muramidase and Necrosis

Topics: Aged; alpha 1-Antichymotrypsin; Chymotrypsin; Collagen; Female; Histiocytes; Histiocytoma, Benign Fibrous; Humans; Mitosis; Muramidase; Necrosis; Stomach; Stomach Neoplasms; Vimentin

Deltamethrin (DM) is one of the most toxic but widely used pyrethroid insecticides. Even though a non-target animal, fish are at high risk as they are deficient in the enzyme system that hydrolyses pyrethroids. Enhancing the immune system is a potential method in preventing fish diseases. The present investigation aims to study the modulations in the immune response-related parameters in Oreochromis niloticus that were exposed to DM, by dietary supplementation of aqueous root extract of Asparagus racemosus (ARE). The experiment compared fish in control, DM (1 μg/L) exposed (added to water), ARE (10 g, 20 g, and 30 g ARE/kg of feed) supplemented, and DM-ARE cotreated groups. After 21 days of experimental period, serological, histopathological, and immune response related-gene and protein analysis were carried out. The DM-ARE cotreated group showed significant increase in weight gain, specific growth rate, and decreased feed conversion ratio compared to the DM exposed group. The ARE cotreatment could significantly revert the alteration induced by DM in lysozyme, respiratory burst, myeloperoxidase, C-reactive protein, glucose, cortisol, total protein, albumin, and triglyceride levels. The liver histopathology showed membrane breakage, severe necrosis, infiltration of inflammatory cells, melano-macrophages, and nuclear atrophy, and the kidney showed tubular necrosis, hematopoietic necrosis, Bowman's capsule edema, and glomerulus degeneration in DM exposed group. In ARE cotreated group, the liver showed regenerative cellular changes and only mild to moderate cellular damages, and the kidney tubules and glomerulus had intact structure. ARE discernibly regulated the expression of immune-related genes and proteins (IgM, TNFα, IFN-γ, IL-1β, and IL-8) in fish. The DM-ARE cotreated groups showed reduced cumulative mortality and higher relative percent survival on experimental challenge with Aeromonas hydrophila compared to the DM group. Thus, ARE possess protective potential against DM-induced toxicity, and can be used as a cost-effective technique in aquafarming.

Topics: Animal Feed; Animals; C-Reactive Protein; Cichlids; Diet; Dietary Supplements; Fish Diseases; Glucose; Hydrocortisone; Immunoglobulin M; Insecticides; Interleukin-8; Muramidase; Necrosis; Nitriles; Peroxidase; Plant Extracts; Pyrethrins; Triglycerides; Tumor Necrosis Factor-alpha; Water

The polymorphism of amyloid fibrils is potentially crucial as it may underlie the natural variability of amyloid diseases and could be important in developing a fuller understanding of the molecular basis of protein deposition disorders. This study examines morphological differences in lysozyme fibrils and the implications of these differences in terms of cytotoxicity. The structural characteristics of amyloid fibrils formed under two different experimental conditions (acidic and neutral) were evaluated using spectroscopic methods, atomic force microscopy and image analysis. Growth curves and apoptotic/necrotic assays were used to determine the cytotoxic effect of fibrils on the LLC-PK1 renal cells. The results reveal that both types of mature lysozyme amyloid fibrils are actively involved in the cytotoxic process, however each exhibit different levels of cytotoxicity. Fibrils formed at acidic pH affect cell growth in a dose-dependent manner, but a threshold-dependent inhibition of cell growth was observed in the case of lysozyme fibrils prepared at neutral pH. Experiments examining the mechanism of the cell death suggest that both types of mature lysozyme fibrils trigger late apoptosis/necrosis at different fibril concentrations. Our findings clearly indicate that the intrinsic differences between amyloid fibrils due to their polymorphism result in different degrees of cytotoxicity.

