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A L Sandberg

Publications and source records attributed to A L Sandberg.

At least 37 records · Page 2Linked to original sources
PubMed1986

A 160-kilodalton epithelial cell surface glycoprotein recognized by plant lectins that inhibit the adherence of Actinomyces naeslundii.

The adherence of Actinomyces naeslundii to human epithelial (KB) cells is mediated by the interaction of a fimbrial lectin on this oral bacterium with epithelial cell receptors exposed by sialidase. The D-galactose- and N-acetyl-D-galactosamine-reactive plant lectins from peanut and from Bauhinia purpurea inhibit this interaction. This report describes the partial purification and characterization of a 160-kilodalton (kDa) cell surface glycoprotein which is the principal receptor for these lectins. Radioiodinated lectins detected a band of 160 kDa on sialidase-treated Western blots of epithelial cell extracts but did not detect bands on nontreated filters. However, wheat germ agglutinin was reactive with the 160-kDa band on filters that were not treated with sialidase, suggesting that this lectin recognizes the sialic acid residues of this molecule. The 160-kDa component was partially purified from n-octylglucoside extracts of the epithelial cells by wheat germ agglutinin affinity chromatography. This molecule was metabolically labeled with D-[14C]glucosamine and labeled at the cell surface by lactoperoxidase-catalyzed iodination or periodate oxidation followed by sodium borotritide reduction. Incubation of epithelial cells with sialidase before extraction resulted in the loss of the 160-kDa band and the appearance of a band at 200 kDa which was directly reactive with 125I-labeled peanut agglutinin. These results indicate that the 160-kDa glycoprotein on the surface of the epithelial cell serves as a receptor for the agglutinins from the peanut and B. purpurea and presumably the fimbrial lectin of actinomyces.

Actinomyces↗
PubMed1986

Type 2 fimbrial lectin-mediated phagocytosis of oral Actinomyces spp. by polymorphonuclear leukocytes.

Phagocytosis of Actinomyces viscosus T14V and A. naeslundii WVU45 by human polymorphonuclear leukocytes in the absence of antibody or complement was mediated by the lectin associated with the type 2 fimbriae of these bacteria. This effect was markedly enhanced by exogenous sialidase, an enzyme also secreted by these actinomyces. Since sialidase treatment of the bacteria did not result in increased phagocytosis, this enzyme presumably acts by unmasking receptors for the fimbrial lectin on phagocytic cells. The viability of A. viscosus T14V, which possesses type 1 and type 2 fimbriae (1+ 2+), and A. naeslundii WVU45, which possesses only type 2 fimbriae (2+), was decreased by at least 98% following incubation with polymorphonuclear leukocytes in the presence of sialidase. Entirely analogous findings were obtained with a 1- 2+ mutant of A. viscosus T14V. In contrast, the phagocytosis of 1+ 2- and 1- 2- mutants of A. viscosus T14V and a 2- mutant of A. naeslundii WVU45 was minimal or absent. Lactose and beta-methylgalactoside inhibited the destruction of the bacteria, whereas cellobiose and alpha-methylgalactoside were ineffective. Thus, the type 2 fimbriae of the oral actinomyces recognize galactose-containing receptors on polymorphonuclear leukocytes which have been exposed by the removal of sialic acid, an interaction that is followed by internalization and subsequent killing of the bacteria.

Actinomyces↗
PubMed1984

Lectin-dependent attachment of Actinomyces naeslundii to receptors on epithelial cells.

The adherence of Actinomyces naeslundii WVU45 to monolayer cultures of human epithelial cell lines was mediated by the lactose-sensitive fimbriae (type 2) of strain WVU45. The attachment of Actinomyces viscosus T14V, which has both types 1 and 2 fimbriae, was approximately half that of A. naeslundii, and only minimal attachment of A. naeslundii and A. viscosus mutants lacking type 2 fimbriae was detected. The adherence of strain WVU45 was enhanced two- to threefold by neuraminidase treatment of the epithelial cells. The Fab fragments of antibodies which recognize the type 2 fimbriae inhibited the adherence of A. naeslundii WVU45 to the epithelial cells. The bacterial interaction with epithelial cells was inhibited by lactose, methyl-beta-D-galactoside, and N-acetyl-D-galactosamine, but not by methyl-alpha-D-galactoside, cellobiose, N-acetyl-D-glucosamine, L-fucose, or D-mannose. To further characterize the epithelial cell receptors for the bacterial lectin, we utilized several plant and invertebrate lectins as potential inhibitors of bacterial adherence. Lectins from Bauhinia purpurea and Arachis hypogaea which recognize N-acetyl-D-galactosamine, D-galactose, and D-galactose-beta-(1----3)-N-acetyl-D-galactosamine inhibited bacterial attachment, and binding of these lectins to epithelial cells was enhanced by the addition of neuraminidase. Lectins reacting with alpha-linked D-galactose, alpha-linked N-acetyl-D-galactosamine, D-mannose, or sialic acid were not inhibitory. Under similar assay conditions, adherence of a mannose-sensitive strain of Escherichia coli was inhibited by concanavalin A but not by the lectin from Bauhinia purpurea. These results indicate that certain plant lectins have specificities similar to that of the actinomyces fimbrial lectin and are, therefore, useful probes for identifying receptors on epithelial cells for certain bacteria.

