acid-phosphatase and Chediak-Higashi-Syndrome

Chediak-Higashi syndrome (CHS) is an inherited immunodeficiency disorder characterized by giant lysosomal granules in all granule-containing cells. Prior examination of lysosomal enzyme activities in granulocytes and other cells derived from patients with CHS have revealed multiple abnormalities, with the predominant finding being diminished activity of many of the enzymes tested. Abnormalities in lysosomal enzyme activity are also found in animal models of CHS (cattle, aleutian mink, and beige mice). In this study, we have examined lymphoblastoid cell lines derived from a patient with CHS and from an individual heterozygous for the CHS gene for acid phosphatase, beta-glucuronidase, and alpha-mannosidase activity. These cell lines have recently been shown to be satisfactory in vitro models for the disease. Acid phosphatase activity was increased in the heterozygous-derived cell line when compared to control while other enzyme activities were normal both in the CHS- and heterozygous-derived cell lines. We have reviewed the literature and summarized published abnormalities of lysosomal enzyme activities in humans and animals with CHS.

Topics: Acid Phosphatase; alpha-Mannosidase; Animals; Cell Line, Transformed; Cells, Cultured; Chediak-Higashi Syndrome; Disease Models, Animal; Glucuronidase; Humans; Lysosomes; Mannosidases

Topics: Acid Phosphatase; Animals; Cathepsins; Chediak-Higashi Syndrome; Fabry Disease; Inflammation; Keratins; Langerhans Cells; Light; Lysosomes; Melanophores; Microscopy, Electron; Peptide Hydrolases; Phagocytosis; Pigmentation; Protease Inhibitors; Sebaceous Glands; Skin; Skin Diseases; Skin Neoplasms; Vitamin A

Topics: Acid Phosphatase; Agranulocytosis; Blood Bactericidal Activity; Chediak-Higashi Syndrome; Chemotaxis; Child, Preschool; Complement System Proteins; Cytoplasmic Granules; Female; Glucosephosphate Dehydrogenase Deficiency; Humans; Immunologic Deficiency Syndromes; Infant, Newborn; Infant, Premature; Leukocytes; Liver; Lysosomes; Macrophages; Male; Monocytes; Mononuclear Phagocyte System; Muramidase; NADH, NADPH Oxidoreductases; Neutrophils; Opsonin Proteins; Peroxidases; Phagocyte Bactericidal Dysfunction; Phagocytosis; Spleen

Topics: Acid Phosphatase; Acid-Base Equilibrium; Chediak-Higashi Syndrome; Cytoplasm; Diffuse Cerebral Sclerosis of Schilder; Gaucher Disease; Genes, Recessive; Glycogen Storage Disease; Humans; Hydrolases; Lipidoses; Lysosomes; Metabolism, Inborn Errors; Niemann-Pick Diseases

Chediak-Higashi syndrome (CHS) is a rare disease occurring in several animal species. Recently, mutant beige rats with CHS were found among DA strain rats in Japan. In the present study, histological examination of beige rats revealed giant granules in the hepatocytes, renal proximal tubules, submandibular ducts, thyroid follicular cells, granulocytes, mast cells, melanocytes, retinal pigment epithelial cells and globular leucocytes. Ultrastructurally, these granules varied from enlarged lysosomes, which were amorphous, granular or filamentous, to giant mast cell granules, crystalloid granules of eosinophils and slightly enlarged neutrophil granules. These findings bore many similarities to those in the beige mouse, which is a well known animal model for CHS, but some differences were apparent. Thus the giant granules of beige rats were larger and more easy to observe than those in beige mice. The study indicated that the beige rat may prove useful as an animal model for CHS.

Topics: Acid Phosphatase; Animals; Chediak-Higashi Syndrome; Cytoplasmic Granules; Female; Leukocytes; Male; Mast Cells; Melanocytes; Mice; Mice, Mutant Strains; Microscopy, Electron; Rats; Rats, Mutant Strains

We report the first prenatal diagnosis of an affected fetus with Chediak-Higashi syndrome (CHS). Diagnosis was accomplished via fetal blood sampling at 17 menstrual weeks and was confirmed after birth. Retrospective measurement of the largest acid phosphatase-positive lysosomes in cultured amniotic fluid cells and chorionic villus cells showed that in CHS these lysosomes are significantly larger than those in normal cells. This method may be used for prenatal diagnosis of CHS by amniocentesis and chorionic villus sampling (CVS).

