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Biomedical subjects

M Ballow

Publications and source records attributed to M Ballow.

At least 37 records · Page 2Linked to original sources
PubMed1986

Development of the immune system in very low birth weight (less than 1500 g) premature infants: concentrations of plasma immunoglobulins and patterns of infections.

Plasma immunoglobulin concentrations of premature infants of birth weight less than 1500 g were measured longitudinally from birth to 10 months chronological age. Infants were divided into two groups based on gestational age (group I: 25-28 wk; group II: 29-32 wk). In the 1st wk of life, plasma IgG levels correlated with gestational age (r = 0.5, p less than 0.001). At 3 months chronological age, the geometric mean plasma IgG levels were 60 mg/dl in group I and 104 mg/dl in group II infants. Most infants remained hypogammaglobulinemic at 6 months with seven of 11 infants in group I and 13 of 21 infants in group II having plasma IgG levels below 200 mg/dl. In the 1st wk of life, plasma IgM concentrations were 7.6 and 9.1 mg/dl in groups I and II, respectively. They rose to 41.8 and 34.7 by 8 to 10 months of life. Plasma IgA concentrations were comparable for groups I and II in the 1st wk of life (1.2 and 0.6 mg/dl, respectively), but at 1 month of age group I infants had a transient increase in IgA which was not seen in the group II infants (4.5 versus 1.9 mg/dl, respectively, p less than 0.02). This transient elevation in IgA did not correlate with type or route of feeding or amounts of transfused blood. Group I and group II infants had comparable rates of infections prior to discharge from the nursery (p = 0.27). After discharge, the 43 preterm infants followed until 10 months chronological age had a significantly higher incidence of infections than 41 term infants (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1985

The aetiological agent of cat scratch disease.

A highly pleomorphic, gram-positive bacterium was cultured from an excised lymph node of a patient with cat scratch disease (CSD). The organism had morphological forms similar to those of the bacterium observed in Warthin-Starry stains of lymph node sections from CSD patients and may be the aetiological agent of this disease. Electron microscopic examination of lymph node sections from another patient with CSD showed organisms with morphological forms similar to those of the isolated bacterium. Biochemical and physiological analyses of this isolate suggested that it is not a commonly recognised contaminant or human pathogen and that it may be a member of the genus Rothia. This organism appears to resemble the bacterium that was identified as the aetiological agent of Parinaud's oculoglandular syndrome, a specific form of CSD, over 70 years ago.

Actinomycetaceae↗
PubMed1985

Modulation of suppressor-cell activity by cimetidine in patients with common variable hypogammaglobulinemia.

Because of evidence of a possible immunoregulatory role for cimetidine, an antagonist to histamine H2 receptors, we studied the effects of this drug in five adult patients with common variable hypogammaglobulinemia. Three patients had excessive suppressor-cell function associated with panhypogammaglobulinemia, whereas the other two had no apparent T-cell defects. The patients were given a one-month course of oral cimetidine (1200 mg daily in four divided doses). Subsequently, the three patients with excessive suppressor-cell function had a marked reduction in suppressor activity along with a decrease in the number of suppressor cells (T8+). One of these three had a marked rise in both in vitro immunoglobulin secretion and serum immunoglobulin concentrations, which was reversible after the drug was stopped for three months and reproducible when therapy with cimetidine was repeated. There was no difference in immunoglobulin secretion or suppressor-cell activity while taking cimetidine between the two patients with common variable hypogammaglobulinemia without excessive suppressor-cell activity and control patients with duodenal ulcers. The data suggest that H2-receptor antagonists may decrease excessive suppressor-cell activity and allow endogenous immunoglobulin production in some patients with common variable hypogammaglobulinemia.

Adult↗
PubMed1985

Varicella pneumonia in a bone marrow-transplanted, immune-reconstituted adenosine deaminase-deficient patient with severe combined immunodeficiency disease.

Bone marrow transplantation provides an important modality for "enzyme replacement" and the immune reconstitution of patients with adenosine deaminase (ADA) deficiency and severe combined immunodeficiency disease. We report a patient with ADA deficiency who develops severe varicella pneumonia 6 years after successful bone marrow transplantation and immune reconstitution. Marked abnormalities in T-cell mitogen responsiveness and pokeweed mitogen-induced polyclonal immunoglobulin synthesis occurred. Coculture experiments suggested the presence of increased suppressor activity. T-cell phenotyping showed decreased T3 and T4 subsets. These abnormalities slowly resolved over several months as the patient recovered from the varicella infection. ADA enzyme levels and metabolite concentrations in urine and erythrocytes remained unchanged. These findings, together with the chromosome and immune studies, suggested that the bone marrow graft remained intact. These studies indicate that immunologically reconstituted ADA-deficient patients may be at higher risk for complications related to varicella infection and suggest that the institution of preventive measures is important.