Actinomyces↗
PubMed1983

Enhancement of macrophage invasion of tumors by administration of chemotactic factor-antitumor antibody conjugates.

The numbers of macrophages in peritoneal guinea pig hepatomas were significantly (P less than 0.005) elevated by the intraperitoneal injection of a covalent conjugate of the chemotactic peptide, formylmethionylleucylphenylalanine (fMLP), and IgG reactive with surface antigens on the hepatoma cells. These conjugates, which were previously shown to be chemotactic for guinea pig peritoneal exudate macrophages in vitro, increased the numbers of macrophages in the tumors approximately twofold when injected either in a single dose or in five doses. Although five injections of unconjugated fMLP were nearly as effective as the IgG-fMLP conjugates, free fMLP did not enhance the numbers of macrophages in tumors when injected as a single dose. Unconjugated IgG had no effect. The mean tumor weights were decreased in those groups of guinea pigs which received IgG-fMLP but statistical significance was not achieved due to tumor weight variability in all groups.

Animals↗
PubMed1982

Activation of serum complement inhibits collagen synthesis in fetal rat bone in organ culture.

Activation of rabbit serum complement caused a marked reduction in collagen synthesis but a much smaller change in noncollagen protein synthesis in fetal rat calvaria maintained in organ culture. In the periosteum of the fetal rat calvarium, both collagen and noncollagen protein synthesis were reduced, whereas in the central bone, presumably enriched in osteoblasts, only collagen synthesis was inhibited. This large decrease in bone collagen synthesis could not be attributed to enhanced degradation of newly synthesized collagen or its release into the culture medium. Activation of complement also stimulated the production of PGE in fetal rat calvaria. Antagonists of prostaglandin cyclooxygenase decreased prostaglandin synthesis but did not restore collagen synthesis in complement-treated bones, suggesting that complement decreases osteoblast collagen synthesis by a mechanism largely independent of prostaglandin production.

Animals↗
PubMed1982

Enhancement of complement-mediated prostaglandin synthesis and bone resorption by arachidonic acid and inhibition by cortisol.

Arachidonic acid enhances the resorption of fetal rat long bones cultured in the presence of complement and antibodies reactive with rat cell surface antigens as determined by the release of previously incorporated 45Ca by the bones. This effect is attributed to enhanced complement-mediated synthesis of PGE2 by the bones since the levels of PGE2 detectable by radioimmunoassay were greater in cultures containing arachidonic acid, complement and antibody than in those containing only complement and antibody. In addition indomethacin, RO 20-5720 and cortisol inhibited the arachidonic acid induced elevation of PGE2 and 45Ca levels in the supernatants of bones cultured in the presence of complement and antibody. The stimulatory activity of arachidonic acid was not observed if complement was destroyed by heating or if C6 deficient serum was utilized. However, arachidonic acid was effective in cultures containing C6 deficient serum supplemented with functionally purified C6, demonstrating a requirement for late complement components. The increased membrane phospholipid turnover known to be initiated by complement activation is apparently a prerequisite for stimulation of prostaglandin synthesis and resultant bone resorption by arachidonic acid.

Animals↗
PubMed1982

Coexistence of defective and normal immunologic functions in lymphocytes and macrophages from osteopetrotic (op) rats.

The restoration of normal bone remodeling in osteopetrotic animals by transplantation of spleen or bone marrow cells from normal littermates has suggested that the connective tissue abnormalities associated with this disease may be attributed to defective functions of the cells of the immune system. Examination of several immunologic parameters has revealed that both thymocytes and macrophages from osteopetrotic (op) rats express some dysfunctions but retain other activities. Mitogen-induced proliferation of thymocytes from affected rats is significantly lower than that of thymocytes from normal littermates. However, mitogen-activated thymocytes from op rats produce levels of a chemotactic lymphokine that are similar to those produced by the thymocytes from normal animals. Peritoneal exudate macrophages from op rats are defective in that they migrate minimally in response to a chemotactic lymphokine or C5a. These macrophages do, however, produce lymphocyte-activating factor as efficiently as those from the unaffected littermates. The results presented here, which document immunologic defects in the lymphocytes and macrophages from the op rat, indicate that multiple immunoregulatory mechanisms involved in the degradation of connective tissue may contribute to the skeletal malformations that are present in this animal model.