Topics: Acid Phosphatase; Adult; Amniocentesis; Chediak-Higashi Syndrome; Chorionic Villi Sampling; Cordocentesis; Female; Humans; Lysosomes; Pregnancy; Pregnancy Trimester, Second

The autosomal recessive disease Chediak-Higashi syndrome (CHS) is a progressive and generally fatal disease of humans. The underlying genetic defect in CHS is unknown and prenatal diagnostic methods have not been applied to this disease. The purpose of this study was to determine if CHS chorionic cells expressed a characteristic of CHS--enlarged lysosomes--that would permit the prenatal diagnosis of the disease. Cats with CHS, which have been shown to be homologous with human CHS, were used as the model system in this study. Chorionic tissue samples were obtained from CHS and control cat fetuses and cultures of cells were established. Acid phosphatase was utilized as a marker of lysosomes and cultures of chorionic fibroblasts from CHS and control fetuses were stained histochemically for acid phosphatase. The diameter of the largest lysosomes in 150 cells of each fetus was determined. The mean (+/- SD) diameter (in microns) of the largest lysosomes of normal fetuses was 0.9 +/- 0.13 (range 0.5-7.0 microns), whereas the mean diameter of lysosomes in CHS chorionic cells was 3.9 +/- 0.65 microns (range 0.5-25 microns). These means were significantly different (P less than 0.0001). These data suggest that it should be possible to diagnose human CHS in the first trimester by chorionic villus sampling.

Topics: Acid Phosphatase; Animals; Cats; Cells, Cultured; Chediak-Higashi Syndrome; Chorion; Disease Models, Animal; Lysosomes; Prenatal Diagnosis; Statistics as Topic

The ultrastructure of lysosomes from megakaryocytes (MK) and platelets of cattle with the Chediak-Higashi syndrome (CHS) was characterized using acid phosphatase histochemistry with beta-glycerophosphate as substrate and cerium as a capturing agent. Acid phosphatase was localized in the trans aspect of the Golgi complex and/or granules in MK at all stages of maturation. Morphometric analysis of the diameter of each lysosome was performed on MK from CHS cattle and compared to MK from normal cattle. Lysosomes in CHS MK were neither enlarged nor different with respect to classification as secondary lysosomes, which composed 35% of the lysosomes in CHS MK. Lysosomes were demonstrated in 22% of the CHS platelet sections and appeared similar to those from normal cattle, 56% of them being classified as secondary lysosomes. Why lysosomes are not enlarged in bovine CHS MK and platelets, whereas they are enlarged in most other cell types, remains unknown.

Topics: Acid Phosphatase; Animals; Blood Platelets; Cattle; Cattle Diseases; Cell Survival; Chediak-Higashi Syndrome; Histocytochemistry; Lysosomes; Megakaryocytes; Microscopy, Electron

Chediak-Higashi syndrome (CHS) is an autosomal recessive disease in humans, cats, and 8 other species. The homology of CHS in humans and cats has been demonstrated. Since human CHS is a progressive, serious, and eventually fatal disease, a method for prenatal diagnosis would be desirable. This study was designed to determine whether CHS could be diagnosed prenatally by examination of amniotic fluid cells. The amniotic fluid samples were obtained from CHS and control cat fetuses on the 45th day of gestation and cultures of cells were established. Because the underlying enzyme deficiency in CHS has not been identified, it was necessary to use a secondary manifestation of the syndrome in these studies. The secondary manifestation used was the characteristic enlargement of lysosomes associated with the disease. The lysosomes of these cells were stained by acid phosphatase histochemistry and the diameter of the largest lysosome in each cell was measured by light microscopy with a calibrated ocular micrometer. The diameters of the largest lysosomes in cells of normal fetuses ranged from 0.5 to 7.0 micron (means ranged from 0.9 to 1.8 micron), whereas the diameter of the largest lysosomes in the cells of CHS fetuses ranged from 0.5 to 30 microns (means ranged from 6.4 to 12.8 microns). The approximate t-test for independent samples with unequal variances disclosed that the largest acid phosphatase-positive lysosomes in amniotic fluid cells of CHS cat fetuses were significantly larger than the lysosomes in the cells of normal cat fetuses (P less than 0.0001). This information should, by extrapolation, provide the basis for the prenatal diagnosis of human CHS by amniocentesis.

