Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum angiotensin I converting enzyme (ACE) was measured in 10 patients with Graves' disease and 2 with thyroiditis during different stages of the diseases. The effect of thyroxine on serum ACE levels was also recorded in 12 patients with thyroid cancer, who were on thyroxine suppression. Serum ACE levels correlated positively with clinically assessed thyroid function and peripheral thyroid hormone levels, especially during hyper- or hypofunction. ACE was measured both with an enzyme kinetic and a new, quantitative inhibitor binding assay. The methods gave similar results, which indicates that ACE increments during thyroid hyperfunction were quantitative, and not a result of increased enzyme activity. Serum ACE increments associated with high lysozyme concentrations are signs of immunologic activation or proliferation of monocytic cells. In this study there was no correlation between the two enzymes, which may indicate either increased synthesis or possibly shedding of ACE from endothelial cells or delayed metabolic clearance of this enzyme. Serum ACE measurements may provide a useful tool for assessing thyroid function and the effect of thyroxine treatment.
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PMID:Thyroid hormones affect serum angiotensin I converting enzyme levels. 298 20

Antibodies against the gram negative enteric bacterium Yersinia enterocolitica have been found in a high proportion of persons with autoimmune thyroid disorders, especially in those with Graves' disease or hyperthyroidism (Shenkman & Bottone, 1981). There is strong evidence that Graves' disease is caused by receptor autoantibodies which mimic the bioeffects of thyroid stimulating hormone (TSH) on the thyroid (Manley, Knight & Adams, 1982). Recently, saturable binding sites for TSH were demonstrated in Y. enterocolitica under non-physiological conditions (Weiss et al., 1983). We have characterized TSH binding sites on Y. enterocolitica under physiological conditions and studied their interaction with Graves' immunoglobulins (Ig's). Saturable and specific binding of receptor-purified 125I-TSH to lysozyme/EDTA-treated Y. enterocolitica (serotype 03) was demonstrated under both non-physiological and physiological conditions. Scatchard binding plots were linear indicating a single class of binding site (Kd 1 X 10(-7) M, maximum of 30,000 binding sites per cell). In the presence of Graves' Ig's the binding of 125I-TSH to Y. enterocolitica was significantly inhibited. Graves' Ig's also precipitated a protein of relative molecular mass (Mr) 64,000 from Triton-solubilized, 125I-labelled Y. enterocolitica, similar in size to one of the proteins precipitated by Graves' Ig's from human thyroid membranes. These findings are consistent with the hypothesis that thyroid autoimmunity may be triggered by bacterial infection via a mechanism involving crossreactivity at the level of the TSH receptor. They also suggest that elements of mammalian endocrine systems are highly conserved and have a function in prokaryotes.
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PMID:Thyrotrophin (TSH) binding sites on Yersinia enterocolitica recognized by immunoglobulins from humans with Graves' disease. 301 19

An enzymatic activity present in high-speed supernatant fluids of rat skeletal muscle was found that catalyzes the release of ADP-ribose from ADP-ribosylated-modified lysozyme. The nature of the product was proved by chromatographic studies and proton nuclear magnetic resonance spectroscopy. The enzyme activity is stimulated by Mg2+, dithioerythritol, and flouride. These results and those published earlier (Soman, G., Mickelson, J.R., Louis, C.F., and Graves, D.J. (1984) Biochem. Biophys. Res. Commun. 120, 973-980) show that ADP-ribosylation is a reversible process in skeletal muscle.
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PMID:Identification of an enzymatic activity that hydrolyzes protein-bound ADP-ribose in skeletal muscle. 376 8

Graves' Disease results from the production of autoantibodies against receptors for thyroid stimulating hormone (TSH) on thyroid epithelial cells, and represents the prototype for numerous autoimmune diseases caused by autoantibodies that bind to organ-specific cell membrane antigens. To study how humoral tolerance is normally maintained to organ-specific membrane antigens, transgenic mice were generated selectively expressing membrane-bound hen egg lysozyme (mHEL) on the thyroid epithelium. In contrast to the deletion of autoreactive B cells triggered by systemic mHEL (Hartley, S.B., J. Crosbie, R. Brink, A.B. Kantor, A. Basten, and C.C. Goodnow. 1991. Nature. 353:765-769), selective expression of mHEL autoantigen on thyroid cells did not trigger elimination or inactivation of circulating HEL-reactive B cells. These results provide evidence that tolerance is not actively acquired to organ-specific antigens in the preimmune B cell repertoire, underscoring the importance of maintaining tolerance to such antigens by other mechanisms. The role of an intact endothelial barrier in sequestering organ-specific antigens from circulating preimmune B cells is discussed.
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PMID:Self-reactive B cells are not eliminated or inactivated by autoantigen expressed on thyroid epithelial cells. 939 69

