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Biomedical subjects

D B Lowrie

Publications and source records attributed to D B Lowrie.

At least 55 records · Page 3Linked to original sources
PubMed1988

HLA typing in the Hong Kong Chest Service/British Medical Research Council study of factors associated with the breakdown to active tuberculosis of inactive pulmonary lesions.

As part of a multifactorial study of the causes of breakdown to active tuberculosis of inactive pulmonary lesions, HLA-A, -B, and -DR typing was performed on 256 Hong Kong Chinese patients and 100 healthy control subjects. Patients were classified into those with smear-positive, active pulmonary tuberculosis (n = 103), those with inactive disease (n = 113), and those with breakdown to active disease after 6 months or more of inactivity (n = 40). Separately, 21 multiple-case families comprising 38 available parents and 93 offspring were examined for HLA haplotype segregation in relation to infection. Results of both studies indicate that among Hong Kong Chinese there is no statistically significant association between HLA and susceptibility to pulmonary tuberculosis.

Adolescent↗
PubMed1988

Demonstration of increased anti-mycobacterial activity in peripheral blood monocytes after BCG vaccination in British school children.

A blood sample was taken from children aged 13-15 years immediately before BCG vaccination and 8 weeks after. The children were tuberculin skin-test negative to PPD-S before vaccination and positive after. Mononuclear cells were separated from the blood, infected with Mycobacterium microti at a low bacterium/monocyte ratio and allowed to form monolayers in microtitre wells. The infected monolayers were rinsed daily and the change in number of live bacteria in monolayers and supernatants was monitored by colony counts on agar. The cells were bacteriostatic during the first day, thereafter growth accelerated in pre-vaccination monolayers. When monolayers received pulsed exposures to autologous lymphocytes that had been incubated with whole dead tubercle bacilli the growth rates of M. microti were increased. However, growth rates in lymphocyte-pulsed monolayers were significantly lower after vaccination than before. It is proposed that this difference reflects the protective effect of vaccination.

Adolescent↗
PubMed1987

Induction of synthesis of components of the hydrogen peroxide-generating oxidase during activation of the human monocytic cell line U937 by interferon-gamma.

Increased amounts of cytochrome b-245 and a 45 kDa polypeptide component of the hydrogen peroxide-generating oxidase were detected in the human monocytic cell line U937 after incubation in interferon-gamma. The time course of increase in cytochrome b-245 paralleled the induction of oxidase activity. Induction of the 45 kDa component had a different time course, having a greater lag before increased amounts were seen.

Cell Line↗
PubMed1986

Recombinant interferon-gamma and chemotherapy with isoniazid and rifampicin in experimental murine tuberculosis.

Viable bacterial counts in the lungs and spleens of mice infected intravenously with Mycobacterium tuberculosis, strain H37Rv were reduced by intravenous recombinant murine interferon-gamma (IFN-gamma) 1000-5000 u, but not by 200 u. Reduction in counts was greatest when IFN-gamma was given 1 day before infection and was not increased by additional doses in the preceding 2 days. The effect was complete in 1 day and was not increased by successive doses during the next week. Giving IFN-gamma in multilamellar liposomes further reduced the spleen viable counts, but this appeared due to the liposomes themselves and not to encapsulation of IFN-gamma within them. Only a minimal reduction in organ viable counts, not statistically significant, occurred when IFN-gamma was given 5 days after infection. Although IFN-gamma alone and isoniazid 25 mg/kg alone reduced the organ viable counts, combined treatment with IFN-gamma and isoniazid was no more bactericidal than isoniazid alone. Similarly, the bactericidal activity of rifampicin 25 mg/kg was not increased by simultaneous administration of IFN-gamma. There seems little likelihood that IFN-gamma would increase the efficacy of the early stages of the chemotherapy of tuberculosis.

Animals↗
PubMed1986

Effects of recombinant interferon-gamma and chemotherapy with isoniazid and rifampicin on infections of mouse peritoneal macrophages with Listeria monocytogenes and Mycobacterium microti in vitro.