Topics: Amyloid; Animals; Apoptosis; Cell Proliferation; Cytotoxins; Epithelial Cells; Hydrogen-Ion Concentration; Kidney; Muramidase; Necrosis; Protein Multimerization; Protein Structure, Secondary

The present study was designed to investigate the immunotoxicity of atrazine (ATZ) in male Balb/c mice. ATZ (175, 87.5, and 43.75 mg/kg bw/day) was administered by gavage method for 28 days. The following indexes were determined in various groups of mice: body and organ weight; antibody aggregation of serum hemolysin; proliferative response of splenocytes to ConA; delayed-type hypersensitivity (DTH); natural killer cell activity; clearance of neutral red and nitric oxide (NO) release from peritoneal macrophages; apostosis and necrosis of splenocytes and thymocytes; cytokine production; and serum lysozyme. Results showed that cell-mediated, humoral immunity, and non-specific immune function in the high-dose ATZ group were suppressed; NO release and interferon-γ(IFN-γ)/interleukin-4 (IL-4) were also significantly decreased in the high-dose group. In the medium-dose group, the proliferation response and IFN-γ production was significantly decreased. In the low-dose group, the proliferation response was significantly decreased. Serum lysozyme was decreased in the ATZ-treated groups. The percentage of early apoptosis in thymocytes was increased significantly in high- and medium-dose ATZ groups. In conclusion, ATZ elicited an inhibitory effect on cell-mediated immunity, humoral immunity, and non-specific immune function of mice.

Topics: Animals; Apoptosis; Atrazine; Body Weight; Dose-Response Relationship, Drug; Dose-Response Relationship, Immunologic; Herbicides; Immunity, Humoral; Interferon-gamma; Interleukin-4; Macrophages, Peritoneal; Male; Mice; Mice, Inbred BALB C; Muramidase; Necrosis; Organ Size; Spleen; Thymocytes; Toxicity Tests, Acute

The prevalence of infections with enterococci is increasing worldwide. However, little is known about the mechanisms which enable these opportunistic pathogens to cause infections of their host. Here we demonstrate that Enterococcus faecium in the presence of lysozyme induces necrosis in human and mouse cells after 4 h indicated by disrupted cellular membranes of epithelial (HeLa), myeloid (U937, J774A.1) and lymphoid (Jurkat J16, thymocytes), but not intestinal epithelial cells (CaCo-2, CMT-93). Using an appropriate mutant strain it was shown that the enterococcal surface-protein SgrA is involved in cell death induction in mouse cells (J774A.1, thymocytes). Microscopic analyses of epithelial cells 30 min post infection revealed that lysozyme increases adhesion of E. faecium to HeLa, but not CaCo-2 cells. At that time the phalloidin-FITC-stained cytoskeleton of infected cells was still intact, whereas 2 h post infection the F-actin network of HeLa, but not CaCo-2 cells was disrupted. Hence, the early, lysozyme-mediated increase of bacterial adherence plays an important role for cell death induction by E. faecium in HeLa cells. Moreover, bacterial extracellular hydrogen peroxide might contribute to necrosis induction, since the rate of propidium iodide-positive HeLa and J774A.1 cells was lowered after infection with a ROS-deficient E. faecium mutant.

Topics: Animals; Bacterial Adhesion; Bacterial Proteins; Caco-2 Cells; Cell Death; Cell Line; Enterococcus faecium; Epithelial Cells; Gram-Positive Bacterial Infections; HeLa Cells; Humans; Mice; Muramidase; Necrosis; Reactive Oxygen Species; U937 Cells

Enterococci are commensal organisms in the alimentary tract. However, they can cause a variety of life-threatening infections, especially in nosocomial settings. We hypothesized that induction of cell death might enable these facultative pathogenic bacteria to evade the innate immune response and to cause infections of their host. We demonstrate that E. faecium when exposed to lysozyme induces cell death in macrophages in vitro and in vivo. Flow cytometric analyses of J774A.1 macrophages infected with E. faecium revealed loss of cell membrane integrity indicated by uptake of propidium iodide and decrease of the inner mitochondrial transmembrane potential DeltaPsi(m). Inhibition of caspases, treatment of macrophages with cytochalasin D, or rifampicin did not prevent cells from dying, suggesting cell death mechanisms that are independent of caspase activation, bacterial uptake, and intracellular bacterial replication. Characteristics of necrotic cell death were demonstrated by both lack of procaspase 3 activation and cell shrinkage, electron microscopy, and release of lactate dehydrogenase. Pretreatment of E. faecium with lysozyme and subsequently with broad spectrum protease considerably reduced cell death, suggesting that a bacterial surface protein is causative for cell death induction. Moreover, in a mouse peritonitis model we demonstrated that E. faecium induces cell death of peritoneal macrophages in vivo. Altogether, our results show that enterococci, under specific conditions such as exposure to lysozyme, induce necrotic cell death in macrophages, which might contribute to disseminated infections by these facultative pathogenic bacteria.

