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PubMed1976

Metabolic inhibition of polymorphonuclear leucocytes in fulminant hepatic failure.

A high incidence of bacterial infections in patients with fulminant hepatic failure (F.H.F.) has led to an investigation of polymorpho-nuclear-leucocyte (P.M.N.) function. No intrinsic leucocyte abnormality was demonstrable but a factor present in F.H.F. serum was shown to inhibit the metabolic activity of the leucocyte hexose-monophosphate shunt. This effect was due neither to low serum-complement nor to associated renal failure. The inhibitory factor, however, was removed either by pre-incubation with activated charcoal or by in-vitro dialysis, raising the possiblity that charcoal haemoperfusion or other forms of artificial liver support may improve P.M.N. function in this condition.

Bacterial Infections↗
PubMed1976

Characterisation of the enzyme defect in chronic granulomatous disease.

Strikingly reduced activity of an enzyme, normally located in the plasma membrane of human neutrophils, has been demonstrated in a male patient with chronic granulomatous disease (C.G.D.). The subcellular distribution of N.A.D.H.-dependent reduction of nitroblue tetrazolium (N.B.T.) was determined in neutrophils because reduction of this dye by these patients is grossly impaired. Assayed at high concentrations of N.A.D.H. (1 mmol/1), N.B.T. is reduced by enzymes in the cytosol and mitochondria in addition to the plasma membrane by both normal and C.G.D. cells--properties which previously obscured the identity and location of this enzyme. At a more physiological concentration of N.A.D.H. (25 mumol/1), reduction of the dye by the plasma membrane, the principal site of N.B.T. reduction by normal neutrophils, was absent in the patient with C.G.D. It is suggested that absence or imperfect function of this reductase enzyme is the primary lesion in this disease.

Adolescent↗
PubMed1985

[Anomalies of the membrane receptors of blood phagocytic cells in nosocomial pulmonary infections].

Patients in intensive care units have frequent and severe opportunistic bacterial pneumoniae, even if they were previously free from respiratory disease. A search was made in these patients for possible immune deficiencies. Granulocyte and monocyte phagocytic activities were studied separately in 17 patients with bacterial bronchopneumonia (male: 13, female: 4; age: 41 +/- 5 yr). The ability of three types of particles (opsonized zymosan, immunoglobulin coated and glutaraldehyde-treated sheep red cells) to trigger ingestion was measured. Cells were tested either in normal AB serum or in the presence of patient's serum. A substantial 40% decrease of the fraction of granulocytes ingesting zymosan was found in our experimental conditions (p less than 0.001). Activity with the other particles was not significantly altered. Patients' sera were at least as efficient as a pool of normal sera in opsonizing zymosan. Furthermore, no phagocytic inhibitor was found in the patients tested. Underlying mechanisms for these abnormalities remain unknown, but a better understanding of the aetiology of the altered bactericidal function of phagocytic cells is required before suggesting immunomodulating treatments.

Adult↗
PubMed1999

Defective priming of the phagocyte oxidative burst in a child with recurrent intracellular infections.

Human phagocytes (polymorphonuclear neutrophils and monocytes) play a critical role in host defense against invading microorganisms. Recent studies reported that circulating phagocytes undergo a final maturation process, in particular in terms of oxidative burst, during extravasation and migration to local sites of inflammation. This process is known as priming. We report here on a nine-year-old boy with successive disseminated infections due to intracellular microorganisms (Mycobacterium bovis, BCG, and Salmonella typhimurium). No T- or B-cell quantitative or qualitative defects were found. Polymorphonuclear neutrophil (PMN) migration and NADPH oxidase in PMNs and monocytes stimulated with various agents at optimal concentrations were normal, ruling out a leukocyte adhesion deficiency syndrome, a Chediak Higashi syndrome, and a chronic granulomatous disease. Nevertheless, the patient's PMNs and monocytes showed defective priming capacity, as measured by H(2)O(2) production after pretreatment with LPS (5 microg/mL for 30 min), TNFalpha (100 units/mL for 30 min), or IL-8 (50 ng/mL for 30 min) in response to bacterial N-formyl peptides (fMLP 10(-6) M for 5 min). In these conditions, H(2)O(2) production of PMNs and monocytes from the patient did not exceed that of the samples treated with fMLP or LPS alone, while the controls strongly produced H(2)O(2). Moreover, monocytes from the patient showed an impaired capacity to kill S. typhimurium in vitro. Such an impairment could be related at least in part to the priming deficiency of phagocyte oxidative burst. This case suggests, for the first time, that in vivo priming processes are critical in host defence against intracellular pathogens.

Adult↗
PubMed2000

Primary immunodeficiency diseases in Norway.