Topics: Acid Phosphatase; Amniocentesis; Amniotic Fluid; Animals; Cats; Cells, Cultured; Chediak-Higashi Syndrome; Disease Models, Animal; Female; Fetal Diseases; Lysosomes; Male; Phenotype

Topics: Acid Phosphatase; Animals; Chediak-Higashi Syndrome; Fibroblasts; Histocytochemistry; Lysosomes; Rats; Rats, Inbred Strains

The Chediak-Higashi syndrome (CHS) is an autosomal recessive genetic disease of humans, and clinically similar diseases occur in cats, mink, cattle, mice, killer whales, blue foxes, and silver foxes. It is characterized by incomplete albinism, increased susceptibility to infection, and the most distinctive hallmark, the presence of enlarged cytoplasmic granules in many cell types. The acid phosphatase-positive granules, lysosomes, of fibroblasts from control and CHS humans, cats, mink, cattle, and mice were examined. These studies represent the initial characterization of the lesions in fibroblasts of CHS cats, mink, and cattle. Fibroblasts from each species and genotype were stained histochemically for acid phosphatase, and morphometric analysis of the distribution of acid phosphatase-positive granules was performed. The lysosomes in the CHS fibroblasts tended to be restricted to the perinuclear area of the cytoplasm, whereas the lysosomes in the normal fibroblasts were generally more widely distributed in the cytoplasm. The lysosomes in the CHS fibroblasts of all species examined were also more enlarged and heterogeneous than those in the control fibroblasts.

Topics: Acid Phosphatase; Animals; Cats; Cattle; Cells, Cultured; Chediak-Higashi Syndrome; Disease Models, Animal; Fibroblasts; Genotype; Histocytochemistry; Humans; Lysosomes; Mice; Mink

Topics: Acid Phosphatase; alpha-Macroglobulins; Animals; Cell Membrane; Cells, Cultured; Chediak-Higashi Syndrome; Exocytosis; Fibroblasts; Inclusion Bodies; Lysosomes; Mice

Fibroblasts cultured from the skin of beige mice manifesting the Chédiak-Higashi syndrome (CHS), unlike cells derived from normal black mice, exhibited giant dense bodies in the cytoplasm. These megabodies were membrane-delimited and exhibited dense content by electron microscopy, with myelin figures, highly osmiophilic, thick membranous contours, and lucent areas. The megabodies evidenced acid phosphatase ultrastructurally. Cells of both normal and CHS mice contained smaller dense bodies. During a 2--6 hour exposure to colloidal gold, the smaller dense bodies of normal and CHS fibroblasts selectively incorporated the gold spherules and, accordingly, were identified as secondary lysosomes of heterophagic origin. With longer exposure to colloidal gold, the small dense bodies of the normal and CHS cells disclosed increased content of colloidal gold. After 24 hour exposure to colloidal gold, many giant dense bodies also exhibited gold particles, evidencing uptake of endocytosed material into the giant structures and the heterophagic origin of at least some of the content of the bodies. The gold spherules initially incorporated into the giant dense bodies were concentrated in foci along their periphery and indicated fusion of small dense bodies into the giant structures. Transformed normal and CHS cells appeared to contain more abundant myelin figures than nontransformed cells, and these were larger in transformed CHS cells and constituted a major component of their giant dense bodies. The giant inclusions of the transformed CHS cells generally contained little colloidal gold, suggesting their derivation principally through cellular autophagy.

Topics: Acid Phosphatase; Animals; Cells, Cultured; Chediak-Higashi Syndrome; Colloids; Endocytosis; Fibroblasts; Gold; Inclusion Bodies; Lysosomes; Mice; Mice, Inbred C57BL; Microscopy, Electron; Skin

Nine lysosomal enzyme activities were examined in granulocytes and lymphocytes from two unrelated patients with Chediak-Higashi syndrome (CHS) in "accelerated phase" and from their family members. In CHS granulocytes, there was a marked reduction of alpha-mannosidase (E.C. 3.2.1.24), alpha-galactosidase (E.C. 3.2.1.22), and alpha-fucosidase (E.C. 3.2.1.51) activities, which were below 21, 24, and 43% of mean control values, respectively. In CHS lymphocytes, beta-glucuronidase (E.C. 3.2.1.31) and alpha-mannosidase activities were also decreased. In granulocytes of family members, the activities of acid phosphatase (E.C. 3.1.3.2), N-acetyl-beta-glucosaminidase (E.C. 3.2.1.30), aryl sulphatase (E.C. 3.1.6.1), and beta-glucuronidase were significantly higher than the control values (P < 0.001), which were 262, 218, 414, and 180% of mean control values. Neither the inhibitor in CHS granulocytes nor the activator in the heterozygous granulocytes to those enzymes could be found by mixing experiments with normal ones.

