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Biomedical subjects

N I Abdou

Publications and source records attributed to N I Abdou.

At least 55 records · Page 3Linked to original sources
PubMed1986

Study of anti-DNA antibodies prepared by DNA cellulose or Cibacron blue chromatography.

We prepared anti-DNA antibodies from sera of lupus patients by either DNA cellulose or by Cibacron blue chromatography. Eluates from both columns were studied with respect to recovery of IgG, recovery, purification and specificity of anti-DNA activity. An attempt was made to raise rabbit anti-idiotypic antibodies against both eluates. DNA cellulose chromatography--if DNA leakage was prevented--yielded 58% recovery and 58-fold purification of the anti-DNA activity present in the original purified IgG sample. 1% of loaded IgG was recovered. Cibacron blue chromatography yielded 32% recovery and 1.1-fold purification of the anti-DNA activity. 29% of loaded IgG was recovered. Eluates of Cibacron blue were not pure as shown by their high binding activity against an unrelated antigen, tetanus toxoid. Eluates from DNA cellulose were pure and did not show anti-tetanus toxoid activity. Rabbit anti-idiotypic antibodies could be raised only against eluates of DNA cellulose suggesting that the eluates of Cibacron blue did not contain enough idiotypes to induce anti-idiotypic antibodies. The characterization of the rabbit anti-idiotypic antibodies showed that it contained two populations, one against site-specific idiotypes and the other against framework idiotypes. Anti-DNA antibodies prepared by Cibacron blue had idiotypes similar to those prepared by DNA cellulose. The present study demonstrates that DNA cellulose chromatography--if leakage of DNA is prevented--can yield excellent recovery and purification of anti-DNA activity. Anti-DNA antibodies prepared by DNA cellulose were enriched and could induce anti-idiotypic antibodies in rabbits. Tube chromatography on Cibacron blue yielded poor recovery and minimal enrichment of anti-DNA activity.

Animals↗
PubMed1986

Effect of exchange transfusion with Fluosol DA 20% on splenic distribution and immunocompetence of rat lymphocytes.

T- and B-splenic lymphocyte frequency, immune response 4 days after immunization with sheep red blood cells (SRBC), and proliferative response to concanavalin A (Con A) were determined 1, 3, and 5 days after exchange transfusion with Fluosol DA 20% (FDA) in adult, male Sprague-Dawley rats vs sham transfused rats. T-cell, T-helper, T-suppressor, and B-lymphocyte were reduced 1 day after transfusion (P less than or equal to 0.001). T- and B-lymphocyte frequencies were still reduced at day 3 (P = 0.0372). By day 5, there were no significant reductions in T-cell, T-helper, T-suppressor, and B-cell frequencies in the FDA-transfused rats. The frequency of cells with cytoplasmic IgG was reduced (P less than or equal to 0.025) in cells harvested from spleens of FDA-transfused rats and tested fresh. Proliferative response of splenic lymphocytes to Con A was unaffected by transfusion with FDA (P greater than or equal to 0.078). Splenic hemolytic plaques in response to SRBC were unaffected if rats were transfused 3 days after immunization with SRBC and 1 day prior to study (P = 0.941), enhanced if rats were transfused 1 day after SRBC immunization and 3 days prior to study (P = 0.0015), and suppressed if rats were transfused 1 day before SRBC immunization and 5 days before study (P less than 0.0001). Transfusion with FDA causes transient decreases in identifiable T and B lymphocytes, depresses cytoplasmic IgG-positive B cells, does not affect proliferative response to Con A, does not affect an ongoing specific immune response, enhances an early specific immune response, and inhibits the induction of a specific immune response.

Animals↗
PubMed1984

Takayasu's arteritis: reversal of pulse deficit after early treatment with corticosteroids.

Takayasu's arteritis is a rare disease characterized by inflammation and stenosis of large arteries. The aortic arch and its branches are most often affected. Initial symptoms are nonspecific and the diagnosis may be delayed until signs of vascular insufficiency appear. Results of medical treatment have been conflicting. We report a case of a young woman with a short history of pulse deficits, high erythrocyte sedimentation rate, narrowing of the subclavian arteries on arteriography, and a complete return of pulses after high dose corticosteroids. Takayasu's arteritis is a treatable disease in its early phase, but treatment response may be disappointing after irreversible vascular lesions develop.

Adult↗
PubMed1983

Heterogeneity of bone marrow-directed immune mechanisms in the pathogenesis of neutropenia of Felty's syndrome.

Twenty-seven patients with Felty's syndrome were studied by the colony forming unit in culture (CFU-C) assay for possible immune mechanisms within the bone marrow compartment that could contribute to the neutropenia. Depletion of bone marrow suppressor T cells resulted in normal CFU-C numbers in 7 patients. In 5 patients serum antiprecursor cell activity was detected. Blood monocytes failed to generate colony stimulating factor in 5 patients. Bone marrow-directed immune mechanisms are heterogeneous and could play a role in the pathogenesis of neutropenia in some patients with Felty's syndrome.

Adult↗
PubMed1983

In vitro growth promotion of T-lymphocyte colonies from normal human bone marrow with 12-O-tetradecanoylphorbol-13-acetate (TPA).

