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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↗
PubMed1980

Neutrophil dysfunction associated with states of chronic and recurrent infection.

Infants, children, and young adults who suffer chronic and recurrent bacterial or fungal infection despite adequate numbers of circulating granulocytes and normal or elevated levels of immunoglobulins should be suspected of having fundamental defects in granulocyte functioning. This article considers clinical disorders for which there is evidence for associated defects of polymorphonuclear leukocytes.

Adolescent↗
PubMed1980

[The NBT test--a review].

The NBT-test is a technique particularly used in its stimulated variant for testing granulocyte metabolism and in this capacity it is an integrated part of the test programme for differentiating neutrophilic dysfunctions. Its sphere of application is the diagnosis of progressive septic granulomatosis. The variety of the methods used makes it difficult to compare the results described by the various authors. Therefore, standardization is urgently necessary. A differentiation of bacterial and non-bacterial infections as well as of other febrile diseases is not possible with the unstimulated test. Investigations of the longitudinal section, however, allow the activity of the disease to be evaluated (with initially high numbers of granulocytes being positive in the nitroblue tetrazolium test).

Animals↗
PubMed1978

Recurrent Pseudomonas infection associated with neutrophil dysfunction.

A 72-year-old male is described with a history of 4 episodes of Pseudomonas aeruginosa sepsis and chronic otitis media caused by pseudomonas species. In vitro testing of the patient's polymorphonuclear leukocytes (PMNs) revealed profoundly abnormal chemotactic responses and defective intracellular killing of Ps. aeruginosa, Staphylococcus aureus and Escherichia coli. Chemiluminescence production by the patient's PMNs in response to opsonized zymosan as well as endotoxin stimulated nitroblue tetrazolium dye reduction were markedly depressed. These data indicate the presence of a profound, apparently acquired, defect in PMN function in an elderly male. Detailed evaluation of adult patients with recurrent infections may reveal similar, apparently acquired defects in PMN function.

Aged↗
PubMed1983

Ocular findings in patients with neutrophil dysfunction.

Of 32 patients (19 females and 13 males, ranging in age from 2 to 44 years), nine had ocular problems related to neutrophil dysfunction. Four patients had blepharokeratoconjunctivitis and pannus formation. In one of these, severe visual loss secondary to corneal thinning and scarring occurred. Five patients had inactive chorioretinal scars without visual loss. Although some of the other 23 patients had minor ocular abnormalities, we could not demonstrate that they were related to the neutrophil dysfunction. However, none of the control subjects (20 patients with systemic lupus erythematosus and 20 randomly selected eye clinic patients) had lesions resembling those of the patients with neutrophil dysfunction. Fisher's exact test (one-tailed) gave the following values: P less than .03 for keratitis; P less than .01 for chorioretinal scars; and P less than .001 for keratitis and chorioretinal scars. Abnormal neutrophil function probably interferes with the control of normal eyelid flora and predisposes the eye to the development of marginal keratitis. Eyelid hygiene and topical administration of antibiotics and corticosteroids during inflammatory episodes may prevent the progression of corneal vascularization. The chorioretinal scars do not appear to be progressive.

Adolescent↗
PubMed1981

Immune-enhanced phagocytic dysfunction in pulmonary macrophages infected with parainfluenza 1 (Sendai) virus.

Cultured alveolar macrophages infected with parainfluenza 1 (Sendai) virus were treated with specific antiviral immune serum and their phagocytic activity for opsonized erythrocytes (EA), Candida krusei, and Staphylococcus epidermidis quantitated. Membrane Fc receptor and candida binding activity were unaffected by the viral infection. In contrast, the virus infection decreased the phagocytic ingestion of EA. The addition of immune serum induced new phagocytic defects in that the treatment of virus-infected macrophages decreased the binding of EA and candida and reduced the ingestion of the yeast and the staphylococci. In addition, treatment with immune serum also enhanced the phagocytic defects induced by the virus infection alone, further reducing the binding and ingestion of EA. Neither virus infection nor treatment with immune serum affected the intracellular killing of S. epidermidis. These data demonstrated that virus infection of alveolar macrophages in vitro induce phagocytic defects that are accentuated by the treatment of the macrophages with antiviral antibody.

Animals↗
PubMed1997

[Chronic granulomatous disease (CGD): dysfunction of the neutrophil granulocyte NADPH-oxidase enzyme system].

Dysfunction of NADPH oxidase results in chronic granulomatous disease (CGD), a syndrome characterized by severe bacterial and fungal infections. Phagocytes of the patients are unable to kill ingested microorganisms which leads to the formation of granulomas and abscesses. Predominant pathogens are the catalase-positive bacteriae (Staphylococcus aureus) and some fungi (Aspergillus species). Infections of these patients should be treated by antimicrobial agents, which penetrate cells and kill pathogens inside. The aim of this study was to give a short description of the structure and function of the NADPH oxidase enzyme and to summarize the results obtained during the diagnostic of 10 patients with chronic granulomatous disease. Characterization of the disease was confirmed by mutation analyses.

