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)

Lysozyme has been shown to be associated with damaged elastic fibers in many tissues and organs. To better characterize this interaction, binding of lysozyme to elastin was studied using solution-based binding assays. Under physiologic conditions, radio-labeled lysozyme bound specifically to elastin in a time- and concentration-dependent manner. Binding was reversible and was inhibited by unlabeled human and hen lysozyme but not by other proteins. Lysozyme had no elastolytic activity as assessed by a standard tritium-release assay, but, importantly, prevented the proteolytic degradation of elastin by human leukocyte elastase, pancreatic elastase, thermolysin, and Pseudomonas elastase. A striking feature of lysozyme's anti-elastase activity was that it did not function in the classical sense of inhibiting directly the enzymatic activity of the protease. Instead, by binding to elastin, lysozyme prevented the protease from interacting with the elastin substrate in ways that normally favor proteolysis. These results show that lysozyme binds to the elastin component of elastic fibers and that this interaction has important biological consequences for elastic fiber degradation. By preventing degradation of elastin, lysozyme can function as an important natural inhibitor that exerts a protective effect on elastic fibers at sites of tissue injury.
J Invest Dermatol 1996 May
PMID:Lysozyme binds to elastin and protects elastin from elastase-mediated degradation. 861 42

A 30-year-old Japanese woman relapsed into sarcoidosis after two successive parturitions. The cutaneous lesions consisted of scar sarcoidosis, papular type, nodular type, and subcutaneous nodules with histologically typical "naked tubercles". Hypergammaglobulinemia, elevation of both serum angiotensin converting enzyme and lysozyme levels, and bilateral hilar lymphadenopathy were found in the acute and subacute stages, and spontaneously returned to normal levels 16 months after the onset. Our case suggests that parturition may trigger the onset of sarcoidosis.
J Dermatol 1995 Dec
PMID:A case of sarcoidosis which relapsed twice after successive parturitions. 864 5

Malacoplakia, an inflammatory disease characterized by accumulations of phagocytic macrophages, occurs primarily in immunocompromised individuals. Cutaneous involvement is rare. Two men, each with a renal allograft, had expanding nodules on the temple and perianal area (case 1) and perianal, inguinal, and scrotal skin (case 2). Lesions resolved after combined surgical and antibiotic therapy. Histopathologic examination showed dense infiltration with large phagocytic macrophages containing round, concentric, laminar Von Kossa stain-positive inclusion bodies. Histiocytes had positive results for CD 68, lysozyme, and alpha 1-antitrypsin. Electron microscopic examination demonstrated rare intracytoplasmic inclusion bodies with concentric electron-dense laminations of calcium (Michaelis-Gutmann bodies.) Cutaneous malacoplakia should be considered in the differential diagnosis of nodules or draining ulcers, particularly in immunocompromised patients. Because Michaelis-Gutmann bodies are difficult to identify, specimens should be evaluated for cutaneous malacoplakia by immunohistochemical or electron microscopic means.
J Am Acad Dermatol 1996 Feb
PMID:Cutaneous malacoplakia: a report of two cases and review of the literature. 865 20

The wavelength dependence for UVA-induced cumulative damage was investigated in human skin. Epidermal changes (stratum corneum thickening, viable epidermal thickening sunburn cell production), as well as dermal alterations (lysozyme deposition, inflammation), were used as indices of cumulative photoperturbation. UVA wavelengths between 320 nm and 345 nm were more effective than longer wavelengths (360-400 nm) in inducing viable epidermal thickening. Similarly, the shorter wavelengths (320-345 nm) elicited more sunburn cells, although these differences did not reach statistical significance. All UVA bands were equally effective in inducing the dermal markers. At equal fluences, wavelengths > 400 nm produced no measurable cutaneous alterations. These findings suggest that (i) chronic epidermal and dermal damages have different spectral dependence and (ii) the action spectrum for dermal damage in the UVA is broad, extending up to 400 nm, and is different from the acute erythema spectrum in humans.
J Invest Dermatol 1997 Jan
PMID:The spectral dependence for UVA-induced cumulative damage in human skin. 898 Feb 80

Granulomatous slack skin is an uncommon cutaneous T-helper cell lymphoma closely related to mycosis fungoides. To the best of our knowledge this disease has not been previously described in children. We report on an 11-year-old boy who presented with painless slack skin masses in the neck, right axilla and arm, anterior wall of the abdomen, both inguinal regions, and the malleolar and dorsal aspects of the feet. The disease started 3 years earlier with erythematous lesions on the neck and wrists. Histologic examination of a specimen from the abdominal mass revealed an extensive lymphoid infiltrate with scattered multinucleated giant cells extending from the papillary dermis to the subcutis. The lymphoid cells showed the following immunophenotype: CD43+ (MT1), CD45+, CD45RO+, CD20-. The phenotype of the giant cells was lysozyme positive, CD68+ and Mac387-. The tumoral lymphoid cells had clonal rearrangement for the gene of the beta chain of the T-cell receptor (C beta TCR). The disease could be controlled with systemic glucocorticoids. Due to the presence of many histiocytes arranged in aggregates in the papillary and mid-dermis, this case was initially considered to be a cutaneous form of histiocytosis. We recommend deep and extensive biopsies in patients with slack skin disease.
Pediatr Dermatol
PMID:Granulomatous slack skin in childhood. 919 13