Topics: Acetylglucosaminidase; Acid Phosphatase; alpha-L-Fucosidase; Arylsulfatases; Chediak-Higashi Syndrome; Child, Preschool; Fabry Disease; Female; Glucuronidase; Granulocytes; Heterozygote; Humans; Infant; Lymphocytes; Lysosomes; Male; Mannosidases

Topics: Acid Phosphatase; Adolescent; Chediak-Higashi Syndrome; Cytoplasmic Granules; Female; Humans; Leukemia, Monocytic, Acute

The beige mouse (bg/bg) is an analogue of the Chediak-Higashi syndrome (CHS) in man. The disorder is characterised by the presence of enlarged cytoplasmic granules, said to be lysosomes, in many cell types. The present report describes giant lysosomes defined as lysosomes greater than 1.0 micrometers in diameter, in osteoclasts of beige mice. The giant lysosomes contained both acid phosphatase and aryl sulphatase and were present in osteoclasts of beige mice aged from at least 4 days to 3 months. There is some evidence that the giant lysosomes form by fusion of smaller structures. Since giant lysosomes were also seen in osteoclasts from mouse strains not suffering from CHS, e.g., CBA mice, a quantitative survey was carried out. It was shown that osteoclasts from beige mice aged from 4 days to 3 months contain significantly increased numbers of giant lysosomes when compared with osteoclasts from CBA mice and CBAXbg/bg F1 hybrids. The giant lysosomes of the beige mouse osteoclast are currently being used as cytoplasmic markers in experiments on the cell of origin of the osteoclast.

Topics: Acid Phosphatase; Animals; Arylsulfatases; Bone Marrow; Chediak-Higashi Syndrome; Femur; Histocytochemistry; Ilium; Kidney Tubules, Proximal; Lysosomes; Mice; Mice, Inbred CBA; Microscopy, Electron; Osteoclasts

2 cases of acute myeloid leukaemia with inclusion bodies are presented. The inclusions were found mainly in the blast cells but could also be encountered in lymphocytes and plasma cells. Cytochemical and ultrastructural studies showed a great resemblance of these inclusions to the ones found in Chediak-Higashi anomaly, i.e., high acid phosphatase activity, varying in size of inclusions from clusters of small granules to hugh inclusion, sometimes found in vacuoles, featuring fusion of lysosomes.

Topics: Acid Phosphatase; Adult; Chediak-Higashi Syndrome; Female; Humans; Inclusion Bodies; Leukemia, Myeloid, Acute; Lymphocytes; Male; Middle Aged; Plasma Cells

The giant inclusion anomaly of leukocytes from three patients with the Chédiak-Higashi syndrome (CHS) has been reexamined by the ultrastructural and cytochemical techniques placing emphasis on the monocyte. Contrary to previous assumptions that all CHS leukocytes shared a common form of giant granule with similar mechanisms of formation, it is shown that CHS monocytes contain ring-shaped organelles as their principle manifestation of the disease. These granules consist of a double membrane surrounding a segment of cytoplasm, which may or may not be sequestered from the remaining cytoplasm and which usually contains one or more normal-sized azurophilic granules. The material lying between the double membranes contains the specific reaction products for peroxidase and acid phosphatase. Therefore, the ring-shaped organelles share identity with the azurophilic granules and probably share a common origin with the primary lysosomes. The double-ring form of giant CHS organelle has also been found infrequently in neutrophils, eosinophils, and lymphocytes.

Topics: Acid Phosphatase; Adolescent; Chediak-Higashi Syndrome; Humans; Leukocytes; Lysosomes; Male; Monocytes; Organoids; Peroxidases

We used immunofluorescent microscopy to characterize the abnormal granules in neutrophils from five patients with Chediak-Higashi disease. Monospecific antiserums to the azurophilic markers myeloperoxidase, elastase, cathepsin G and lysozyme, and to the specific granule markers lactoferrin and lysozyme, were labeled with fluorescein and rhodamine and were used to demonstrate two antigens in the same cell simultaneously. The abnormal granules in Chediak-Higashi neutrophils contained both azurophilic and specific granule markers. Normal-appearing lactoferrin-positive granules were also present, but normal azurophilic granules were not seen. Analysis of bone-marrow samples from two of these patients suggested that the abnormal granules were formed during granulocyte maturation by the progressive aggregation and fusion of normally formed azurophilic and specific granules. These results are consistent with a membrane abnormality or a defect of microtubular function leading to inappropriate granule fusion, and suggest that the granular abnormality is more generalized than previously appreciated.

