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J Frerichs

Publications and source records attributed to J Frerichs.

3 recordsLinked to original sources

Transforming Growth Factor-beta2 protects the small intestine during methotrexate treatment in rats possibly by reducing stem cell cycling.

During chemo- and radiation therapy, the balance between epithelial cell proliferation, differentiation, and cell death at the villus tip is disrupted by premature death of dividing epithelial cells. This will subsequently lead to the onset of mucosal barrier injury in the whole gastrointestinal tract. Up till now there is no validated method to treat side effects occurring due to therapy. An approach to manage this side effect might be to reversibly arrest growth of epithelial stem cells during therapy using Transforming Growth Factor-beta2. A Transforming Growth Factor-beta2 enriched fraction prepared from bovine milk was shown to protect small intestinal epithelial cells against cell cycle specific chemotherapeutic agents by arresting the cells in G1-phase. Secondly, in a rat model for induced small intestinal damage, oral supplementation of rats exposed to methotrexate with the Transforming Growth Factor-beta2 enriched fraction significantly reduced the chemotherapy-associated weight loss and ileal villus atrophy by reducing cell proliferation in the normal stem cell population. Thus oral supplementation with a bovine milk fraction enriched for Transforming Growth Factor-beta2 attenuated the side effects of chemotherapy in the small intestine in rats.

Administration, Oral↗

Induction of antibody and T-cell responses by immunization with ISCOMS containing the 38-kilodalton protein of Mycobacterium tuberculosis.

In this study, we investigated the influence of different amounts of N-(palmitoyloxy) succinimide (PA-NHS): attachment of lipid tails to the protein and Quil A on the immunogenicity of the 38-kDa mycobacterial protein incorporated into immunostimulating complexes (ISCOMS; 38-kDa ISCOMS). The addition of higher amounts of Quil A during the ISCOMS preparation increased the amount of protein incorporated into ISCOMS, whereas the use of higher amounts of PA did not influence this parameter. Low antibody responses were observed after primary immunization with all 38-kDa ISCOMS preparations which, however, strongly increased after booster injections. IgG2a is the major subclass IgG induced by these ISCOMS preparations. There were only slight differences between the various ISCOMS formulations in their capacity to induce cytotoxic T-lymphocytes (CTLs). Spleen cells primed with ISCOMS prepared with the highest amount of Quil A produced high levels of IFN-gamma after stimulation with T helper cell type one (Th1) peptide of the 38-kDa protein (aa 70-84), 38-kDa protein or purified protein derivate (PPD). Spleen cells primed with ISCOMS prepared with the lowest amount of Quil A only substantial IFN-gamma levels were detected after stimulation with 38-kDa protein. IL-4 secretion was very low or not detectable with all ISCOM preparations. These results therefore demonstrated that all 38 kDa-ISCOMS preparations were: (1) immunogenic by inducing antibodies, Th1 and CTL responses; (2) that the way in which the ISCOMS were prepared, e.g. the amount of Quil A used, modulates the epitope specificity of the Th1 response.

Adjuvants, Immunologic↗

Types and sensitivity patterns of ocular pathogens.

The total number of specimens received for microbiologic examination and culture in a teaching hospital department of ophthalmology for the years 1974 and 1975 has been reviewed. The results have been analyzed, and information is presented on (a) the relative frequency of different types of bacteria, fungi, and viruses as causal agents of ocular inflammatory diseases and (b) the current pattern of antibiotic sensitivities.

Bacteria↗