Topics: Animals; Apoptosis; Bacterial Proteins; Caspase 3; Caspases; Cell Death; Cross Infection; Enterococcus faecium; Female; Macrophages; Macrophages, Peritoneal; Membrane Potentials; Mice; Mice, Inbred C57BL; Mitochondria; Muramidase; Necrosis

A cage study was conducted to demonstrate the effect of Entegard REV, a lysozyme-based antimicrobial blend, on the performance of broiler chickens and necrotic enteritis (NE) disease reduction of birds that were challenged with Eimeria maxima and Clostridium perfringens. In the experiment, challenge by the infectious agents without medication resulted in impaired feed consumption, weight gain, and feed conversions and caused high incidence of gross NE lesions and NE mortality rate. Entegard REV included in feed at 200 g/metric ton (MT) was very effective in reducing negative health effects in the birds after NE challenge, and its ability to control the disease was not statistically different from a commonly used antibiotic growth promotant, bacitracin methylene disalicilate, at 55 g/MT.

Topics: Animal Feed; Animals; Anti-Bacterial Agents; Chickens; Clostridium Infections; Clostridium perfringens; Coccidiosis; Eimeria; Enteritis; Muramidase; Necrosis; Poultry Diseases

Among the newly discovered amyloid properties, its cytotoxicity plays a key role. Lysozyme is a ubiquitous protein involved in systemic amyloidoses in vivo and forming amyloid under destabilising conditions in vitro. We characterized both oligomers and fibrils of hen lysozyme by atomic force microscopy and demonstrated their dose (5-50 microM) and time-dependent (6-48 h) effect on neuroblastoma SH-SY5Y cell viability. We revealed that fibrils induce a decrease of cell viability after 6 h due to membrane damage shown by inhibition of WST-1 reduction, early lactate dehydrogenase release, and propidium iodide intake; by contrast, oligomers activate caspases after 6 h but cause the cell viability to decline only after 48 h, as shown by fluorescent-labelled annexin V binding to externalized phosphatidylserine, propidium iodide DNA staining, lactate dehydrogenase release, and by typical apoptotic shrinking of cells. We conclude that oligomers induce apoptosis-like cell death, while the fibrils lead to necrosis-like death. As polymorphism is a common property of an amyloid, we demonstrated that it is not a single uniform species but rather a continuum of cross-beta-sheet-containing amyloids that are cytotoxic. An abundance of lysozyme highlights a universal feature of this phenomenon, indicating that amyloid toxicity should be assessed in all clinical applications involving proteinaceous materials.

Topics: Amyloid; Animals; Annexin A5; Apoptosis; Caspases; Cell Survival; Electrophoresis, Polyacrylamide Gel; Fluorescence; Hydrophobic and Hydrophilic Interactions; Kinetics; L-Lactate Dehydrogenase; Microscopy, Atomic Force; Muramidase; Necrosis; Oxidation-Reduction; Protein Structure, Quaternary; Solubility; Tetrazolium Salts

Pathological examination in the spleen of an 81-year old female with hemoperitoneum, hypovolemic shock, anemia, thrombocytopenia and hyperglicemia revealed the presence of an angiosarcoma. On histological examination, characteristically the neoplasm was formed by vascular lumina and cystic spaces into which papillary fronds projected and solid nests. Neoplastic cells had scant cytoplasm, hyperchromatic, oval or reniform nuclei, with prominent nucleoli. The necrosis was evident and mitoses were frequent. Immunohistochemical analysis revealed positivity for endothelial (CD31, CD34) and histiocytic markers (CD68 and lysozyme) and negativity for CD21. Ultrastructural examination also disclosed a biphasic differentiation, showing the presence of organelles associated with histiocytic and endothelial differentiation. These findings suggest that this lesion can be considered a conventional splenic angiosarcoma with focal histocytic differentiation.

