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Biomedical subjects

T Lehner

Publications and source records attributed to T Lehner.

At least 253 records · Page 14Linked to original sources
PubMed1977

A functional comparison of blood and gingival inflammatory polymorphonuclear leucocytes in man.

Polymorphonuclear leucocytes from the human gingival crevice (CREV-PMN) have a defective phagocytic capacity when compared with peripheral blood polymorphonuclear leucocytes (PB-PMN) from the same individual. In a study of fourteen clinically healthy subjects, significantly smaller numbers of CREV-PMN phagocytosed fewer Candida albicans blastospores as compared with PB-PMN. The intracellularkilling capacity of the two cell populations was similar. Removal of specific antibody but not complement significantly depressed blastospore uptake by both cell types. It is postulated that the intrinsic defect of the CREV-PMN is acquired in vivo and may be a general property of PMN from inflammatory sites.

Adult↗
PubMed1977

The role of Fc and C3b receptors in phagocytosis by inflammatory polymorphonuclear leucocytes in man.

Polymorphonuclear leucocytes from the gingival crevice (CREV-PMN) in man have a defective capacity to phagocytose Candida albicans blastospores. Phagocytosis of zymosan particles, which detect C3b receptors, is also impaired but ingestion of latex beads coated with heat-aggregated IgG, which detects Fc receptors, is normal compared to peripheral blood polymorphonuclear leucocytes (PB-PMN). If phagocytosis is inhibited by Cytochalasin B, fewer CREV-PMN bind Candida and zymosan but the binding of IgG-coated latex beads remains unchanged. CREV-PMN have IgG (88%), IgM (45%) and C3 (48%) on their cell membrane, whilst less than 5% of PB-PMN have any of these components. Incubation of PB-PMN in fluid from the gingival crevice confers surface IgG and C3 to the cells. Such treatment also inhibits the subsequent binding of IgG coated latex beads. The results suggest that the deficiency of phagocytosis by CREV-PMN is due to decreased binding of particles to the C3b receptor of PMN, whilst the Fc receptor system remains intact.

Adult↗
PubMed1977

Interdependence of in vitro responsiveness of cord and maternal blood lymphocytes to antigens from oral bacteria.

A group of thirty-five mothers and their babies at parturition were examined by the in vitro lymphocyte transformation test to determine sensitization by oral bacterial antigens, B-cell mitogens and dental plaque. Lymphocytes from babies of sensitized mothers with gingival or periodontal disease gave the highest frequency (70 and 63%) and magnitude (mean stimulation index of 3.4 and 3.3) of response in cultures stimulated by Actinomyces viscosus and Veillonella alcalescens. However, IgM antibodies to V. alcalescens antigen were absent from cord sera. With one exception, stimulation of lymphocytes from babies of unsensitized mothers with clinically healthy gingiva was not found with these antigens. The response of cord lymphocytes from mothers with gingival or periodontal disease to antigens from oral bacteria, as compared with the response of cord lymphocytes from mothers with clinically healthy gingiva, seemed specific, since a corresponding difference in response to unrelated antigen PPD was not found. The response of cord and maternal lymphocytes to B-cell mitogens was also determined. Maternal lymphocytes responded in the following decreasing order of effectiveness: dextran sulphate, levan, lipopolysaccharide and dextran B1355; whereas cord lymphocytes were stimulated in the reverse order of effectiveness.

Adolescent↗
PubMed1976

Double blind crossover trial of levamisole in recurrent aphthous ulceration.

A double blind crossover trial of levamisole has been carried out in 47 patients with recurrent oral ulceration. Significant decreases in the number of ulcers and ulcer days were found after 2 months of intermittent administration of levamisole. About 64% of patients responded to the drug by a decrease in the number of ulcers of more than 50%, for two or more months. The remaining 36% of patients failed to respond to levamisole and 23% of these had an increased number of ulcers. The side-effects recorded in patients taking levamisole were comparable with those in patients on placebo, except for a flu-like syndrome in 1 patient and urticaria in another, necessitating withdrawal of the drug. The mechanism of action of levamisole in recurrent oral ulceration is not known, but it is suggested that levamisole may correct a deficiency of suppressor cells, or potentiate the cellular responses to crossreacting microbial agents.

Clinical Trials as Topic↗
PubMed1976

Cell-mediated immunity to herpes simplex virus types 1 and 2 antigens in leukoplakia and carcinoma in man.

Cell-mediated immune responses to herpes simplex virus 1 and type 2 virion and non-virion antigens were assessed in patients and in controls with oral leukoplakia, carcinoma and recurrent herpes labialis. Enhanced proliferation was found in lymphocytes from patients with recurrent herpes labialis or with leukoplakia showing epithelial atypia, and depressed responses were found in carcinoma. Very significantly positive correlations were shown between the responses to each of the herpes virus antigens. A specific increase in cell-mediated immunity to herpes virus in epithelial atypia was confirmed, but separation of the nonvirion from virion antigen is necessary before specific cell-mediated immune responses to the non-virion antigen can be assessed.

Antigens, Neoplasm↗
PubMed1976

Serum and salivary antibodies to cariogenic bacteria in man.

Antibodies in serum and parotid saliva against cell wall preparations from four serotypes of S mutans were examined in 110 subjects aged 18 to 25 years. In subjects with no detectable carious lesions, significant negative correlations were found between the DMF index and serum IgG and IgM antibodies, especially in S mutans of serotype c, whereas positive correlations were found between the DMF index and salivary IgA antibodies. In subjects with active caries, positive correlations were found between serum IgG antibodies and S mutans (serotypes c and a) and the DMF index. Sequential antibody analysis during a period of up to 32 months showed that development of carious lesions was associated with a rise in serum antibody titer to S mutans, but no change was detectable in salivary antibodies. Treatment of caries led to a decrease in serum IgG and IgM antibodies to S mutans cell wall, but in parotid saliva an increase in antibody titer to a culture extract of S mutans was found. The results support the concept of dental caries as an infective disease and suggest that serum antibodies may contribute to caries immunity in man.