Adenosine Deaminase↗
PubMed1985

Erythroderma with spongiotic dermatitis. Association with common variable hypogammaglobulinemia.

Two middle-aged men presented with generalized erythroderma, diffuse alopecia, and hyperkeratosis of the palms and soles. Histopathologic study demonstrated spongiosis (epidermal intercellular edema) with a perivascular lymphohistiocytic infiltrate. Complete immunologic evaluation demonstrated that both patients had panhypogammaglobulinemia and markedly depressed in vitro pokeweed mitogen-induced immunoglobulin secretion. One of the patients also showed poor lymphocyte responses in vitro to T cell mitogens and antigens and had a decreased ratio of helper to suppressor cells. In both patients, the cutaneous lesions improved with systemic corticosteroids, but no significant alteration in the immunologic abnormalities was observed. This report illustrates that chronic erythroderma may be the presenting clinical manifestation of common variable hypogammaglobulinemia.

Agammaglobulinemia↗
PubMed1985

Complement proteins and C3 anaphylatoxin in the tears of patients with conjunctivitis.

Previous studies in our laboratory have demonstrated pollen-specific IgG antibodies in the tears of patients with vernal conjunctivitis (VC) and elevated tear IgG levels in patients with contact lens-induced giant papillary conjunctivitis (GPC). Tear secretions were examined for complement (C) proteins to determine the role of this effector system in the pathogenesis of these ocular disorders. The tears of VC (15) and GPC (10) patients with active disease had elevated tear levels of both C3 and factor B. By use of transferrin as a marker for the leakage of plasma proteins into the tears, most C3 was locally produced by the conjunctival tissues. Although immune complexes could not be detected in the tear secretions, increased levels of C3 des Arg were present in the tears that suggested complement activation with the generation of anaphylatoxins. These studies suggest that complement may be important in the inflammatory ocular process of VC and GPC and that the generation of anaphylatoxins (C3a), even by nonimmune mechanisms, may contribute to basophil and mast cell activation with the release of inflammatory mediators into the tear secretions.

Complement C3↗
PubMed1978

Diphenylhydantoin interstitial nephritis. Roles of cellular and humoral immunologic injury.

A child with diphenylhydantoin hypersensitivity developed an associated interstitial nephritis. Circulating autoantibody of the IgG class which reacted with normal human tubular basement membrane was linearly deposited along host renal TBM. Cell-mediated immunity to the DPH antigen was also present. In addition, deposits of DPH were demonstrated along the renal TBM. It is suggested that initial alteration of host renal TBM by DPH deposition with secondary immune injury directed at the DPH-TBM antigen may have altered the TBM or uncovered new antigenic sites, rendering it susceptible to further injury on an autoimmune basis.

Autoantibodies↗
PubMed1978

Modulation of mixed lymphocyte culture reactivity following alloimmunization between H-1 (Ag-B)-histocompatible rat strains.

H-1 (Ag-B)-histocompatible rats were cross-immunized to study the effects of presensitization on the mixed lymphocyte culture (MLC) reactivity in normally nonresponsive MLC interactions. Lewis (LEW) rats, H-1 (Ag-B), were given s.c. injections of Fischer (F), H-1 (Ag-B), lymhocytes at weekly intervals for 3 weeks. Immunized LEW (Lew-iF) and F lymphocytes showed increased proliferative responses in MLC after the third immunization. The augmented proliferative responses in the MLC between these H-1 (Ag-B)-histocompatible rat strains following immunization may reflect minor histocompatibility antigenic differences. On the other hand, decreased proliferative responses in MLC between Lew-iF and Ag-B (H-1)-disparate rat strains were demonstrated. Alloimmunization across minor histocompatibility differences led to different types of regulatory effects on the MLC interactions. With low MLC responses, e.g., minor histocompatibility differences, the regulation tends to be positive; whereas for strong MLC responses, e.g., major H-1 (Ag-B) differences, the regulation tends to be negative or suppression.

Animals↗
PubMed1977

Biosynthesis of the third component of complement (C3) in vitro by monocytes from both normal and homozygous C3-deficient humans.

Human monocytes synthesized the third component of complement (C3) up to 5 wk in vitro. Evidence for net C3 synthesis was based on (a) incorporation of 14C-labeled amino acids into C3 protein, (b) indentity of the allotype of C3 produced in vitro with that of the doner's serum C3, even in the presence of carrier C3 protein of a different allotype; (c) correspondence of electrophoretic mobility, size, and subunit structure of C3 protein produced in vitro with serum C3; (d) inhibition of C3 production with cycloheximide. Monocytes from two unrelated C3-deficient patients were studied under conditions that supported C3 synthesis by normal monocytes. Serum from each of the patients contained less than 1% of the normal C3 concentration, buth their monocytes produced C3 at approximately equal to 25% of the normal rate when studied after 2 wk in vitro. The C3 produced in vitro by monocytes from one of the patients had the molecular weight of normal serum C3 and dissociated appropriately under reducing conditions. Monocytes from C3-deficient patients could not be distinguished from normals on the basis of morphology, rosetting with C3-coated erythrocytes, or rates of C2, and total protein synthesis.