Topics: Aged, 80 and over; Antigens, CD; Biomarkers, Tumor; Cell Nucleus; Fatal Outcome; Female; Hemangiosarcoma; Humans; Lysosomes; Muramidase; Necrosis; Rupture, Spontaneous; Splenic Neoplasms; Splenic Rupture

Atlantic salmon parr were injected intraperitoneally with salmon pancreas disease virus (SPDV) grown on CHSE-214 cells. The viraemia, the histopathological changes in target organs and some immune parameters were taken at intervals up to 30 days post-infection (dpi). The earliest kind of lesion was necrosis of exocrine pancreas, appearing as soon as 2 dpi. It progressed towards complete tissue breakdown at 9 dpi before resolving gradually. Concurrent to this necrosis, a strong inflammatory response was in evidence from 9 dpi in the pancreatic area for a majority of fish. A necrosis of the myocardial cells of the ventricle occurred in infected fish mainly at 16 dpi and it faded thereafter. The monitoring of the plasma viral load showed a rapid haematogenous spreading of SPDV, peaking at 4 dpi, but also the absence of a secondary viraemia. No interferon (IFN) was detected following the infection of parr with SPDV, probably owing to an IFN activity in Atlantic salmon below the detection level of the technique. Neutralising antibodies against SPDV were in evidence from 16 dpi and they showed a time-related increasing titre and prevalence. The phagocytic activity in head-kidney leucocytes was always significantly higher in the infected fish than in the control fish, being particularly high by 9 dpi. Lysozyme and complement levels were both increased and they peaked significantly in the infected fish at 9 and 16 dpi respectively. These results demonstrated that an experimental infection of Atlantic salmon parr with SPDV provoked a stimulation of both specific and non-specific immunity with regards to the viraemia and the histopathology.

Topics: Alphavirus; Alphavirus Infections; Animals; Antibodies, Viral; Cells, Cultured; Complement Pathway, Classical; Fish Diseases; Immunohistochemistry; Injections, Intraperitoneal; Interferons; Muramidase; Necrosis; Pancreas; Pancreatic Diseases; Phagocytosis; Salmo salar; Time Factors; Viremia

Recent studies have demonstrated that circulating antibodies against malondialdehyde-acetaldehyde (MAA)-haptenated proteins are significantly increased in patients with alcohol-induced cirrhosis and hepatitis and correlate with the severity of liver damage. Additionally, when proteins are haptenated with MAA, they become highly immunogenic in vivo in the absence of adjuvants. However, the mechanism(s) of this immunogenicity are currently unknown. Initial in vitro studies on the effects of MAA-modified proteins on cells demonstrated an increase in cell death at concentrations that were cell type specific and time-dependent. Since immunogenicity due to cell death has been described, we investigated the mechanism(s) by which cell death was occurring. Assessment of cell death in splenocytes after 1 h found significant levels of apoptosis as compared to controls. After 5 h, a significant and dose-dependent necrosis occurred in which cells were exposed to >62.5 microg/ml (43.1 mM) MAA-haptenated protein. After 24 h, exposure to >31.3 microg/ml (21.6 mM) MAA-haptenated protein resulted in significant levels of necrosis, although DNA laddering studies found apoptosis was occurring as well. Morphological changes in the cells were observed by light microscopy that correlated with a "low" forward scatter population by flow cytometry. Since necrosis has been implicated in enhancing both primary and secondary immune responses, and necrosis was predominantly occurring in response to MAA-haptenated proteins, a possible mechanism by which the immunogenicity of MAA modification of proteins in vivo may occur is suggested. Specifically, MAA modification of self proteins may result in the death of various cell types, most likely those in the liver. These necrotic materials may induce anti-MAA antibodies and other auto antibodies, whose levels may then correlate with the severity of ALD.

