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)

Mononuclear phagocytes secrete a number of materials into the extracellular environment. The materials secreted by phagocytes can be grouped into three categories: a) enzymes affecting extracellular proteins (collagenase, elastase, lysosomal proteases, plasminogen activators), b) materials involved in defense processes (complement proteins, interferons, lysozyme), and c) factors regulating activities of surrounding cells. The latter include lymphostimulatory molecules, a colony-stimulating factor, and inhibitors of cell growth. The conditions for secretion of the materials depend on the activity of the phagocytes. The lymphostimulatory molecules secreted by macrophages exert various effects: 1) an increase in DNA synthesis of lymphocytes, 2) a maturation of early thymocytes to mature T cells, and 3) the differentiation of some B cells to antibody-secreting cells. The mitogenic principle has been partially isolated as a protein of 15,000 to 20,000 daltons. The secretion of lymphostimulatory molecules is increased following uptake of various materials by macrophages or by addition of activated T cells to macrophage cultures.
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PMID:Regulation of immunity and inflammation by mediators from macrophages. 13 1

Mediators released from injured human skin that initiate the inflammatory response have not been adequately identified. Organ culture of full-thickness skin explants enables us to do so, because injury to the skin can be made in vitro, eliminating the rapid leakage of serum and infiltration of leukocytes that occur in vivo. In our studies, the military vesicant sulfur mustard (SM) (10 microliters of a 0.01 to 1.0% dilution) was topically applied to injure the epidermis of the explant. Then, the explants were cultured in small Petri dishes, usually for 18 h at 36 degrees C, and the organ-culture fluids were assayed for various inflammatory mediators. We found that the culture fluids from SM-exposed and control explants contained similar amounts of angiotensin-converting enzyme, trypsin-like and chymotrypsin-like proteases, acid phosphatase, beta-glucuronidase, beta-galactosidase, lysozyme, deoxyribonuclease, ribonuclease, interleukin 1, and lactic dehydrogenase. However, the culture fluids from SM-exposed explants contained increased amounts of histamine and plasminogen-activating activity, and often prostaglandin E2, when compared to culture fluids from control explants. After 3 to 4 d in culture, full-thickness human skin explants, when exposed to 0.2% SM (but not when exposed to 1.0% SM), sometimes showed separation of the epidermis and increased collagenase activity (i.e., hydroxyproline release). Thus, histamine (from local mast cells), and prostaglandin E2 and plasminogen-activating activity (probably from both mast cells and epidermal cells) are apparently involved in early mediation of the inflammatory response.
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PMID:Mediators, initiating the inflammatory response, released in organ culture by full-thickness human skin explants exposed to the irritant, sulfur mustard. 171 Jun 39

A unique type of Ag-specific hypersensitivity was induced by challenging the Ag-sensitized mice at the ear. It was elicited within 1 h after the Ag challenge, and thus was distinct from either the delayed-type hypersensitivity (DTH) which developed in 24 h or the immune complex-mediated hypersensitivity which evolved in 4 to 6 h. This hypersensitivity was referred to as early-type hypersensitivity (ETH). The time required for these types of hypersensitivity to develop after immunization was also different; DTH required 4 to 6 days, ETH 9 to 11 days, whereas plasma protein-induced immune complex-mediated hypersensitivity needed 18 to 21 days. The ETH could be induced by a smaller amount of Ag than DTH, and unlike DTH could be transferred by either immune sera or T cell-derived culture factor which was small m.w. Although the ETH developed later than DTH after sensitization, it lasted longer once developed and the pattern of response was inversely related to DTH. Furthermore, the denatured hepatitis B surface Ag induced DTH but not ETH, in contrast to native hepatitis B surface Ag that induced both, suggesting that the epitopes recognized by TETH cells were distinct from those recognized by TDTH cells. The ETH could be induced by most Ag tested including poly(Glu60Ala10Tyr10, L-lactic dehydrogenase, insulin, chicken egg white lysozyme, polymerized human serum albumin, horse gamma-globulin, transferrin, fibrinogen, and plasminogen, but not by purified protein derivative. Because poly(Glu60Ala10Tyr10, L-lactic dehydrogenase, egg white lysozyme and insulin were under the Ir gene control and the inducibility of ETH was Ag dependent and was closely correlated with that of DTH, the expression of ETH also must be regulated by Ir gene. The histopathologic changes in ETH consisted of capillary congestion and edema. The vasopermeability was increased and there was the leakage of plasma proteins into the tissue. Based on these data, we concluded that the ETH reported in this study was a novel type of Ag-specific hypersensitivity.
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PMID:An antigen-specific hypersensitivity which does not fit into traditional classification of hypersensitivity. 247 37