Adolescent↗
PubMed1976

Immunologic basis for vaccination against dental caries in rhesus monkeys.

The effects of immunization with Streptococcus mutans on the development of caries and the immune responses were investigated in 37 young rhesus monkeys (Macaca mulatta) during a period of up to 33 months. The monkeys were supplied a human type of carbohydrate-rich diet that contained about 15% sucrose. The monkeys were separated into seven groups, and the effects of two whole cell vaccines and an extracellular culture extract of S mutans in Freund's incomplete adjuvant were compared with a vaccine of a noncariogenic Streptococcus CHT, the adjuvant alone, and a sham immunized group. Sequential analysis of complement fixing, hemagglutinating and precipitating antibodies to the cell wall, and extracellular culture extract have shown that a significant reduction in smooth surface and fissure caries resulted from immunization with the S mutans vaccines, if antibodies reached an optimum level before caries development started. Protection was not elicited by the culture extract of S mutans or the noncariogenic Streptococcus CHT vaccines. A recently developed bacteriological sampling technique of crevicular fluid, plaque, and saliva showed that caries reduction in immunized animals was associated with a significantly decreased percentage of S mutans in crevicular fluid. Immunochemical studies showed IgG and IgM classes of antibodies in serum and secretory IgA antibodies in saliva, but it appears that reduction in caries was best associated with serum IgG antibodies to the culture extract of S mutans. The humoral and cellular mechanisms involved in the immunologic control of caries are discussed in terms of a central afferent mechanism required for antigen processing and cellular proliferation, and two peripheral effector mechanisms that function in the crevicular and salivary domains.

Animals↗
PubMed1976

Acute phase proteins and C9 in patients with Behcet's syndrome and aphthous ulcers.

Estimation of the concentration of C9, C-reactive protein (CRP) and alpha1-antitrypsin in forty sera from patients with Behcet's syndrome and recurrent oral ulcers showed significantly increased amounts of C9 and CRP in Behcet's syndrome. The concentration of C9 was also significantly raised in recurrent oral ulceration, though to a lesser extent than in Behcet's syndrome. The assay C9 and CRP might be useful in the differential diagnosis of Behcet's syndrome, especially from recurrent oral ulcers. It is suggested that during epithelial inflammation in recurrent oral ulcers some of the acute phase proteins are increased and in some patients these may modulate the immunological mechanism in such a way as to induce a transition from focal oral ulceration to the multifocal Behcet's syndrome.

Behcet Syndrome↗
PubMed1976

Serum glucosyltransferase-inhibiting antibodies and dental caries in rhesus monkeys immunized against Streptococcus mutans.

Serum antibodies to glucosyltransferase (GTF) of Streptococcus mutans serotype c were assayed sequentially by means of an enzyme inhibition radio-assay in twenty-six Rhesus monkeys immunized with S. mutans. Pre-immune and control sera had a GTP-enhancing effect which was shown also by albumin and non-immune immunoglobulin fractions. GTF-inhibitory activity was found in IgG fractions from some immune sera and could be absorbed by S. mutans cells possessing cell-bound GTF. Inhibitory antibodies to GTF developed in the sera of four monkeys immunized with hydroxylapatite extract of culture supernatant (HACS), and in four out of fifteen monkeys immunized with S. mutans cells, but in none of the seven sham-immunized control animals. The monkeys immunized with HACS showed no reduction in caries. A correlation has been demonstrated between protection against caries and the early development of serum IgG antibodies to antigens present in HACS but there was no consistent association between protection against caries and GTF-inhibitory antibodies. The results also suggest the possibility that other antibodies, possibly present in the IgM or IgA fractions and having an enhancing effect on GTF, may increase the incidence of caries.

Animals↗
PubMed1975

Immunological basis for latency, recurrences and putative oncogenicity of herpes simplex virus.

The development of latency and recurrent infection after primary herpes simplex virus (H.S.V.) infection can be interpreted in terms of cell-mediated and antibody responses to virus-specific antigens and Fc receptors on the surface of the infected cells. Primary infection will induce immune responses to the virus, and antibody and cell-dependent cytotoxic mechanisms will kill most of the virus and virus-infected cells which are accessible to killer cells. H.S.V. will be sequestrated to the nerves and will migrate centripetally along the axons to the trigeminal or sensory ganglia. Latency in the trigeminal ganglion may be mediated by IgG antibodies binding to both H.S.V. antigens and Fc receptors. Derepression of the viral genome may be induced by factors which weaken the binding of antibodies to the antigen and Fc receptor; the virus will replicate and migrate centrifugally along the axon, to be shed at the nerve endings. In the presence of some defect in T lymphocytes, acting at the neuroepithelial junction, a recurrent herpetic lesion will be precipitated. There is some evidence that H.S.V. may be associated with squamous-cell carcinoma, and it is postulated that the enhanced cell-mediated and antibody responses to H.S.V. may destroy cells containing the viral genome but allow the emergence of an oncogenic genome. Double binding of the Fc receptor and H.S.V. antigen by IgG antibodies or immune complexes on the surface of carcinoma cells may prevent killing and allow these cells to proliferate into invasive tumours.

Antibodies, Viral↗