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.
Australas J Dermatol 1998 May
PMID:Antineutrophil cytoplasmic antibody (ANCA)-positive cutaneous leucocytoclastic vasculitis associated with antithyroid therapy in Graves' disease. 961 79

Secretory leukocyte protease inhibitor (SLPI) is a small, cationic protein that is known to be constitutively expressed by several glandular epithelia. SLPI inhibits leukocyte-derived proteinases, has anti-HIV-1, antibacterial, and anti-fungal properties, and interferes with the induction of synthesis of proinflammatory mediators in monocytes and macrophages. We now report that at both the mRNA and the protein level, SLPI shows inducible expression in a nonglandular epithelium. A weak expression of SLPI was found in the stratum granulosum of adult normal human epidermis; however, in lesional psoriatic epidermis and in migrating keratinocytes of healing wounds, a strong cytoplasmic staining was seen in the suprabasal keratinocytes. Remarkably, in the dermis adjacent to SLPI-expressing keratinocytes, SLPI was found extracellularly associated with elastin fibers, whereas the dermis in normal skin was negative. In cell culture, SLPI was hardly expressed in monolayers of proliferating keratinocytes. Differentiating cultures with a phenotype of normal skin expressed low levels of SLPI, whereas cultures with a regenerative/psoriatic phenotype expressed high levels. Functional studies with recombinant SLPI indicated that its antibacterial spectrum and potency are distinct from other anti-microbial peptides such as lysozyme and defensins. In view of the multiple functions of SLPI and the inducibility, we propose that it acts as an important first line defence mechanism in cutaneous injury.
J Invest Dermatol 1998 Dec
PMID:Induction of SLPI (ALP/HUSI-I) in epidermal keratinocytes. 985 7

We describe a widespread papular eruption in a 5-year-old girl with rheumatic fever. Histological examination revealed a dense histiocytic infiltration in the dermis. On immunohistochemical studies, the cells were positive for vimentin, CD68, MAC387, alpha1-antichymotrypsin and lysozyme, but negative for CD1a and S-100 protein. Electron microscopic studies showed no Birbeck granules in their cytoplasm. A diagnosis of generalized eruptive histiocytoma of childhood was established. The skin lesions completely disappeared within 8 months.
Eur J Dermatol
PMID:Generalized eruptive histiocytoma of childhood associated with rheumatic fever. 1052 34

We describe a 61-year-old woman who presented with multiple small, firm, shiny, skin-coloured papules in a symmetrical pattern on the dorsum of the hands, sides of the fingers and extensor aspect of the forearms. These had slowly increased in number over a period of 40 years, and were asymptomatic. Both laboratory results and systemic review were unremarkable. Histological examination of six papules revealed well-circumscribed but unencapsulated dermal nodules composed of epithelioid histiocytes and abundant alcian blue-positive mucin separating broad bundles of collagen. Histiocytes within the nodule stained positively with vimentin, and were focally positive for alpha1-antitrypsin and lysozyme. The interstitium was positive for tenascin. On electron microscopy, the histiocytes showed numerous circular, osmophilic myelin bodies and zebra bodies reminiscent of those seen in lysosomal storage diseases. Our patient's clinical, histological and ultrastructural features have been previously described as hereditary progressive mucinous histiocytosis, a rare familial form of eruptive histiocytoma characterized by multiple persistent papules with prominent mucinosis.
Br J Dermatol 1999 Dec
PMID:Hereditary progressive mucinous histiocytosis. 1060 60

We report a case of toxic epidermal necrolysis-type drug eruption. A 23-year-old man took an oral over-the-counter preparation for the common cold. A few days later, generalized erythema developed with systemic malaise and pain. A multiple blister formation followed, and Nikolsky's sign was noted on each blister. A lymphocyte stimulation test (LST) with the patient's peripheral lymphocytes strongly suggested that the eruption was attributable to lysozyme chloride which was included in the preparation taken. Following an intravenous drip of betamethasone for two weeks, the eruptions improved favorably.
J Dermatol 2000 Jun
PMID:A case of toxic epidermal necrolysis-type drug eruption induced by oral lysozyme chloride. 1092 May 87


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