Twenty biopsies of lesions of cutaneous leishmaniasis were classified according to the mechanism of parasite elimination, on the basis of macrophage activation (five cases) or macrophage lysis (15 cases). The immunoperoxidase technique was used to demonstrate free Leishmania antigen, immunoglobulins, complement, lysozyme, C-reactive protein, beta-lipoprotein, alpha 1-antitrypsin, alpha 2-macroglobulin, plasminogen and factor VIII, which were quantitated and comparatively assessed. The fall in the parasite load during the course of the infection was associated with rising levels of IgG, IgM and IgE, and of the complement components of the classical pathway. Macrophage lysis supervened when there was an approximate equivalence of antigen and antibody, and was associated with the deposition of immune complex components. Lysis of the acute focal type (C response) was accompanied by a massive liberation of free Leishmania antigen, followed by a fall indicative of parasite elimination. The lysis of small numbers of macrophages scattered diffusely in the lesion, which was slow to reach completion (B response), was less effective and immunologically closer to the non-lytic (A) response. A terminal fall of the immunological factors other than the globulins, suggestive of resolution, was observed mainly in the C response. Lymphocytes may be important in macrophage activation associated with the macrophage A response and in the later stage of the B and C responses. However immunologically induced host-cell lysis is more important than macrophage activation for the elimination of Leishmania in the acute stage of most skin lesions. It is associated with, and may be caused by, the formation in situ of immune complexes of Leishmania antigen and antibody at an appropriate ratio.
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PMID:Cutaneous leishmaniasis: immune complex formation and necrosis in the acute phase. 637 41

The immunoperoxidase technique was used to assess the quantity and situation of various immunological factors in 24 skin biopsies which represented the leprosy spectrum from TT to LL. The factors were immunoglobulins (IgG and IgM), complement components (C3, C3d and Clq), plasminogen, muramidase (lysozyme), C-reactive protein and alpha-1-antitrypsin. The results were compared with previous reports on the assessment of these factors in serum. The quantities of these factors in the lesions produced peaks at TT and LL, with a dip in the BT-BB region (C-reactive protein and alpha-1-antitrypsin excepted). The immunoglobulins, present mainly in plasma cells and lymphocytes, correlated in general with reports of serum levels. The complement components were present in appreciable amounts, though the serum levels are depressed; they were seen in young mononuclear cells with a low bacterial load. All factors produced an ascending gradient in active lesions from BT to BL or LL, which correlated with the bacterial load and its viability. In regression (studied only in LL) there was a decrease in all factors. In TT there was an increase in most factors which did not correlate with the antigen load, and which probably resulted in an excess of antibody over antigen. In active LL there is probably an antigen excess. The results suggest the possibility that there is a common defect from BT to LL, in which the generation of immunological factors within the lesion of immunological factors within the lesion is a secondary response to the antigenic load. In TT alone (a rare group) is there an enhanced immunological response unrelated to the antigen load. In support of this was the finding of Ia antigen only in TT lesions.
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PMID:An immunoperoxidase study of immunological factors in skin lesions across the spectrum of leprosy. 704 10

The epithelioid cell granuloma in high resistant tuberculoid (TT) leprosy was contrasted with the pure macrophage granuloma of anergic lepromatous leprosy (LL) by evaluating various immunological factors operating in these lesions. The immunoperoxidase technique using antisera to immunoglobulin IgG, IgM, complement C3, C3d and C1q and other products of macrophage secretion, lysozyme, plasminogen, a1 antitrypsin and C-reactive protein and of Ia antigens revealed peak levels in tissues of most of these factors in both types of granuloma. The tuberculoid response was linked to low antigenic load and Ia-like antigen and the lepromatous response was secondary to a high antigenic load in the absence of Ia antigen. Complement and other mediators were found intracellularly in both tuberculoid and lepromatous granulomas, but extracellularly only in tuberculoid lesions. This may indicate local hypersensitivity in the tuberculoid granuloma. It is suggested that the mediators in LL macrophages remain bound to lipids of mycobacterial degenerations in the phagocytic vacuole. Secretory cells were differently sited in the two types of granulomas: peripheral in epithelioid cell lesions and central around capillaries over the whole lesion in pure macrophage granulomas of LL. In tuberculoid leprosy many of the central vessels in the granuloma were obliterated. C1q was found in fibroblasts. However, the marked absence of fibrosis in any of the lesions of leprosy, except following severe reactions, casts some doubt on the link which has been postulated between epithelioid cells and fibroblasts as an explanation of fibrosis in granulomas.
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PMID:An immunoperoxidase study of immunological factors in high immune and low resistance granulomas in leprosy. 704 10