Topics: Acid Phosphatase; Chediak-Higashi Syndrome; Cytoplasmic Granules; Female; Humans; Inclusion Bodies; Infant; Microtubules; Neutrophils; Peroxidase; Staining and Labeling

The phenomenon of giant anomalous lysosome formation in human Chediak-Higashi syndrome leukocytes was analyzed. Ultrastructure findings combined with cytochemical procedures for visualizing acid phosphatase and peroxidase activity showed giant anomalous granules in addition to normal, small and enlarged granules. Massive granules in lymphocytes had an appearance and structure different from those found in other leukocytes. The giant granules seem to be a product of an active fusion between primary and secondary normal sized or enlarged lysosomes. This fusion occurs in polymorphonuclear neutrophils, eosinophils and in monocytes. No fusion was found in lymphocyte granules.

Topics: Acid Phosphatase; Cell Fusion; Chediak-Higashi Syndrome; Child, Preschool; Cytoplasmic Granules; Eosinophils; Granulocytes; Humans; Leukocytes; Lysosomes; Male; Monocytes; Neutrophils; Peroxidases; Staining and Labeling

Topics: Acid Phosphatase; Animals; Cathepsins; Chediak-Higashi Syndrome; Cyclic AMP; Dermatitis; Fabry Disease; Humans; Keratins; Lupus Erythematosus, Systemic; Lysosomes; Psoriasis; Skin; Ultraviolet Rays; Vacuoles; Vitamin A Deficiency

A method of blood granylocyte concentration and isolation of granules from both normal and neutropenic Chediak-Higashi syndrome (CHS) patients is described. the intracellular distribution of activity for several hydrolases in CHS granulocytes differs from normal; significantly more activity is present in the cytoplasmic fraction and correspondingly less is granule-associated. Isolated CHS granules are not more sensitive to the labilizing agents vitamin A, progesterone, or etiocholanolone. Specific activities of myeloperoxidase and ss-glucuronidase in CHS granulocytes are lower than normal while alkaline phosphatase is elevated. Other lysosomal enzyme activities are normal. Lysosomal enzyme distribution and content are similar in CHS and normal mononuclear cells. The possible significance of these findings is discussed.

Topics: Acid Phosphatase; Alkaline Phosphatase; Cathepsins; Chediak-Higashi Syndrome; Cytoplasmic Granules; Etiocholanolone; Female; Glucuronidase; Heparin; Humans; Leukocytes; Lysosomes; Male; Muramidase; Peroxidase; Progesterone; Vitamin A

The origin of giant granules in the retinal pigment epithelium of the beige mouse was investigated with electron microscopy and ultrastructural histochemistry. These granules were found to contain melanin and acid phosphatase. Apparently they arise from fusions of primary lysosomes with melanin granules which are already enlarged from multiple fusions among melanosomes. Therefore, the giant granules are not primary lysosomes, nor are they simply enlarged melanin granules as suspected from light microscopic studies. A deficiency of primary lysosomes in the pigment epithelium results, suggesting a defect in intracellular digestion similar to that found in the leukocytes of Chediak-Higashi patients and several animal models. Affected humans probably have defective digestion in their retinal pigment epithelium also; which could impair the renewal process for rod outer segments. Thus, Chediak-Higashi patients may show an increased susceptibility to light damage due not only to hypopigmentation, but to defective intracellular digestion, as well.

Topics: Acid Phosphatase; Animals; Chediak-Higashi Syndrome; Cytoplasmic Granules; Disease Models, Animal; Epithelium; Histocytochemistry; Lysosomes; Melanins; Mice; Mice, Inbred Strains; Microscopy, Electron; Mutation; Retina

Bone marrow from a child with Chediak-Higashi-Steinbrinck disease was cultured. It was found that all cells with granulocytic colony forming ability were affected by the disease. Cytoplasmic vacuoles were identified as lysosomes by their cytochemical staining. The cloning rates suggest that granulopoiesis is largely ineffective.