Topics: Acetaldehyde; Animals; Annexin A5; Apoptosis; B-Lymphocytes; DNA Fragmentation; Female; Flow Cytometry; Haptens; In Situ Nick-End Labeling; Malondialdehyde; Mice; Mice, Inbred C3H; Muramidase; Necrosis; Spleen; T-Lymphocytes

Haemophilus ducreyi is the causative bacterium of genital ulcers, which are collectively known as chancroid. Little is known about the cytotoxicity of H. ducreyi. The virulent strains are relatively resistant to phagocytosis and apoptosis by neutrophils. Therefore, experiments were designed to examine whether neutrophil degranulation caused by H. ducrey would provide insights into the virulence mechanisms through which cellular damage is affected by the organism. Clinical isolates of eight strains of H. ducreyi and the culture strain type CIP542 (Collection Institute Pasteur) were incubated with neutrophils harvested from human donor blood. The release by the organism of lysosomal enzymes from intracellular granules of neutrophils was indicative of degranulation. The results showed that H. ducreyi triggered the release of lysosomal enzymes from human neutrophils, and that the magnitude of the release was dependent both on the ratio of bacteria to neutrophils and the duration of incubation. In vitro experiments involving HeLa cells were designed to determine the manner in which H. ducreyi initiated the process of degranulation. The morphological changes associated with degranulation were visualized by confocal and transmission electron microscopy. This is the first report that describes degranulation of neutrophils induced by H. ducreyi which causes chancroid infection.

Topics: Cathepsin D; Coculture Techniques; Cytoplasmic Granules; Haemophilus ducreyi; HeLa Cells; Humans; Microscopy, Confocal; Microscopy, Electron; Muramidase; Necrosis; Neutrophils; Peroxidase

Flow cytometry was used to quantify apoptotic and necrotic polymorphonuclear (PMN) cells in an exudate generated by biomaterials, and the results were compared with determinations of spontaneous apoptosis and necrosis in PMN cells from the bloodstream. The exudate formed inside cylindrical tubes subcutaneously implanted in the dorsal region of rats was collected over a 1-week period. A rapid and simple staining procedure based on the spectral properties of the bisbenzemide Hoechst 33342 was used to identify apoptotic PMN cells. Quantification of permeabilized PMN cells stained by propidium iodide was possible in the same unfixed specimens. The percentages of apoptotic and permeabilized PMN cells in peripheral rat blood were low (1.8 +/-0 0.5% and 1.7 +/- 0.7%, respectively), similar to results found in humans. In exudates generated by polyvinyl chloride (PVC), the percentages of apoptotic and permeabilized PMN cells were higher than in the blood. The percentage of PMN cells undergoing apoptosis progressively increased with time and reached a maximum at day 2 (27% +/- 6%). The percentage of permeabilized cells progressively increased with time and was much higher than the percentage of apoptotic cells on days 4 and 8. Apoptosis and necrosis of PMN cells at day 2 were inhibited when tubes were filled with 10% serum. Selective inhibition of apoptosis with a caspase inhibitor in vivo indicated that apoptosis and necrosis are two separate pathways leading to the death of PMN cells in the exudate. At day 2, polyurethane (PU) was associated with a lower rate of apoptosis than PVC or a random copolymer of trimethylene carbonate (TMC) and epsiloncaprolactone (ECL). Apoptosis was interpreted as an organized cell removal process that limits inflammation. Apoptosis was the natural route of PMN cell death at the early stage of inflammation.

