetemcomitans colony-forming units released from the minced tissues (r = 0.90, p = 0.000), as well as; (2) the colony-forming units from the periodontal pocket (r = 0.62, P = 0.017).(ABSTRACT TRUNCATED AT 250 WORDS)

Actinobacillus↗

In vitro translation of rat intestinal RNA prepared from isolated villus and crypt cells and from the epithelium-denuded intestine. Synthesis of intestinal basement membrane.

RNA purified from rat intestinal epithelial cells, obtained as isolated cell fractions of a villus-to-crypt gradient, were shown to be capable of directing peptide synthesis in a cell-free system. Analysis of products have demonstrated differences between villus and crypt and between jejunum and ileum. RNA purified from epithelium-denuded intestine was also shown to be capable of directing cell-free protein synthesis. Precipitation of products by antisera to rat IBM showed differences between epithelial and nonepithelial cells. Anti-laminin derived from mouse EHS sarcoma laminin precipitated products synthesized, in vitro, only by nonepithelial intestinal cells. Further studies on the control of the synthesis of rat IBM should provide valuable information on the relative contributions of epithelial and nonepithelial cells to the synthesis of basement membrane components of this organized tissue system.

Animals↗

[Mercuric chloride-induced enteropathy in the rat: a model of gastrointestinal disease with immunologic pathogenesis].

Protein-loss into the gastrointestinal tract is a feature of many different diseases, a number of which are immunologically mediated, e.g. systemic lupus erythematosus or Crohn's disease. The pathogenic mechanism of protein-losing enteropathy in diseases without obvious enterocyte injury are unknown. Brown-Norway-rats (BN-rats) were gavaged with low doses of HgCl2 for 39 weeks. Within 2 weeks, the intestines showed strong linear staining for IgG and IgA along vascular and intestinal basement membranes. Granular deposits containing IgG and C3 were present along intestinal basement membrane only in the late stages of the experiment; only in these animals increased intestinal protein loss as measured by fecal Cr-51 excretion was found. These findings suggest that immune complex deposition along the intestinal basement membrane can lead to protein-losing enteropathy. This disease may be used as a model for the study of immunologically mediated intestinal disease.

Animals↗