Blood Proteins↗
PubMed1975

C1-bypass complement-activation pathway in patients with chronic urticaria and angio-oedema.

During the routine screening of 152 patients with urticaria or angio-oedema for hypocomplementaemia, 4 patients were found to have low serum levels of the third component of complement (C). These patients were noteworthy and differed from previous reports of patients with urticaria-like skin lesions and hypocomplementaemia because of the absence of immune-complex disease. In addition to the low C3, 2 of these patients were unique on the basis of low serum levels of haemolytic C1, C1q, C1s, and properdin factor B, but normal concentrations of C4 and C2. These C abnormalities may reflect a new clinical entity, and these cases form the first description in man of the C1-bypass complement-activation pathway.

Adult↗
PubMed1975

Complete absence of the third component of complement in man.

A 4-yr-old female patient who has recurrent infections with encapsulated bacteria and gramnegative organisms was found to have a complete absence of total hemolytic complement and C3. Total hemolytic complement was reconstituted by the addition of functionally pure C3. With the exception of a moderately reduced homolytic C4, all other C components, measured homolytically and by radial immunodiffusion, were present in normal amounts. By Ouchterlong analysis, the patient's serum contained C3b inactivator and properdin but no antigenic C3. Activation of the alternate pathway was examined by purified cobra venom factor (CVF) and inulin. Neither of these substances led to activation of properdin factor B to B. On addition of partially purified Cordis C3, in four out of four instances and with different preparations of Cordis C3, activation of factor B to B occurred in the inulin-serum-C3 mixture. In contrast, activation of factor B to B occurred only once out of four times with CVF-serum-C3 mixtures. Immune adherence was found to be normal in the patient's serum and could be removed by anti-C4 antiserum of hydrazine treatment. A marked opsonic defect was present against Escherichia coli. Serum bactericidal activity against a rough strain of E. coli was also defective. The ability to mobilize an infalmmatory response was examined by Rebuck skin window technique. A delay in neutrophil migration occurred until the 6th h. In vitro lymphocyte transformation and serum immunoglobulins were normal. The proportion of peripheral blood T cells forming spontaneous sheep erythrocyte rosettes and the percentage of B cells forming EAC rosettes by the C3 receptor were normal. The significance of the absence of C3 in our patient is emphasized by the increased number of infections with encapsulated bacteria and the decreased functional biological activities of the C system, important in host defense mechanism(s).

Blood Bactericidal Activity↗
PubMed1975

Complement in graft versus host disease: IL Depletion of complement components during a systemic graft versus host reaction in the rat (38499).

Serum complement (C) and C components were examined during a systemic graft versus host (GVH) reaction in the rat. In our series of experiments (Lewis times Brown Norway) F-1 hybrid rats (60-80g) were given 200 times 10-6 or 400 times 10-6 Lewis spleen cells intravenously. Clinical GVH disease appeared 5-7 days after cell injection. Five of six rats in the experimental groups had a fall in levels of serum C2 (20-76%) and C4 (75-98%). Only one of six rats in the control group had a significant fall in C components. In a subsequent experiment (Fisher 344 times Brown Norway) F-1hybrid rats (60g) were given 400 times 10-6 Fischer 344 spleen cells or 200 times 10-6 Fischer 344 Ficoll-Hypaque separated spleen lymphocytes. Clincal GVH disease in this instance appeared on day 10. As in the previous experiments C2 and C4 fell markedly, 20-60% and 60-8-%, respectively, from baseline titers. The control groups did not have a significant fall in C2 or C4. Further examination showed reduction in C3, C5, C6,AND C8 suggesting a sequential activation of the C system via the classical pathway. We have postulated that the cells undergoing blast transformation may be activating the C system through membrane changes during the GVH reaction. Furthermore, the deficiency of C AND C components during GVH disease may contribute to the increased susceptibility of the host to infection and sepsis.

Animals↗
PubMed1975

Transfer factor therapy: evidence for nonspecificity.

Four patients were treated with multiple doses of dialyzed transfer factor in which one Wiskott-Aldrich patient with abnormal IgG monocyte receptors obtained benefit. All patients converted skin reactivity, and had improved in vitro lymphocyte responses to varying degrees. Three patients developed positive reactivity to allogeneic cells in MLC, and one patient developed DNCB reactivity. These latter two findings suggest transfer factor may act by inducing a nonspecific maturation of lymphocyte function. A possible mechanism for the action of transfer factor is discussed.

Antibody Formation↗