Topics: Animals; Apoptosis; Biocompatible Materials; Cell Membrane Permeability; Cells, Cultured; Cysteine Proteinase Inhibitors; Exudates and Transudates; Fibroblasts; Flow Cytometry; Foreign-Body Reaction; Humans; Lactones; Male; Materials Testing; Muramidase; Necrosis; Neutrophils; Polyesters; Polymers; Polyurethanes; Polyvinyl Chloride; Prostheses and Implants; Prosthesis Implantation; Rats; Rats, Wistar; Time Factors

T cell receptor (TCR) transgenic mice specific for hen egg lysozyme (HEL) were crossed with mice expressing HEL on the thyroid epithelium, on pancreatic islet beta cells, or systemically. Depending on the pattern of HEL expression, deletion of double-positive thymocytes ranged from minimal to complete, and peripheral CD4 cells exhibited graded reduction in TCR expression, in vitro responsiveness, and in vivo helper ability. CD4 cells were least tolerant in TCR/thyroid-HEL and TCR/islet-HEL mice, which developed an extensive lymphocytic thyroiditis or insulitis that nevertheless did not eliminate HEL-expressing endocrine cells. Autoreactive CD4 clones thus escape the thymus under a range of circumstances, retain sufficient function to initiate subclinical autoimmune inflammation when self-antigens are concentrated in the thyroid or pancreas, and may regulate progression of subclinical inflammation to destructive autoimmune disease.

Topics: Animals; CD4-Positive T-Lymphocytes; Cell Movement; Chickens; Enzyme Activation; Epitopes, T-Lymphocyte; Immune Tolerance; Immunophenotyping; Inflammation; Islets of Langerhans; Lymphocyte Count; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Muramidase; Necrosis; Organ Specificity; Receptors, Antigen, T-Cell, alpha-beta; Thyroid Gland; Thyroiditis, Autoimmune

The material comprised 15 cases of ischemic brain stroke at the age of 45 to 101 years. Six brain of subjects deceased at the age of 45 to 57 years and 9 brains of those deceased at the age of 80 to 101 years were studied. Phagocytic cell immunoreactivity in both age groups during the first 5 days and on the 11th and 12th were compared. Phagocytic reactivity in cases of patients who died on the 6th, 15th and 35th days after stroke onset was also estimated. Colliquative necrosis with cavitation was observed in middle-aged cases from the 3rd infarction day. In the senile group the beginning of tissue breakdown was noted on the 5th day, but colliquative necrosis with cavitation was found on the 11th infarction day. Senile alterations in the biochemical components in various brain tissue elements are probably the cause of the different course and dynamics of the pathological process.

Topics: Aged; Aging; Autopsy; Brain; Brain Ischemia; Female; Humans; Immunohistochemistry; Male; Middle Aged; Muramidase; Necrosis; Phagocytes

Since gender can influence the renal toxicity of a drug in a given species, the present study was undertaken to evaluate the role of sex in the protection against gentamicin (G)-induced nephrotoxicity afforded by diabetes mellitus (DM) in the rat. We have compared the effects of administration of G (40 mg/kg/day, for 14 days) on male and female DM Sprague-Dawley rats. Non-diabetic animals of both sexes receiving identical doses of G served as controls. At the end of the experiment on day 14, both female (F) and male (M) control groups had similar and marked evidence of nephrotoxicity: elevation of plasma creatinine (F 1.7 +/- 0.7; M 2.8 +/- 0.6 mg/dl), decrease in endogenous 24-h creatinine clearance (Ccr) (F0.3 +/- 0.1; M 0.2 +/- 0.1 ml/min/100 g BW), and histological evidence of severe acute tubular necrosis. In marked contrast, the DM rats showed no functional or morphological evidence of renal damage throughout the study regardless of their gender (day 14: plasma creatinine: F 0.2 +/- 0.03; M 0.2 +/- 0.02; Ccr: F 1.2 +/- 0.1; M 1.6 +/- 0.1 ml/min/100 g BW), and they also accumulated less G in their kidney cortex than the C rats. The male controls exhibited higher renal cortex accumulation of G than the female controls (p < 0.05), whereas the opposite occurred in the DM groups (p < 0.01). Because the validity of using Ccr for the evaluation of GFR changes in experimental nephrotoxicity has been questioned, we have compared, in a separate experiment, three different methods of estimation of GFR (simultaneous short clearances of inulin and Ccr, and 24-h Ccr) in conscious female Sprague-Dawley rats undergoing the same treatment with G described above. At no time during the study did the method used for estimation of the GFR influence the results. We conclude that male and female Sprague-Dawley rats with diabetes are functionally and morphologically equally protected against G. Furthermore, no gender-related differences in the magnitude of G-induced nephrotoxicity was demonstrated in the non-diabetic control animals.