We cloned the streptokinase (STK) gene of Streptococcus equisimilis in an expression vector of Escherichia coli to overexpress the profibrinolytic protein under the control of a tac promoter. Almost all the recombinant STK was exported to the periplasmic space and recovered after gentle lysozyme digestion of induced cells. The periplasmic fraction was chromatographed on DEAE Sepharose followed by chromatography on phenyl-agarose. Active proteins eluted between 4.5 and 0% ammonium sulfate, when a linear gradient was applied. Three major STK derivatives of 47.5 kDa, 45 kDa and 32 kDa were detected by Western blot analysis with a polyclonal antibody. The 32-kDa protein formed a complex with human plasminogen but did not exhibit Glu-plasminogen activator activity, as revealed by a zymographic assay, whereas the 45-kDa protein showed a K(m) = 0.70 microM and kcat = 0.82 s-1, when assayed with a chromogen-coupled substrate. These results suggest that these proteins are putative fragments of STK, possibly derived from partial degradation during the export pathway or the purification steps. The 47.5-kDa band corresponded to the native STK, as revealed by peptide sequencing.
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PMID:Cloning, expression and purification of recombinant streptokinase: partial characterization of the protein expressed in Escherichia coli. 968 61

Although the tear film has been extensively studied as it exists in the open eye state, until recently very little was known as to what happens to the tear film on eye closure. Recent studies have shown that eye closure results in a profound change in the composition, origins, turnover and physiological functions of the tear film. These changes include a shift from an inducible, neurologically controlled, lacrimal secretion containing among other proteins primarily lysozyme, lactoferrin and tear specific lipocalin, to a much slower, constitutive-type of secretion, composed almost exclusively of sIgA. This change is accompanied by the build-up of sialoglycoproteins of epithelial and goblet cell origin, the build-up and activation of complement and the build-up of serum proteins. In addition, various cytokines and proinflammatory mediators accumulate, including some which are potent inducers of angiogenesis and leukochemotaxis. The closed eye also exhibits the recruitment and activation of massive numbers of PMN cells. This results in a stagnant, closed eye layer, which is extremely rich in reactive complement products, PMN cell proteases including protease-3, elastase, capthepsin G, MMP-9 and urokinase. We have postulated that this shift represents a fundamental change in host-defense strategies from a passive-barrier defense to an active immune, inflammatory, phagocyte-mediated process and that this shift is necessitated in order to protect the cornea from entrapped microorganisms. Studies have shown that autologous cell damage is avoided in closed eye tear fluid, by the accumulation of several modulators of complement activation, which shift activation towards opsonization of entrapped microorganisms and the build-up of a wide array of antiproteases. Some of the latter are likely to arise from the ocular surface tissues. Corneal neovascularization may be avoided in part by the build-up of alpha2-macroglobulin and the conversion of plasminogen to angiostatin. It is highly probable that other bioactive protein fragments are produced in the closed eye, which contribute to homeostasis. Areas of future study are indicated.
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PMID:Towards a closed eye model of the pre-ocular tear layer. 1102 50

Photonic induced immobilization is a novel technology that results in spatially oriented and spatially localized covalent coupling of biomolecules onto thiol-reactive surfaces. Immobilization using this technology has been achieved for a wide selection of proteins, such as hydrolytic enzymes (lipases/esterases, lysozyme), proteases (human plasminogen), alkaline phosphatase, immunoglobulins' Fab fragment (e.g., antibody against PSA [prostate specific antigen]), Major Histocompability Complex class I protein, pepsin, and trypsin. The reaction mechanism behind the reported new technology involves "photonic activation of disulfide bridges," i.e., light-induced breakage of disulfide bridges in proteins upon UV illumination of nearby aromatic amino acids, resulting in the formation of free, reactive thiol groups that will form covalent bonds with thiol-reactive surfaces (see Fig. 1). Interestingly, the spatial proximity of aromatic residues and disulfide bridges in proteins has been preserved throughout molecular evolution. The new photonic-induced method for immobilization of proteins preserves the native structural and functional properties of the immobilized protein, avoiding the use of one or more chemical/thermal steps. This technology allows for the creation of spatially oriented as well as spatially defined multiprotein/DNA high-density sensor arrays with spot size of 1 microm or less, and has clear potential for biomedical, bioelectronic, nanotechnology, and therapeutic applications.
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PMID:Photonic activation of disulfide bridges achieves oriented protein immobilization on biosensor surfaces. 1643 46

Streptococcus suis serotype 2 (SS2) is a zoonotic pathogen that is distributed throughout the world. Virulence factors and/or markers of the virulent serotype 2 strains have not been fully identified. In this study a simple, rapid, and non-destructive method was used to extract cell wall-associated proteins from SS2 strains. Two virulent strains were compared with one avirulent strain by 2-dimensional electrophoresis (2DE). When the results of the 2DE analyses were combined with the results of mass spectrometry analyses, a total of 40 unique proteins were identified, including 26 antigens (2DE immunoblotting was used as a preliminary study). In addition to a known virulence factor, muramidase-released protein, two new proteins, catabolite control protein A and leucyl aminopeptidase, and nine potential virulence factors were also identified. The formers may be a potential virulence regulator or drug target, and the latter contains plasminogen-binding proteins and molecular chaperones. Our results complemented previous immunoproteomics studies of SS2 strains.
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PMID:Comparative proteomic analyses of Streptococcus suis serotype 2 cell wall-associated proteins. 2082 77


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