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Results for “Phagocyte Bactericidal Dysfunction”

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At least 19 recordsLinked to original sources
PubMed1975

The role of superoxide anion generation in phagocytic bactericidal activity. Studies with normal and chronic granulomatous disease leukocytes.

The capacity of human phagocytes to generate superoxide anion (O2-), a free radical of oxygen, and a possible role for this radical or its derivatives in the killing of phagocytized bacteria were explored using leukocytes from normal individuals and patients with chronic granulomatous disease (CGD). Superoxide dismutase, which removes O2-, consistently inhibited phagocytosis-associated nitroblue tetrazolium (NBT) reduction indicating the involvement of O2- in this process. Similarly, superoxide dismutase inhibited the luminescence that occurs with phagocytosis, implicating O2- in this phenomenon, perhaps through its spontaneous dismutation into singlet oxygen. Subcellular fractions from homogenates of both normal and CGD leukocytes generated O2- effectively in the presence of NADH as substrate. However, O2- generation by intact cells during phagocytosis was markedly diminished in nine patients with CGD. Leukocytes from mothers determined to be carriers of X-linked recessive CGD by intermediate phagocytic reduction of NBT elaborated O2- to an intermediate extent, further demonstrating the interrelationship between NBT reduction and O2- generation in phagocytizing cells. Activity of superoxide dismutase, the enzyme responsible for protecting the cell from the damaging effects of O2-, was approximately equal in homogenates of normal and CGD granulocytes. Polyacrylamide electrophoresis separated this activity into a minor band that appeared to be the manganese-containing superoxide dismutase associated with mitochondria and a more concentrated, cyanide-sensitive, cytosol form of the enzyme with electrophoretic mobility that corresponded to that of erythrocyte cuprozinc superoxide dismutase. Superoxide dismutase inhibited the phagocytic killing of Escherichia coli, Staphylococcus aureus, and Streptococcus viridans. A similar inhibitory effect was noted with catalase which removes hydrogen peroxide. Neither enzyme inhibited the ingestion of bacteria. Peroxide and O2- are believed to interact to generate the potent oxidant, hydroxyl radical (.OH). A requirement for .OH in the phagocytic bactericidal event might explain the apparent requirement for both O2- and H2O2 for such activity. In agreement with this possibility, benzoate and mannitol, scavengers of .OH, inhibited phagocytic bactericidal activity. Generation of singlet oxygen from O2- and .OH also might explain these findings. It would seem clear from these and other studies that the granulo cyte elaborates O2- as a concomitant of the respiratory burst that occurs with phagocytosis. To what extent the energy inherent in O2- is translated into microbialdeath through O2- itself, hydrogen peroxide, .OH, singlet oxygen, or some other agent remains to be clearly defined.

Catalase↗
PubMed1977

Disorders of phagocytic function: ultrastructural aspects.

The electron microscopic changes in genetic and acquired disorders of granulocytes have been reviewed. In rare situations, such as the Chédiak-Higashi syndrome, there are bizarre giant lysosomes. In other conditions associated with abnormal phagocytic function, such as chronic granulomatous disease, there are no qualitative morphologic abnormalities. In chronic infection and in protein calorie malnutrition (kwashiorkor) granulocytes contain frequent Döhle bodies and cytoplasmic vacuolization. The development of new cytochemical methodology and the combination of electron microscopy with in vitro techniques offers the potential for further understanding of the relationship between cell structure and functional disorders of the granulocyte.

Animals↗
PubMed1977

Phagocytosis. Clinical disorders of recognition and ingestion.

Tentative conclusions concerning the role of recognition and ingestion of microorganisms by phagocytes in host defense and the consequences of disorders of phagocytosis can be derived by correlating a) knowledge about recognition and ingestion derived from studies in vitro, b) investigations of the clearance of particulate matter from the circulation of animals and man, and c) analyses of the behavior of phagocytes in patients susceptible to recurrent pyogenic infections. Deficiency of the major serum recognition-conferring (immunoglobulins and complement proteins that deposit a fragment of C3 on microbes) prevents the optimal clearance of virulent encapsulated pathogens by fixed mononuclear phagocytes. Confrontation of phagocytes with particulate matter appearing in pathologic states (viruses, immune complexes, damaged erythrocytes in sickle cell anemia and other hemoglobinopathies) diverts them from their normal task of clearing opsonized encapsulated microorganisms. Corticosteroids impair the phagocytic capacity by an unknown mechanism. Major impediments to progress in this field are inadequate assays for phagocytosis and the difficulty in measuring phagocytosis in the intact organism.

Anemia, Sickle Cell↗
PubMed1978

[Phagocytosis].

Explore the source record for details and available documents.

Humans↗
PubMedDate not supplied

[Chronic granulomatous disease (CGD): in vitro enhancement of bactericidal activity of CGD phagocytes by rifampicin].