Common Variable Immunodeficiency↗
PubMed1975

An appraisal of the nitroblue tetrazolium reduction test.

The available literature on the nitroblue tetrazolium reduction test is reviewed. The mechanism of this test is poorly understood. There are two basic methods of performing the test, namely, the stimulated and the spontaneous methods. However, the test procedure has not been standardized, and numerous modifications have ensued resulting in a number of technics. The stimulated test has proved to be valuable for screening patients or carriers with chronic granulomatous disease of childhood. It is one of the useful tests in studying neutrophil dysfunction. On the other hand, extensive accumulated data indicate that this test, be it stimulted or spontaneous, cannot be relied upon as an absolute test to differentiate bacterial from nonbacterial infectious disease as there have been numerous false-positive and false-negative results. When this test is used, the result should be interpreted in the context of other laboratory test results and the clinical picture of the patient. Preliminary data indicate that in certain diseases, if the initial test is positive in a particular patient, it may be useful as one of the follow-up tests to ascertain the activity of the disease process.

Bacterial Infections↗
PubMed1984

Neutrophil bactericidal dysfunction towards oxidant radical-sensitive microorganisms during experimental iron deficiency.

We developed a clear-cut nutritional iron deficiency anemia without concomittant malnutrition in rats given a low iron diet, and we restored normal iron and hemoglobin levels in these same animals with iron dextran injections. The neutrophil function studies performed during and after a period of iron deficiency showed the following: Phagocytosis of Staphylococcus aureus 502A, Streptococcus pneumoniae, and Salmonella typhimurium was not altered by iron deficiency or by the administration of iron; phagocytosis of Candida albicans was moderately abnormal during iron deficiency, and became normal with the restoration of iron sufficiency. Microbicidal activity towards Staphylococcus aureus 502A and Candida albicans, two catalase-positive microorganisms, was markedly decreased (to 50% of control values) and returned to normal when iron sufficiency was restored. Killing of a catalase-negative organism, Streptococcus pneumoniae was normal in iron-deficient rats. This pattern of differential bactericidal activities suggested an abnormality of the oxidant radical-generating machinery in neutrophils of iron-deficient animals. Indeed, iron deficiency caused a marked decrease of neutrophil nitroblue tetrazolium dye reduction, which disappeared after iron administration. Neutrophil myeloperoxidase activity was slightly decreased in iron deficient rats and returned to normal after iron administration. Microbicidal activity towards a gram-negative, catalase-positive organism, Salmonella typhimurium, was equal in iron deficient and iron sufficient animals. Our combined results suggest that a definite microbicidal defect is the consequence of nutritional iron deficiency, apart from any protein-calorie malnutrition. This defect affects the disposal in PMNs of two catalase-positive microorganisms (which require intracellular production of oxidant radicals for their destruction) but not of a catalase-negative bacterial species.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia, Hypochromic↗
PubMed1991

Mononuclear phagocyte system dysfunction in murine SLE: abnormal clearance kinetics precede clinical disease.

Although several studies have reported abnormal immune clearance in murine models of systemic lupus erythematosus (SLE), a consistent defect in mononuclear phagocyte function in SLE-prone mice has not been described. To evaluate the mechanism(s) of immune clearance in murine SLE, we applied the technique of kinetic analysis to clearance studies of radiolabeled, immunoglobulin-sensitized red blood cells in normal BALB/c and autoimmune BXSB, MRL-lpr/lpr, New Zealand black (NZB) and New Zealand black/white (NZB/W) mice. Clearance studies were performed in 4-week-old to 18-month-old mice with a complement-fixing rabbit IgG antimouse red blood cell antibody. Four clearance rate constants governing complement- and Fc-mediated clearance function were evaluated: complement-mediated sequestration (k1), C3b deactivation and release (k2), complement-dependent phagocytosis (k4), and Fc-mediated sequestration and phagocytosis (k3). BXSB male, MRL-lpr/lpr female and male, NZB female, and NZB/W female and male mice all had significantly decreased Fc-mediated clearance function (k3) when compared with control BALB/c mice (p less than 0.0001). This defect in Fc-mediated clearance was present in all four strains of autoimmune mice by 6 months of age and preceded the onset of serologic and clinical disease activity in NZB mice. Abnormal complement-mediated clearance was detected in MRL-lpr/lpr female and male mice, NZB female, and NZB/W female and male mice, but not in BXSB mice. In MRL-lpr/lpr mice decreased complement-mediated sequestration (k1, p less than 0.0001) and complement-dependent phagocytosis (k4, p less than 0.0001) were present as early as 4 weeks of age. In contrast, the change in complement-mediated clearance in NZB and NZB/W mice was characterized by decreased C3b deactivation and release (k2, p less than 0.001) and resulted in an enhanced early phase of clearance. Decreased k2 values in New Zealand mice occurred as early as 2 months of age, preceding serologic and clinical disease activity as well as decreased Fc receptor function. These studies demonstrated an early, progressive, and uniform defect in Fc-mediated clearance in the four murine strains of SLE studied. Complement-mediated clearance, however, varied considerably in lupus-prone mice, ranging from severe impairment in MRL-lpr/lpr to normal function in BXSB and accelerated clearance in NZB and NZB/W mice. Accelerated clearance in New Zealand mice was characterized by decreased C3b deactivation and release of antibody sensitized cells, which in turn led to increased phagocytosis of sensitized cells sequestered by complement-dependent processes.