Topics: Animals; Creatinine; Diabetes Mellitus, Experimental; Female; Gentamicins; Glomerular Filtration Rate; Kidney; Kidney Cortex; Kidney Tubules; Male; Muramidase; Necrosis; Rats; Rats, Sprague-Dawley; Sex Characteristics

Thirty-six cases of necrotizing lymphadenitis--including 33 cases of unknown etiology, 1 typhoid lymphadenopathy, and 2 cases of suspicious lupus lymphadenopathy--were clinico-pathologically reviewed and analyzed with immunostaining for s-100 and lysozyme. All cases histologically showed architectural effacement by paracortical lesions composed of nuclear karyorrhexis and mononuclear cell proliferation. Immunohistochemical study revealed proliferation of lysozyme-positive macrophages in the necrotizing areas and an increase in the number of s-100-positive cells in the uninvolved paracortical areas. This observation suggests that necrotizing lymphadenitis may be a common morphologic expression of a T cell-mediated hyperimmune condition induced by diverse etiologies.

Topics: Adolescent; Adult; Female; Humans; Immunohistochemistry; Lymphadenitis; Male; Muramidase; Necrosis; S100 Proteins

A study was made of the disease pathogenesis in 58 patients with recurrent chronic erosions of the gastric mucosa. It has been established that an important role in the relapses of the pathological process is played by pathological microflora, disturbances in humoral immunity and local microcirculation, and long existence of the zone of fibrinoid necrosis.

Topics: Adult; Chronic Disease; Complement System Proteins; Enterococcus faecalis; Escherichia coli; Female; Gastric Mucosa; Humans; Hypergammaglobulinemia; Immunoglobulin G; Male; Middle Aged; Muramidase; Necrosis; Recurrence; Stomach Ulcer; Time Factors

The number and distribution of lysozyme and S100 immunoreactive cells were analyzed in ten cases of lymph node sarcoidosis. Three phases of granuloma development could be differentiated, each showing a typical immunohistological pattern. The early small granulomas consisted of lys- or very weakly lys+ mononuclear phagocytes and developed within an area of focalized accumulation of S100+ antigen-presenting cells. The mature large granulomas were composed of polygonal epithelioid cells with abundant cytoplasm showing very strong granular lysozyme positivity. S100+ cells could still be observed, mainly around the granulomas, but in diminished number. In the final fibrozing phase the epithelioid cells lost their lysozyme immunoreactivity and no S100+ antigen-presenting cells were present within or around the granulomas. In one patient granulomas with central necrosis and palisading, lys- epithelioid cells were also observed, possibly representing a different microenvironment (antigen/antibody equilibrium?). The change in the pattern and number of lysozyme and S100 immunoreactive cells probably reflects the development of the granulomas and is related to the activity of the disease.

Topics: Epithelium; Granuloma; Histocytochemistry; Humans; Lymph Nodes; Lymphatic Diseases; Muramidase; Necrosis; S100 Proteins; Sarcoidosis; Staining and Labeling

Immunohistochemical investigations were carried out on the properties of the cells and extracellular matrix (ECM) in focal hepatic injuries. A liquid nitrogen-cooled syringe needle was thrust into the rat liver. Necrotic areas became permeated with plasma within 24-hour period. Areas became strongly positive for fibronectin and were infiltrated with inflammatory cells positive for lysozyme. By the third day, Ito cells were proliferated in the peripheral portions of the damaged areas. These Ito cells showed enhanced immunostaining for desmin and actin but were negative for lysozyme. Interstitial fibers which were immunochemically positive for Types I and IV collagens, laminin, and fibronectin, began to increase from Day 3. They appeared on the rim of the hepatocytes adjacent to the damaged areas and extended into the injured regions with the Ito cells. An increase in basal laminas associated with capillaries and bile ducts also increased with a 1-day delay. The damaged areas were replaced by granulation tissue by Day 5. A rapid diminution then occurred in the granulation tissue, and normal hepatic tissue was restored in 7-10 days. These observations demonstrate that ECM changed in a sequential manner and then finally disappeared from the damaged site within 10 days. Although various cells, including parenchymal cells, macrophages, endothelial cells, and cholangiolar cells contributed to the healing of the damaged area, Ito cells, which exhibit unique phenotypic changes, presumably had a major role in the process.