In a series of 29 experiments on CGD patients, we have studied the in vitro bactericidal capacity of normal and CGD phagocytes against penicillin, streptomycin and rifampicin sensitive Staphylococcus aureus. The bactericidal activity of phagogyte preparations was tested at different intervals during a 21 hour incubation. The CGD-phagocyte bactericidy peaks after 90 min when penicillin is used; in contrast, a significant enhancement of the bactericidal activity is noted with rifampicin and best noted after 21 hours of incubation. To elucidate the mode of action of this antibiotic, a rifampicin resistant S. aureus was used in a series of experiments; The results point to a mixt type of action: antimicrobial and metabolic.

Blood Bactericidal Activity↗
PubMed1976

Disorders of phagocyte function.

An increasing number of phagocytic defects with cutaneous manifestations and signs in humans are being reported. With the increasing availability of phagocyte assays, detection of phagocyte defects will allow us to dissect the component events and more clearly understand the central role of the phagocytic leukocyte in host defenses of the skin.

Acrodermatitis↗
PubMed1978

Cell biology of leukocyte abnormalities--membrane and cytoskeletal function in normal and defective cells. A review.

In this review I have attempted to explain the processes of chemotaxis, phagocytosis, oxidant generation, and lysosomal degranulation in normal and genetically abnormal human PMN. In my view these leukocyte functions are most importantly dependent on the integrity of three cellular components: the plasma membrane, the submembranous microfilaments, and the cytoplasmic microtubules. These components are often discussed in isolation, and the biochemical and pharmacological aspects of their function are analyzed separately here. However, PMN motile and bactericidal activities require the interdependent functioning of membranes, microtubules, and microfilaments. I have therefore tried to provide an integrated view of cytoskeleton-membrane organization and function in human PMN. I have particularly emphasized dynamic aspects of the cytoskeleton and membranes, eg, the induction of microtubule assembly and membrane enzyme activation by surface ligands and the reorganization of microfilaments in response to the same ligands. With this background established, I have selected for discussion a series of diseases in which abnormalities of chemotaxis, phagocytosis, lysosomal degranulation, and/or oxidant generation can be explained directly or indirectly by abnormalities in dynamic properties of PMN membranes, microtubules, or microfilaments. I emphasize that even preliminary insight into the basis of these disorders has sometimes been sufficient to suggest useful clinical approaches to the management of patients. In several of these neutrophil abnormalities, ie, neutrophil actin dysfunction, Chédiak-Higashi syndrome, and its "antithesis" described by Gallin and co-workers, the cellular dysfunctions were well documented but the molecular basis was completely obscure prior to cell biologic analysis. Snyderman and Pike 159 and Chusid and co-workers 160 emphasized the existence of a large number of other neutrophil bactericidal abnormalities resulting from as yet unexplained cellular defects. Further analyses of the functional interactions between membranes and cytoskeletal components in neutrophils may not only clarify the molecular bases of the disorders described here but also may provide insight into the origins and proper therapeutic approach to other granulocyte dysfunctions.

Cell Membrane↗
PubMed1975

Neutrophil dysfunction in diabetes mellitus.

The neutrophil bactericidal capacity of 31 patients with diabetes mellitus in a nonketoacidotic state, including 21 without infections and 10 with recurrent infections, were evaluated. The killed intracellular bacteria (KICB) expressed as the percentage of the initial inoculum for 25 normal control subjects was 95.4 (SD equal plus and minus (2.7) and that for the diabetic patients, the KICB was 72.8 (SD=+30.7)with a p value of less than or equal to 0.01. In 17 out of 31 diabetic atients, the KICB was greater than minus two standard deviations of the control mean. Using the lysostaphin assay technic, 11 patients were shown to phagocytize poorly, 3 had impaired intracellular killing and 3 had a combined defect. These defects were not correctable by normal serum nor related to blood-glucose levels. No apparent correlation with infection could be demonstrated. Fiver of the 10 patients with recurrent infections and 12 out ot of 21 patients without infections has a neutrophil dysfunction. However, all 3 patients with a combined defect had severe bacterial infections.

Adolescent↗
PubMed1976

Neutrophil dysfunction and granulomatosis in the preleukemic state.

A 40-year-old male had periods of fever, sore throat and anemia for 14 months before acute myeloblastic leukemia could be diagnosed from hematological findings. During the preleukemic state, impaired bactericidal capacity of the granulocytes was repeatedly demonstrated and multiple hepatosplenic and skin granulomas occurred. Results of granulocyte function studies may prove to be of significant aid in the diagnosis of the preleukemic state of acute myeloblastic leukemia.

Adult↗
PubMed1975

Canine granulocytopathy syndrome: neutrophil dysfunction in a dog with recurrent infections.

A male Irish Setter dog had a clinical history of recurrent life-threatening bacterial infections, with associated periods of pyrexia and severe neutrophilia. Examination of a mandibular lymph node biopsy made when the patient was 10 weeks old revealed subacute diffuse suppurative lymphadenitis with reticuloendothelial hyperplasia. Circulating leukocytes isolated from the dog when it was 5 months old had a marked bactericidal defect when compared with cells from clinically normal dogs of the same age. The clinical syndrome in the affected patient resembled that observed in the granulocytopathies described in man and other animals.

Animals↗