Animals↗
PubMed1989

History and implications of the neutrophil glycoprotein deficiencies.

This review focuses on the initial clinical descriptions and subsequent investigation of the syndrome of recurrent infections associated with neutrophil membrane glycoprotein deficiencies. Characterization of the missing group of three glycoprotein heterodimers and their role in adhesion-related neutrophil function is summarized. Study of the clinical consequences of these genetically determined membrane glycoprotein defects has also contributed to the understanding of the role of normal neutrophils in both host defense and host tissue damage.

Glycoproteins↗
PubMed1990

Desferrioxamine improves neutrophil phagocytosis in thalassemia major.

The aims of the present study are: first, to assess the toxic role of serum from thalassemic patients in phagocytosis of PMN from healthy controls, and second, to seek to determine whether serum and cellular disturbances of polymorphonuclear neutrophils (PMN) phagocytosis, observed in thalassemic patients, can be prevented and/or corrected by use of desferrioxamine (DFX). Two kinds of in vitro incubations--without or with DFX--were performed. PMN or serum from thalassemic patients or from healthy controls was used. First, a phagocytosis defect of 3 different bacteria species was induced in PMN from healthy controls by incubation in thalassemic serum. Second, DFX could prevent, already at 1 microM, the phagocytic defect induced in normal PMN by the incubation with thalassemic serum, with disappearance of the toxic role of thalassemic serum at higher concentrations. Third, improvement of the phagocytosis defect of PMN from thalassemic patients was also observed at 1 microM of DFX for the 3 bacteria species. Normalization was obtained at higher concentrations for gram-negative bacteria. In vivo studies revealed, after a 3 hr subcutaneous infusion of DFX into 3 thalassemic patients, an improvement of the phagocytosis results and a decrease of the Prussian Blue reactivity of the PMN. It is concluded first that an iron-mediated defect in phagocytosis can be induced in normal neutrophils by incubation in serum from thalassemic patients, and second that a precautious and intensive chelation therapy seems to be advantageous for increasing PMN defense against infectious agents. Special care must nevertheless be taken in order to detect rapidly opportunistic (such as Yersinia) infections.

Adolescent↗
PubMed1985

p150/95, Third member of the LFA-1/CR3 polypeptide family identified by anti-Leu M5 monoclonal antibody.

Monoclonal antibody (mAb) anti-Leu M5 reacts with a two-chain molecule composed of a 150-kDa alpha subunit noncovalently associated with a 95-kDa beta subunit and probably is specific for an epitope on the 150-kDa alpha chain. This p150/95 antigen is the third member of a family of polypeptides sharing a common 95-kDa beta chain, which includes the lymphocyte function-associated antigen LFA-1 (p177/95) and complement receptor CR3 (Mo1/MAC-1/OKM1; p165/95) antigens. Sequential immunoprecipitation with anti-p95 beta chain mAb specifically removed the antigens detected by anti-LFA-1, anti-CR3 and anti-Leu M5 mAb. Certain patients with recurrent bacterial infections are genetically deficient in expression of the LFA-1 and Mo1 antigens, and have impaired granulocyte function. Granulocytes from a patient with this disease also failed to react with anti-Leu M5. Stimulation of normal granulocytes with f-Met-Leu-Phe, C5a-desArg, or calcium ionophore resulted in increased expression of Mo1 and Leu M5 antigens on the cell surface, but did not significantly increase expression of LFA-1 antigen. In functional assays, anti-Leu M5 did not inhibit T cell-mediated or natural killer cell-mediated cytotoxicity. In addition, anti-Leu M5 neither inhibited the binding of complement-coated particles to CR1 or CR3 nor did it affect the binding of EC3dg to neutrophils (CR4). These studies clearly indicate that the p150/95 antigen recognized by the anti-Leu M5 antibody is a structurally distinct member of the LFA-1/CR3 family.

Antibodies, Monoclonal↗
PubMed1992

Impaired neutrophil bactericidal activity correlates with the infection occurring after surgery for esophageal cancer.

We examined whether or not preoperative impaired bactericidal activities of polymorphonuclear neutrophils (PMN) are associated with infections following surgery for esophageal cancer. Intracellular killing (KI), superoxide anion-producing capacity (SOP), and myeloperoxidase (MPO) activity were measured in 22 patients with esophageal cancer, 27 with gastric cancer, and 13 age-matched controls. The average level of KI was significantly depressed in patients with esophageal cancer or with gastric cancer, to a similar extent, compared to findings in controls, but SOP was not. In esophageal cancer patients, the SOP level was significantly higher in those with postoperative septic complications than in those without such problems, whereas the KI level was depressed to a similar extent in both. Therefore, a depression of KI with elevation of SOP of PMN may serve to predict complications of infection following surgery in patients with esophageal cancer.

Adult↗