Topics: Actins; Animals; Antibodies, Monoclonal; Desmin; Extracellular Matrix; Histocytochemistry; Immunochemistry; Liver; Male; Muramidase; Necrosis; Rats; Rats, Inbred Strains; Time Factors; Wound Healing

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.

Topics: Antigen-Antibody Complex; Antigens; Complement System Proteins; Humans; Immunoenzyme Techniques; Immunoglobulins; Leishmania; Leishmaniasis; Muramidase; Necrosis; Skin

To verify whether renal tubular dysfunction may account for the CAm/CCr enhancement in acute pancreatitis (AP), we have measured the renal excretion of amylase, lysozyme, and gamma-glutamyl-transpeptidase (GGTP) in 22 patients with AP and in 8 with acute tubular necrosis. While the CAm/CCr ratio was elevated in most patients with AP, the CLys/CCr ratio fell within the normal range in 60% of these patients. The subdivision of patients with AP in subgroups with elevated and normal CLys/CCr ratios revealed a mean CAm/CCr not statistically different. Moreover, no correlation was present in AP between amylase vs. both lysozyme and GGTP clearances. These data suggest that tubular dysfunction does occur in some but not in all the patients with AP and seems not to play a major role in the pathogenesis of the increased CAm/CCr ratio in this condition.

Topics: Acute Disease; Amylases; Creatinine; gamma-Glutamyltransferase; Humans; Kidney Tubules; Muramidase; Necrosis; Pancreatitis

Topics: Antigen-Antibody Complex; B-Lymphocytes; Capillary Permeability; Cell Migration Inhibition; Chemotaxis, Leukocyte; Eosinophils; Granuloma; Humans; Immunologic Deficiency Syndromes; Inflammation; Lymphocyte Activation; Macrophages; Monocytes; Muramidase; NAD; NADP; Necrosis; Neutrophils; Opsonin Proteins; Phagocytes; Phagocytosis; T-Lymphocytes

This review deals with those biological activities of peptidoglycan that are not directly analogous to the properties of gram-negative bacterial endotoxin. The report is divided into 3 major parts: 1. A survey of peptidoglycan activities such as the induction of inflammatory skin reactions, lesion-enhancing activity (virulence factor), inhibition of phagocytosis of bacteria, inhibition of cell migration, cytotoxicity to mammalian cells, potentiation of the humoral and cellular immune response (adjuvant activity) and enhancement of tumor defense in experimental animals. 2. A presentation of factors which may influence these biological activities of peptidoglycan. 3. A brief discussion of the potential mechanisms of action of peptidoglycan.

Topics: Adjuvants, Immunologic; Animals; Antibodies, Bacterial; Bacillus megaterium; Cell Migration Inhibition; Chemotaxis; Inflammation; Muramidase; Necrosis; Neutralization Tests; Peptidoglycan; Phagocytosis; Skin Manifestations; Staphylococcal Infections; Staphylococcus; Streptococcus; Virulence

Topics: Biopsy; Conjunctiva; Eye Diseases; Hexosamines; Humans; Keratoconjunctivitis; Lacrimal Apparatus; Lacrimal Duct Obstruction; Methods; Mucus; Muramidase; Necrosis; Pemphigus; Proteins; Radiography; Reflex; Rose Bengal; Secretory Rate; Staining and Labeling; Tears

Topics: Amides; Animals; Antibodies; Bilirubin; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cryptococcosis; Ethanol; Hexachlorocyclohexane; Hyperbilirubinemia; Iron; Liver; Liver Diseases; Male; Muramidase; Naphthalenes; Necrosis; Nitrosamines; Protein Deficiency; Rats; Sulfhydryl Compounds; Thiocyanates