Topics: Acid Phosphatase; Alkaline Phosphatase; Bone Marrow; Bone Marrow Cells; Cell Nucleus; Cells, Cultured; Chediak-Higashi Syndrome; Child, Preschool; Clone Cells; Cytoplasm; Esterases; Granulocytes; Humans; Leukocytes; Peroxidases; Vacuoles

Topics: Acid Phosphatase; Animals; Chediak-Higashi Syndrome; Endoplasmic Reticulum; Lipid Metabolism; Lipoproteins; Liver; Lysosomes; Mice; Microscopy, Electron; Staining and Labeling

The beige mouse is considered to be a homologue of Chediak-Higashi syndrome (CHS). Cytochemical and electron microscopic studies have revealed an inherited lesion in the kidneys of these mice. The alteration was confined to the distal segments (S3) of the proximal tubules and was characterized by the accumulation of numerous massive polysaccharide-rich granules. These granules were reactive for acid phosphatase and beta-glucuronidase activities and were therefore considered to be lysosomes. Small numbers of lymphocytes were also observed in the perivascular spaces and within the tubules of the S3 segment. The fine structure of S3 cells was also markedly altered. In addition to the massive lysosomes, dense material was found associated with the brush border and was present in pinocytotic vesicles at the base of the brush border and between basal invaginations of the plasma membranes. Despite these changes, reabsorption of exogeneous peroxidase by S3 cells appeared to be normal. The presence of a congenital defect in the kidney of the beige mouse appears to provide a useful model for studying the morphology and function of the S3 region of the nephron.

Topics: Acid Phosphatase; Animals; Cell Membrane; Chediak-Higashi Syndrome; Colloids; Cytoplasm; Disease Models, Animal; Endoplasmic Reticulum; Glucuronidase; Histocytochemistry; Iron; Kidney; Kidney Tubules; Lysosomes; Mice; Microscopy, Electron; Peroxidases; Staining and Labeling

Topics: Acid Phosphatase; Animals; Bone Marrow Cells; Chediak-Higashi Syndrome; Female; Histocytochemistry; Jejunum; Kidney; Kidney Tubules; Liver; Lysosomes; Male; Mice; Mice, Inbred Strains; Microscopy, Electron; Microtomy; Thyroid Gland

A giant inclusion filled with structures resembling microtubules was observed in the cytoplasm of a small percentage of circulating lymphocytes from 4 children with the Chediak-Higashi syndrome (CHS). The organelles were similar in many respects to tubule-containing inclusions described previously in normal and abnormal lymphocytes. Tubule-filled organelles appear to develop by cytoplasmic sequestration, and their massive size in CHS cells may result from fusion of small organelles to form a single giant inclusion. Acid phosphatase was found only in giant tubular inclusions which had fused with lysosomal granules. The basis for the existence of these organelles in normal and abnormal lymphocytes remains obscure.

Topics: Acid Phosphatase; Chediak-Higashi Syndrome; Child; Cytoplasmic Granules; Humans; Inclusion Bodies; Lymphocytes; Membranes; Microscopy, Electron; Microtubules; Organoids

Topics: Acid Phosphatase; Adult; Agranulocytosis; Alkaline Phosphatase; Bacterial Infections; Chediak-Higashi Syndrome; Chemotaxis; Female; Glucuronidase; Humans; Leukocytes; Lysosomes; Male; Muramidase; Peroxidases; Skin Window Technique; Staphylococcal Infections; Streptococcal Infections

Topics: Acid Phosphatase; Adult; Alkaline Phosphatase; Azo Compounds; Cell Nucleus; Chediak-Higashi Syndrome; Child; Emulsions; Glucuronidase; Humans; Leukocyte Count; Leukocytes; Lymphocytes; Male; Naphthalenes; Oils; Paraffin; Peroxidases; Phagocyte Bactericidal Dysfunction; Phagocytosis

Topics: Acid Phosphatase; Animals; Blood Bactericidal Activity; Bone Marrow Cells; Cattle; Cattle Diseases; Chediak-Higashi Syndrome; Cytoplasmic Granules; Humans; Kidney; Lipidoses; Lysosomes; Mice; Microscopy, Electron; Mink; Neutrophils; Peroxidases; Phagocytosis; Rodent Diseases; Staphylococcus