An in vitro culture system for the growth of T-lymphocyte colonies from normal human bone marrow has been described. This culture system features the use of 12-O-tetradecanoylphorbol-13-acetate (TPA) at moderately high concentrations (10(-7)-10(-6) M) and daily feeding with growth medium containing leukocyte-conditioned medium primed with phytohemagglutinin. T-lymphocyte colonies in this system can reach a size of over 10,000 cells/colony, suggesting that cells assayed in this system are early progenitors of T-lymphocytes with extensive proliferative capacity. TPA, at a higher concentration (10(-5) M), is inhibitory to the growth of T-lymphocytes, but this level is 5 orders of magnitude higher than the minimum TPA concentration (10(-10) M) inhibitory to myeloid colony forming cells. This demonstrates marked difference in the sensitivity of T-lymphocyte colony forming cells and myeloid colony forming cells to TPA. It appears that this assay system should be useful for the study of the early progenitors of human bone marrow T-lymphocytes.

Bone Marrow Cells↗
PubMed1982

Hidradenitis suppurativa: evidence for a bactericidal defect correctable by cholinergic agonist in vitro and in vivo.

Hidradenitis suppurativa (HS) affects the apocrine sweat glands, giving chronic recurrent abscesses of axillary and perineal areas. We report a patient who had a defect in polymorphonuclear leukocyte killing of bacteria associated with low levels of intracellular cyclic GMP. This defect was corrected with a cholinergic agonist in vitro. Treatment of the patient with a cholinergic agonist, bethanechol chloride, resulted in prolonged clinical improvement, normal bactericidal function, and normal levels of intracellular cyclic GMP. The possible mechanisms responsible for the bactericidal defect and for the patient's improvement are discussed.

Aged↗
PubMed1982

Mycobacterium fortuitum infection: evidence of bactericidal defect due to hyperactive antigen-specific suppressor cells. Correction in vitro and in vivo by cholinergic agonist and indomethacin.

Immunologic studies in a patient with long-standing Mycobacterium fortuitum infection revealed normal numbers of T cells, T inducers, T suppressors, B cells, and monocytes, significant in vitro proliferative response to M. fortuitum antigen, and poor bactericidal activity against M. fortuitum but not against Escherhicia coli. M. fortuitum antigen-activated suppressor cells contributed to the bactericidal defect. The activity of these suppressor cells could be eliminated by the in vitro treatment of blood mononuclear cells with a combination of a cholinergic agonist and indomethacin, but not with either alone. Administration of the two drugs to the patient resulted in reversal of the bactericidal defect and dramatic clinical improvement. Systemic atypical (nontuberculous) mycobacterial infection may activate specific suppressor cells that could compromise the host's phagocytic cell function. Modulation of those suppressor cells by a combination of a cholinergic agonist and prostaglandin synthetase inhibitor could reverse this abnormality and may be beneficial to the patient.

Adult↗
PubMed1982

Modulation of venom-induced leukocyte histamine release by mononuclear cells: effect of venom immunotherapy.

Leukocyte histamine release and blood mononuclear cell proliferative responses to venoms were evaluated in nine patients with sting anaphylaxis. The effect of venom-activated mononuclear cells on the autologous mononuclear cell proliferative response and venom-induced leukocyte histamine release was also studied before and on maintenance immunotherapy. The mononuclear cell proliferative response was low (specific incorporations less than 2.0) and antigen nonspecific both before and during maintenance immunotherapy. Venom-induced in vitro leukocyte histamine release did not change significantly with immunotherapy. However, when patients were on maintenance immunotherapy, venom-activated mononuclear cells cocultured with autologous leukocytes significantly (p less than 0.05) suppressed venom-induced histamine release. The suppressive effect of mononuclear cells was antigen specific and enhanced by in vitro mononuclear cell activation. Suppression of leukocyte histamine release by mononuclear cells extends the regulatory potential of these cells and may identify an additional mechanism by which immunotherapy protects Hymenoptera-sensitive individuals against systemic anaphylaxis.

Adult↗
PubMed1982

Lymphocyte studies in a patient with chronic polyradiculoneuropathy.

We studied immunologic abnormalities in one patient with chronic polyradiculoneuropathy and the effects of immune suppression and plasmapheresis on the clinical course and immune abnormalities. Increased helper T cells and B cells with deficiency of T suppressor cells to B-cell but not to T-cell targets were detected. The patient's blood lymphocytes, but not the controls' lymphocytes, proliferated in vitro on culturing them with P2 antigen in the presence of the patient's CSF. Plasmapheresis combined with corticosteroid and azathioprine reversed the majority of immune abnormalities to normal but did not decrease the patient's lymphocyte-P2 proliferative response; nor did it improve clinical status.

Adult↗
PubMed1982

Specific immunoregulation abnormality in insulin-dependent diabetes mellitus.

We evaluated antigen-nonspecific (Con A) and antigen-specific (islet cell) activation of suppressor cell function in 11 IDD patients. Compared with healthy controls, IDD was associated with both antigen-specific (n = 11, p less than 0.01) and nonspecific (n = 6, p less than 0.03) suppressor cell hypofunction. The specific defect was not present in NIDD patients and correlated negatively with the duration of the disease (r = -0.6, p less than 0.05). No relationship was found between the degree of specific suppressor cell dysfunction and diabetic control as assessed by glycosylated hemoglobin, plasma glucose values, insulin-binding capacity, or C-peptide determinations. Plasma from IDD lacked anti-suppressor cell activity. Low levels of circulating immune complexes were detected in IDD patients whose disease duration was 1 month or less. Specific suppressor cell hypofunction and/or enhanced helper cell activity in early stages of IDD could be contributing to the formation of islet cell autoantibodies, immune complexes, islet cell injury, and the diabetic state.

Adolescent↗