Presented is a case of a 27-year-old male with Graves' disease on long-term propylthiouracil treatment who, when changed to carbimazole, rapidly developed a petechial and purpuric eruption on the legs, which subsequently flared on treatment with radioiodine. The clinical diagnosis of leucocytoclastic vasculitis was confirmed on skin biopsy. High-titre antineutrophil cytoplasmic antibodies in a perinuclear pattern (P-ANCA) were identified. No anti-myeloperoxidase activity was noted; therefore, the P-ANCA were classified in the atypical group. The target antigens, as determined by enzyme-linked immunosorbent assay, were lysozyme, lactoferrin and bactericidal/permeability increasing protein. Propylthiouracil and carbimazole are chemically related antithyroid drugs. There are reports of typical and atypical P-ANCA-positive cutaneous vasculitis due to propylthiouracil. Cutaneous vasculitis associated with atypical P-ANCA has not been noted previously to be temporally related to carbimazole use. The consideration of thionamides as possible aetiological agents in cases of P-ANCA-positive drug-induced vasculitis is suggested.
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PMID:Antineutrophil cytoplasmic antibody (ANCA)-positive cutaneous leucocytoclastic vasculitis associated with antithyroid therapy in Graves' disease. 961 79

Retrospective studies have shown antineutrophil cytoplasmic antibody (ANCA) positivity in patients treated for Graves' hyperthyroidism; ANCA has been attributed to either antithyroid drugs or to the disease itself. The aim of this study was to determine ANCA in Graves' disease patients at diagnosis and after treatment with methimazole and to evaluate the relationship between ANCA and hyperthyroidism evolution. Thirty patients recently diagnosed with Graves' hyperthyroidism were prospectively studied. ANCA were determined by indirect immunofluorescence. ANCA autoantibodies against specific antigens (proteinase 3, myeloperoxidase, bactericidal/permeability-increasing protein (BPI), cathepsin, lysozyme, elastase, and lactoferrin) were detected by ELISA. The median observation period was 22 months. Kaplan-Meier analysis was performed to identify ANCA as an outcome variable. Twenty patients (67%) were ANCA positive before the onset of treatment, and four (19%) remained positive after 1 yr of antithyroid drug treatment. No differences were observed in any clinical or analytical features between patients with or without positive ANCA. Before treatment, BPI-positive patients required radioiodine treatment or presented relapse more rapidly than BPI-negative patients (log-rank test P < 0.0002). Patients with Graves' hyperthyroidism show positive ANCA before medical treatment, which points to a relationship with the autoimmune disease itself. Our results suggest that BPI-positive patients tend to relapse with antithyroid medication.
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PMID:Frequency of antineutrophil cytoplasmic antibody in Graves' disease patients treated with methimazole. 1272 67

The effects of hyperthyroidism on B-cell physiology are still poorly known. In this study, we evaluated the influence of high-circulating levels of 3,5,3'-triiodothyronine (T3) on bone marrow, blood, and spleen B-cell subsets, more specifically on B-cell differentiation into plasma cells, in C57BL/6 mice receiving daily injections of T3 for 14 days. As analyzed by flow cytometry, T3-treated mice exhibited increased frequencies of pre-B and immature B-cells and decreased percentages of mature B-cells in the bone marrow, accompanied by an increased frequency of blood B-cells, splenic newly formed B-cells, and total CD19(+)B-cells. T3 administration also promoted an increase in the size and cellularity of the spleen as well as in the white pulp areas of the organ, as evidenced by histological analyses. In addition, a decreased frequency of splenic B220(+) cells correlating with an increased percentage of CD138(+) plasma cells was observed in the spleen and bone marrow of T3-treated mice. Using enzyme-linked immunospot assay, an increased number of splenic immunoglobulin-secreting B-cells from T3-treated mice was detected ex vivo. Similar results were observed in mice immunized with hen egg lysozyme and aluminum adjuvant alone or together with treatment with T3. In conclusion, we provide evidence that high-circulating levels of T3 stimulate plasma cytogenesis favoring an increase in plasma cells in the bone marrow, a long-lived plasma cell survival niche. These findings indicate that a stimulatory effect on plasma cell differentiation could occur in untreated patients with Graves' disease.
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PMID:High levels of circulating triiodothyronine induce plasma cell differentiation. 2436 50