Animals↗
PubMed1981

Detection and localization of a lectin on Actinomyces viscosus T14V by monoclonal antibodies.

A cell-associated lectin activity that mediates lactose-inhibitable adherence of Actinomyces viscosus T14V has been localized to a specific population of fimbriae by the use of monoclonal antibodies. Nine monoclonal antibodies were produced that reacted with only 1 of 2 immunoelectrophoretically distinct fimbrial components on T14V. The fibrillar morphology of this component was revealed by the immunoelectronmicroscopic examination of bacteria incubated with the monoclonal antibodies. The lectin activity associated with these structures was detected when isolated fimbriae were cross-linked with monoclonal antibodies to form immune complexes with agglutination activity for neuraminidase-treated human erythrocytes, a reaction that was inhibited by lactose. Although the 9 monoclonal antibodies differed in their fine specificities, they reacted only with strains of A. viscosus and A. naeslundii that exhibited lactose-inhibitable adherence. These findings indicate that the lectin activity common to these bacteria resides on fimbriae that are antigenically related to those of T14V.

Actinomyces↗
PubMed1980

Direct stimulation of bone resorption by epidermal growth factor.

Epidermal growth factor, isolated from mouse submaxillary glands (mEGF) and human urine (hEGF; urogastrone), and fibroblast growth (FGF) have been tested for their effect on bone resorption by measuring the release of previously incorporated 45Ca from cultured fetal rat long bone shafts. mEGF produced significant but slow stimulation of bone resorption which was maximal at 30 ng/ml and was not blocked by indomethacin, flufenamic acid, or R0 20-5720, structurally unrelated inhibitors of prostaglandins synthesis. mEGF increased thymidine incorporation in long bones at 1 ng/ml, a concentration which did not stimulate resorption. hEGF at 3-30 ng/ml produced a more rapid stimulation of resorption, which was also unaffected by inhibition of prostaglandin cyclooxygenase. Neither mEGF nor hEGF increased the concentration of prostaglandin E in the medium after 5 days of culture. FGF failed to stimulate resorption at concentrations of up to 1000 ng/ml. We conclude the EGF, but not FGF, is a direct stimulator of bone resorption. In contrast to the previously reported findings in mouse calvaria, this stimulation is not dependent on prostaglandin synthesis. Since there is abundant hEGF in human urine, this factor could be responsible for the calcium-mobilizing activity recently found in human urine concentrates.

Animals↗
PubMed1979

Characterization of mouse allergens.

The major allergens present in mouse skin, serum, and urine have been identified. Skin extracts, serum, and urine were chromatographed, and the activities of the fractions were monitored by histamine release from the leukocytes of individuals sensitive to mice. Fractionation of skin extracts revealed two major allergens. The large allergen has a molecular weight of approximately 67,000 daltons and by biochemical and immunochemical criteria appears to be identical to mouse albumin. The smaller molecular weight allergen is approximately 17,000 daltons. The same two allergens are also found in mouse serum and mouse urine. Histamine release by leukocytes of individuals allergic to mice demonstrated that some individuals react predominantly to the large allergen, some to the small allergen, and one group of patients reacts to both allergens.

Albumins↗
PubMed1979

Defective prostaglandin synthesis by C3H/HeJ mouse macrophages stimulated with endotoxin preparations.

Macrophages obtained from C3H/HeN mice produced significant amounts of prostaglandin E when exposed to phenol-extracted lipopolysaccharides (LPS), whereas macrophages from C3H/HeJ mice were unresponsive. The lipid A fraction from phenol-extracted LPS was an effective inducer or prostaglandin synthesis by macrophages from C3H/HeN mice. The polysaccharide portion of the LPS molecule had no effect. In contrast, the C3H/HeJ macrophages did not produce prostaglandin E in response to the lipid A moiety of phenol-extracted LPS. LPS prepared by butanol extraction stimulated the production of prostaglandin E by macrophages from both C3H/HeN and C3H/HeJ mice. The component of butanol-extracted LPS that stimulated the C3H/HeJ macrophages was shown to be a lipid A-associated protein. Further studies demonstrated a correlation between prostaglandin production by the macrophages of these two strains of mice in response to butanol- and phenol-extracted LPS and the lethal effects of the endotoxin preparations.

Animals↗
PubMed1978

Chemotactic antibody.

Antibody of the immunoglobulin G class to herpes simplex virus and antibody of the immunoglobulin M class to sheep red blood cells were coupled to the synthetic peptide formylmethionylleucylphenylalanine (fMet-Leu-Phe), which is chemotactic for both mononuclear and polymorphonuclear leukocytes. The resulting molecules were chemotactic and retained their antigen-binding activity. When antibodies coupled to fMet-Leu-Phe were incubated with antigen, the resulting immune complexes were also chemotactic. Chemotactic antibody may provide a potent means of enhancing the migration of inflammatory cells to specific sites.

Antibodies↗