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Results for “Phagocyte Bactericidal Dysfunction”

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PubMed1983

Impaired in vitro bactericidal power of polymorphonuclear leukocytes in patients with protein calorie malnutrition.

Bactericidal power of polymorphonuclear leukocytes was determined in eight patients with protein calorie malnutrition before and after nutritional therapy. Oxygen consumption associated with the uptake of zymosan particle by polymorphonuclear leukocytes, which is an exact reflection of the bactericidal power of leukocytes, was significantly decreased in untreated patients in the presence of both autologous and AB serum when compared with two control groups of eight normal patients. After nutritional therapy, oxygen consumption was found to be in the normal range in the presence of both autologous and AB serum. It is concluded that, in patients with protein calorie malnutrition, polymorphonuclear leukocytes have an intrinsic dysfunction, and this dysfunction is corrected after nutritional repletion.

Adult↗
PubMedDate not supplied

Increased susceptibility to infection in hypothermic children: possible role of acquired neutrophil dysfunction.

The addition of hypothermia to regimens to control cerebral edema in children at our institution has been associated with a substantial incidence of infectious complications. Of the 13 children maintained at 30 degrees C to prevent cerebral edema, 3 developed Haemophilus influenzae pneumonia and 2 developed Streptococcus pneumoniae sepsis (one with pneumonia). The importance of neutrophil (PMN) function for elimination of bacterial pathogens prompted in vitro studies of PMN function at clinically attainable hypothermic temperatures. Neutrophils at 30 degrees C had significantly less ability to migrate towards a chemotactic stimulus (45 +/- 10% inhibition; P less than 0.02), to ingest staphylococci (22 +/- 5% inhibition; P less than 0.01) and to be metabolically activated as measured by superoxide production (35 +/- 10% inhibition; P less than 0.01) or by chemiluminescence (18 +/- 8% inhibition; P less than 0.05). These in vitro findings support the clinical observation that persons with decreased body temperature may be at an increased risk for bacterial infections secondary to PMN dysfunction.

Adolescent↗
PubMed1987

[Clinical symptoms, diagnosis and treatment of phagocyte dysfunction].

When patients suffer from recurrent infections with bacteria or fungi that react poorly with the commonly prescribed antibiotics, phagocyte dysfunctions should be considered. In this article, a survey is given of the mechanism of action of these cells, the dysfunctions that may occur, the resulting clinical symptoms, the laboratory diagnostics and some therapeutical approaches.

Cell Adhesion↗
PubMed1996

Immune deficiency in glycogen storage disease type 1B.

Patients with glycogen storage disease type 1B present the clinical features of glycogen storage disease type 1A. In addition, they are susceptible to recurrent bacterial infection and have recurrent oral ulcers and occasionally Crohn's-like disease. There features are due to immune dysfunction caused by a combination of neutropenia and impaired phagocytic functions.

Bacterial Infections↗
PubMed1999

Clinical and laboratory work-up of patients with neutrophil shortage or dysfunction.

Neutrophils have a crucial function in the defense against bacteria and fungi. Indeed, during chronic, severe neutropenia and in case of severe neutrophil dysfunctions, the patients may suffer recurrent and sometimes life-threatening infections. This article describes the clinical symptoms, the theory behind the antimicrobial systems of neutrophils, the methods to diagnose the various aberrations, and the possibilities for treating these patients. A few of the most common causes of neutropenia and neutrophil dysfunctions are described in detail, including recent genetic information regarding the cause of these diseases.

Animals↗
PubMed1985

Gingivitis and oral ulceration in patients with neutrophil dysfunction.

In this study, the gingival condition of patients with neutrophil dysfunction has been evaluated. The data demonstrate increased gingival disease as well as oral ulcerations in patients with neutrophil dysfunction syndromes and are consistent with a critical role of neutrophils in oral health.

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↗
PubMed1980

[Job's syndrome--a case report (author's transl)].

A 4-year old boy with chronic eczema since early infancy had been admitted thrice to the hospital because of recurrent staphylococcal infections including furunculosis, lymphadenitis, pneumonia and pyothorax. Exhaustive immunologic studies revealed normal humoral, cell-mediated and non-specific immunities except extremely high serum IgE level and dysfunctions of granulocytes including decreased Fc and complement receptors, lowered chemotactic response (around the lower range of normal), slightly impaired intracellular killing of staphylococci and possibly impaired reactions to candida and BCG. In spite of long-term antimicrobial prophylaxis, cold abscesses continued to appear and the eczematous skin lesions waxed and waned.

Child, Preschool↗
PubMed1986

Phagocytic defects--monocytes/macrophages.

Mononuclear phagocytes originate from stem cells in the bone marrow which differentiate from monoblasts into promonocytes, then into circulating blood monocytes. Subsequently the monocytes can develop into macrophages and reside in a variety of tissues. Mononuclear phagocytes have cell surface receptors for a variety of substances (e.g., IgG, complement components, fibronectin, and sugars) and are capable of secreting a number of mediators (enzymes, complement components, coagulation components, and monokines). The tissue macrophages adapt to their environment and express unique differentiated functions that are related to various anatomic sites and organs (e.g., Kupffer cells, pulmonary alveolar macrophages, osteoclasts, microglia). Macrophages have the capacity to become "activated" by both specific and nonspecific immunologic stimuli and the "activated" macrophage has enhanced functional capabilities (e.g., tumoricidal, microbicidal, phagocytosis, secretion of mediators). Abnormal monocyte/macrophage function may be acquired or may be due to genetic or developmental disorders. Because of their central role in host defense (in inflammatory responses, in antigen presentation, and in immunoregulatory networks), monocyte/macrophage dysfunction may result in one or more pathophysiologic consequences: defects in monocyte maturation, deficiencies in the clearance of physiologic substrates in lysosomal diseases (e.g., Gaucher's disease, mucopolysaccharidoses, osteopetrosis, metachromatic leukodystrophy), decreased synthesis and secretion of mediators (complement component deficiencies), defects in microbicidal activity (chronic granulomatous disease) and defects which are acquired following infection and during chemotherapy (e.g., acquired immune deficiency syndrome).

Bone Marrow Transplantation↗
PubMed1988

Chemotactic disorders.

Clinical disorders of phagocyte chemotaxis have heterogeneous etiologies. The physiologic defect can involve adherence, the cytoskeleton, deformability, granule dysfunction, regulation of receptors, or a variety of soluble mediators. At present, successful clinical management depends on early and compulsive attention to infectious complications. A host of new immunomodulators (GM-CSF, gamma interferon, tumor necrosis factor, etc.), made available through recombinant gene technology, are now under study and may provide new and more effective means of treatment for these life-threatening disorders.

Chemotactic Factors↗
PubMed1980

Granulocyte dysfunction in transcobalamin II deficiency responding to leucovorin or hydroxocobalamin-plasma transfusion.

Granulocytes from a 6-year-old boy with congenital transcobalamin II (TC II) deficiency were found to have abnormally low antibacterial activity against Staphylococcus aureus and very low intracellular levels of the cobalamin coenzymes. Transfusion of hydroxocobalamin (OH-Cbl) bound to normal plasma temporarily restored granulocyte bactericidal activity and increased cellular levels of the cobalamin coenzymes. Granulocyte function was also temporarily restored by oral Leucovorin. The defect appeared to be causally related to the patient's TC II deficiency and indirectly to a deficiency of cobalamin and folate coenzymes.

Blood Proteins↗