This study represents the first national epidemiological survey of primary immunodeficiency diseases in Norway. Uniform questionnaires were sent out in April 1998 to all hospital departments considered relevant. As of February 1999, a total of 372 patients have been registered, of whom 69 patients are deceased. With a population of 4.45 million people, the total prevalence of primary immunodeficiency diseases in Norway February 1, 1999 is 6.82 per 100000 inhabitants. Distribution between the main immunodeficiency diagnoses is (a) antibody deficiencies 50.8%, (b) combined deficiencies included other immunodeficiency syndromes 12.4%, (c) complement deficiencies 21.0%, (d) phagocytic disorders 6.7%, (e) and immunodeficiency associated with other congenital diseases 9. 1%. Compared to previous reports from other European countries, there is a smaller proportion of antibody deficiencies due to few IgA deficiencies registered and a large proportion of complement deficiencies due to many patients with hereditary angioedema.

Adult↗
PubMed1997

Brazilian report on primary immunodeficiencies in children: 166 cases studied over a follow-up time of 15 years.

One hundred sixty-six cases of primary immunodeficiency diseases (PID) (95 males, 71 females), diagnosed according to WHO criteria, have been registered at the Children's Hospital, University of São Paulo, Brazil. The following frequencies were found: predominantly humoral defects, 60.8% (n = 101); T cell defects, 4.9% (n = 8); combined ID, 9.6% (n = 16); phagocyte disorders, 18.7% (n = 31); and complement deficiencies, 6% (n = 10). IgA deficiency was the most frequent disorder (n = 60), followed by transient hypogammaglobulinemia (n = 14), chronic granulomatous disease (n = 14), and X-linked agammaglobulinemia (n = 9). In comparison to other (national) reports, we observed higher relative frequencies of phagocyte and complement deficiencies. Recurrent infections were the cause of death in 12.7%. Allergic symptoms were observed in 41%, mainly in IgA-deficient, hypogammaglobulinemic, or hyper-IgE patients, and autoimmune disorders in 5%, predominantly in IgA and complement deficiencies. Five patients suffered from BCG dissemination; two of them died. This is the first Brazilian report on PID over an observation time of 15 years.

Adult↗
PubMed2000

In vivo correction of genetic defects of monocyte/macrophages using attenuated Salmonella as oral vectors for targeted gene delivery.

Macrophages are normal targets for Salmonella during natural infections, and it has been demonstrated that attenuated bacteria can deliver nucleic acid vaccine constructs. Therefore, we assessed if attenuated Salmonella can be used for the in vivo delivery of transgenes to their natural cellular target, in an attempt to correct genetic defects associated with monocytes/macrophages. This system would offer the distinct advantage of achieving a specific targeting of defective cells in a non-invasive form. Using a reporter gene, we demonstrated that attenuated Salmonella could be used as an effective in vitro delivery system to transfer genetic material into nondividing cells like murine macrophages. In vivo, the oral administration of attenuated Salmonella allows targeted delivery of transgenes to macrophages and subsequently expression of transgenes at a systemic level. IFNgamma-deficient mice (GKO) were thus selected as a model for the in vivo validation of the Salmonella-based delivery approach. Attenuated Salmonella, used as the carrier for a eukaryotic expression vector encoding the murine IFNgamma gene, was able to restore the production of this cytokine in GKO macrophages. Their oral administration to IFNgamma-deficient mice also re-established, in these immunocompromised animals, the natural resistance to bacterial infections. These results demonstrate, for the first time, that attenuated Salmonella can be successfully used in vivo as a DNA delivery system for the correction of a genetic defect associated with monocyte/macrophages.

Animals↗
PubMed1999

Defective functional activity and accelerated apoptosis in neutrophils from children with cancer are differentially corrected by granulocyte and granulocyte-macrophage colony stimulating factors in vitro.

We have previously shown that polymorphonuclear leucocytes (PMN) harvested from children with cancer and exposed to chemotherapy exhibit defective bactericidal activities against both Gram-positive and Gram-negative microorganisms as well as accelerated apoptosis. In this study, PMN from children with cancer were evaluated to compare in vitro the corrective effects of the two myeloid colony stimulating factors G-CSF and GM-CSF on these defective pathways. Both G-CSF and GM-CSF were able to increase the defective bactericidal activities against S. aureus and E. coli. However, GM-CSF was consistently superior to G-CSF in correcting PMN microbicidal activity; this correction was incomplete since it did not reach the level observed in normal PMN exposed to GM-CSF. The accelerated apoptosis of PMN was not affected by G-CSF. In contrast, GM-CSF significantly prolonged the survival of the PMN although it did not reach the level of survival observed with normal PMN exposed to GM-CSF. These observations were consistent with other studies indicating that in PMN, microbicidal activities and apoptosis are differentially sensitive to the myeloid growth factors G-CSF and GM-CSF.

Adolescent↗