Disease relevance of LYZ

• Here we report on a novel form of systemic ALys amyloidosis, caused by compound heterozygosity in exon 2 (p.T70N) and exon 4 (p.W112R) of the lysozyme gene (LYZ), with both mutations being present on the same allele [1].
• LZM was identified by the capacity of cell lysates or medium to lyse Micrococcus lysodeikticus, and by the presence of a 14.5 Kd protein band which co-migrated with human LZM in SDS-PAGE and which reacted positively in Western blots with antiserum to human LZM [2].
• In Crohn's disease intense LZM staining was seen in epitheloid cell granulomas [3].
• In both ulcerative colitis and Crohn's disease LZM was present in inflammatory cells of crypt abscesses [3].
• RESULTS--Bronchoalveolar lavage fluid from all the patients with sarcoidosis increased LZM secretion by peripheral blood mononuclear cells compared with unstimulated mononuclear cells [4].

High impact information on LYZ

• Genes for CD34 surface antigen, lysozyme (LZM) and myeloperoxidase (MPO) were examined by RNA and DNA analyses [5].
• Wild-type human lysozyme (hLZM) is quantitatively secreted into the media when expressed in mouse fibroblast cells, but some misfolded hLZMs are retained and rapidly degraded in a pre-Golgi compartment (Omura, F., Otsu, M., Yoshimori, T., Tashiro, Y., and Kikuchi, M. (1992) Eur. J. Biochem. 210, 591-599) [6].
• Experiments have been carried out to characterize the binding of lysozyme (LZM) to bacteriol lipopolysaccharide (LPS) [7].
• Thioglycolate-elicited M phi had 75% less intracellular LZM than untreated resident M phi [2].
• Lipopolysaccharide (LPS) treatment of resident mouse peritoneal macrophages (M phi) was found to suppress intracellular as well as secreted lysozyme (LZM) [2].

Chemical compound and disease context of LYZ

• To develop a gene therapy strategy for treating bovine mastitis, a new mammary-specific vector containing human lysozyme (hLYZ) cDNA and kanamycin resistance gene was constructed for intramammary expression and clinical studies [8].

Biological context of LYZ

• A rapid and early downregulation of CD34 transcripts was observed, with concomitant, time-dependent upregulation of expression of both the LZM and MPO genes [5].
• The human lysozyme (LZM) gene also provides a very useful model, because its protein synthesis is continuously increased during myelopoiesis and thus most abundant in mature phagocytes [9].
• When used at concentrations incapable of preventing the target cell recognition by neutrophils, the majority of these agents inhibited both the ADCC and the release of myeloperoxidase (MPO, primary granule marker) and lysozyme (LZM, primary and secondary granule marker) [10].
• Extended methylation analyses of the CpG-poor 5' flanking region and of the exon 4 CpG island (both containing Alu elements) of the LZM gene were now performed [11].
• In conclusion, we demonstrate complex interactions between DNA methylation and histone modifications in mediating LZM repression, which implicate AML1/ETO as one component involved in local chromatin remodeling [11].

Anatomical context of LYZ

• In pathological conditions, such as inflammation and neoplasia, most LZM-positive cells at the site of disease are either granulocytes or members of the mono-nuclear phagocytic system [12].
• After provocation with 25 mg of methacholine or 1 mg of histamine, nasal washings were analyzed for total proteins: the plasma protein albumin, IgG, and nonsecretory IgA (nsIgA), and the glandular proteins secretory IgA (sIgA), lactoferrin (LFN), and lysozyme (LZM) [13].
• The bactericidal and bacteriolytic effects of lysolecithin (LL) and egg-white lysozyme (LYZ) on Staph. aureus and group A streptococci and the solubilization of phospholipids from the bacterial membranes by these agents was studied [14].
• The release of lipids by LYZ (in the presence of LL) from group A streptococci is related to its enzymatic activity, on a still unknown substrate, but not to its cationic nature as this muramidase cannot be replaced by a variety of cation substances (histone, polylysin, leukocyte cationic proteins, polymyxin B, and spermidine) [14].
• Lysozyme (LZM) was identified in ulcerative colitis in granulocytes, monocytes, and macrophages of the intestinal lamina propria [3].

Associations of LYZ with chemical compounds

• Antagonization of LZM repression following conditional expression of AML1/ETO was achieved by TSA [11].
• The antiinflammatory mechanisms of TFLP are probably associated with the inhibition of prostaglandin formation, influence on the antioxidant systems and the suppression of LZM release [15].
• The selective interaction between polyelectrolyte multilayers (PEM) consecutively adsorbed from poly(ethyleneimine) (PEI) and poly(acrylic acid) (PAC) and a binary mixture containing concanavalin A (COA) and lysozyme (LYZ) based on electrostatic interaction is reported [16].
• The solubilization of the bulk of membrane lipids from staphylococci can also be achieved by Triton X-100 and by sodium lauryl sulfate and from group A streptococci by Triton X-100 plus LYZ [14].
• A variety of other detergents (e.g., Cetavlon, sodium taurocholate, cetyl pyrdinium chloride) have no lipid-releasing properties even in the presence of LYZ [14].

Other interactions of LYZ

• Its anti-inflammatory mechanisms are probably associated with the inhibition of prostaglandin formation, the influence on the antioxidant systems, and the suppression of LZM release [17].
• From CD, DLS and AFM the following trend for protein binding at PEC particles under repulsive conditions was obtained: HSA/PEC-1.50 > MYO/PEC-1.50 > LYZ/PEC-0.66 [18].

Analytical, diagnostic and therapeutic context of LYZ

• Histochemical and in particular immunoperoxidase techniques have extended our knowledge about the cellular distribution of LZM [12].
• A reverse haemolytic plaque assay, to detect and quantify LZM release by individual cells was combined with quantitative immunocytochemistry using LZM and the pan-macrophage monoclonal EBM/11 as markers [19].
• In this study, a reverse haemolytic plaque assay for LZM secretion is coupled with immunocytochemistry for the pan macrophage (CD68) marker, EBM/11 [20].
• LZM was analyzed by a new radioimmunoassay (RIA) modification [21].
• The urinary elimination of 3 low molecular weight proteins (LMWP) - beta 2 microglobulin, retinol binding protein and lysozyme (LZM), and the urinary activity of 2 enzymes - alanine aminopeptidase and N-acetyl-beta-glucosaminidase - was measured before, during and after treatment [22].

References