Effect of neuraminidase on immunogenicity of early mouse trophoblast.
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Biomedical subjects
Publications and source records attributed to G Gowland.
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Hyaluronidase from Propionibacterium acnes has been purified 13,000-fold from the culture supernatant to homogeneity (as determined by polyacrylamide disc gel electrophoresis). The molecular weight of the purified enzyme was 85,110 as determined by gel filtration. The purified enzyme had a pH optimum at 6.4, was stable between pH 5 and 5.8 and was completely inactivated after 15 min at 50 degrees C. Preliminary studies suggested that the enzyme is active against chondroitin 4- and 6-sulphates, but not against dermatan sulphate. Analysis by paper chromatography of the reaction products from the degradation of hyaluronic acid by bacterial, testicular and P. acnes enzymes suggested that the P. acnes enzyme is similar in its mode of action to other bacterial hyaluronate lyases. The enzyme from P. acnes may thus be tentatively classified as a hyaluronate lyase.
An immunofluorescence investigation of thirty-six non-inflamed and thirty-four inflamed acne lesions has been carried out. Fluorescence for C3, unaccompanied by fluorescence for immunoglobulins, was found in the walls of dermal blood vessels or at the basement membrane zone of the comedo or at both these sites in fifty-seven lesions. Fluorescence for C3 accompanied by fluorescence for immunoglobulins was found in nine lesions. In two papules and three nodules the comedo was surrounded or replaced by a mononuclear cell infiltrate. These findings have been taken to indicate that cellular immune mechanisms are a late event and activation of complement is an early event in the pathogenesis of inflammation in acne. The mechanism of complement activation remains uncertain.
Patients with varying degrees of acne, acne-free adult controls and samples of cord blood were investigated for cell mediated immunity to P. acnes using a leukocyte migration inhibition test. Despite the fact that the mean migration index tended to decrease with acne severity, only the patients with severe acne showed cell-mediated immunity. It is suggested that when cellular immunity arises it is a late event which may contribute to inflammation but is probably not a factor in its initiation.
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A recently introduced assay of cell mediated immunity and humoral inhibitory factors has been evaluated in colorectal cancer patients. Using a perchloric acid extract of adenocarcinoma of the large bowel as antigen, 16/27 patients with colorectal cancer had significant cellular reactivity when their separated peripheral leucocytes were tested in homologous AB serum. In autologous serum only 7/27 had significant reactivity; 6/20 patients with a variety of other malignancies showed sensitization to the colorectal antigen preparation. It is concluded that the leucocyte adherence inhibiton test may offer a simple method of assaying for serum blocking factors in sequential studies but will be of little value in the diagnosis of large bowel cancer.
There would seem to be no doubt that most stone-forming patients at some time during the course of their disorder excrete substances not present in normal urine. However, considerable doubt must now exist that "Matrix Substance A" is a single antigenic entity or that its presence is confined to the active formation of renal calculi.
The unseparated leucocytes, separated mononuclear cells and granulocytes of six control subjects and nine patients with colorectal cancer have been studied by a direct cell migration inhibition technique. A migratory index was calculated from the migration in the presence and absence of a perchloric acid extract of large bowel tumours. In 10% homologous AB serum, no significant migration inhibition occurred with any of the cells from control subjects. Five of the nine cancer patients showed significant inhibition with their unseparated leucocytes, seven of seven with their mononuclear cells, and none of nine with their granulocytes. In 10% autologous serum, some controls exhibited migration inhibition with their unseparated leucocytes and their granulocyte fraction, but not with the mononuclear cell fraction. Migration inhibition was also now apparent in the granulocyte fraction of the cancer patients. It is concluded that, with a soluble tumour antigen preparation, a mononuclear cell population increases the sensitivity of the direct migration inhibition test and that autologous serum may interfere directly with the migration of granulocytes, by an action not dependent upon the release of inhibitory factors from sensitized lymphocytes. This could explain some of the inconsistencies of the assay when using an unseparated leucocyte population.