The effect of recombinant murine interferon-gamma (IFN-gamma) on the growth of Listeria monocytogenes for 4 h and Mycobacterium microti for up to 3 days in monolayers of peritoneal macrophages from BALB/c mice was examined by serial viable counts of cell-associated bacteria. Macrophages pretreated with 10 u IFN-gamma per ml were bacteriostatic and with 100 u or 1000 u per ml were bactericidal against L. monocytogenes. Addition of IFN-gamma 3 days before infection caused monolayers to be bactericidal against M. microti mainly during the first 15 min after infection. This was just evident with 10 u IFN-gamma per ml and greater with 100 u or 1000 u per ml. If IFN-gamma was added when phagocytosis of M. microti was complete, about 2 h after infection, its action was only bacteriostatic, the viable counts remaining stationary while those of unexposed monolayers increased. IFN-gamma 100 u per ml added before infection did not alter the bactericidal activity of rifampicin 10 mg/l, nor did it alter the killing curves for isoniazid 1 mg/l or for rifampicin 10 mg/l if added after completion of phagocytosis.

Animals↗
PubMed1985

Activation of macrophages for antimycobacterial activity.

The role of macrophage hydrogen peroxide in defense against mycobacterial infection is discussed - not because this is necessarily any more important than other macrophage products (reviews: [1, 2]) but more as a reflection of recently available information. First, we will describe an accumulation of evidence that peroxide has a role, then we will stage an enquiry into whether interferon-gamma (IFN gamma) activates macrophages for peroxide release, and finally we will give an appraisal of direct peroxide toxicity as the mechanism of killing Mycobacterium tuberculosis by activated macrophages.

Animals↗
PubMed1984

Secretion of a macrophage-activating factor distinct from interferon-gamma by human T cell clones.

Supernatants from clones of human T lymphocytes that were responding to a purified Mycobacterium tuberculosis antigen were able to activate macrophages and macrophage-like myeloma cells (U937) to release increased amounts of the microbicidal agent hydrogen peroxide. The activity was not neutralized by monoclonal antibody against interferon-gamma (IFN-gamma), was greater than could be accounted for by the IFN-gamma activity in the supernatants, and was separated from IFN-gamma by high performance liquid chromatography. It is evident that IFN-gamma is not the only macrophage activator released by T lymphocytes responding to microbial antigen, and may not even be the main one to enhance antimicrobial activity in infections such as tuberculosis.

Antibodies, Monoclonal↗
PubMed1984

Profound depression of alveolar macrophage functions in bronchial carcinoma.

Alveolar macrophages (AM) obtained from a patient with advanced bronchial carcinoma have been studied in the course of a series of experiments examining human alveolar macrophage functions. The AM from this single patient exhibited profound depression of function, being unable to phagocytose opsonised Staphylococcus aureus and failing to release hydrogen peroxide when stimulated by phorbol myristate acetate. The relevance of these findings in the context of host-tumour responses is discussed and the case is reported to stimulate prospective, controlled studies.

Carcinoma, Bronchogenic↗
PubMed1983

Extracellular release of hydrogen peroxide by human alveolar macrophages: the relationship to cigarette smoking and lower respiratory tract infections.

It has been suggested that oxidants from pulmonary inflammatory cells may contribute to the development of emphysema by (i) direct tissue toxicity and (ii) inhibition of alpha 1-antitrypsin, thus diminishing protection of the lung from proteolytic damage. The extracellular release of hydrogen peroxide (H2O2) by human alveolar macrophages (AM) has been measured. AM were obtained by bronchoalveolar lavage and adherence from 24 smokers and 17 non-smokers. Smokers' AM released significantly more H2O2 (3.83 nmol h-1 micrograms-1 of DNA; SEM 0.44) than those of non-smokers' (2.33 nmol h-1 microgram-1 of DNA; SEM 0.40) (P less than 0.05). AM from donors with a recent lower respiratory tract infection released increased quantities of H2O2 (5.22 nmol h-1 microgram-1 of DNA; SEM 0.72; P less than 0.01) even when allowance was made for smoking habits. These findings are consistent with the hypothesis that H2O2 of AM origin contributes to the development of emphysema in smokers.

Adult↗