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Biomedical subjects

D A Norris

Publications and source records attributed to D A Norris.

At least 109 records · Page 6Linked to original sources

Fibronectin fragment(s) are chemotactic for human peripheral blood monocytes.

Both plasma-derived and cell-derived fibronectin are deposited at sites of inflammation and wound healing and are associated with migrating cell populations including monocytes/macrophages. We found that fibronectin fragments generated by endogenous protease(s) are potent chemoattractants for human peripheral blood monocytes, whereas intact fibronectin has no activity. Fibronectin preparations produced by gelatin affinity chromatography in the absence of protease inhibitors contained 90 to 220 kd fragments and had potent chemotactic and chemokinetic activity for monocytes but no activity for human neutrophils or lymphocytes. The addition of phenylmethylsulfonyl fluoride to plasma reduced but did not eliminate the recovery of fibronectin fragments and likewise reduced the chemotactic activity. When the preparations were further purified by DEAE ion exchange and Sepharose 4B molecular sieve chromatography, however, intact fibronectin was recovered that lacked both chemotactic and chemokinetic activity. When fragment-poor fibronectin was allowed to sit at 25 degrees C in NaN3 but without protease inhibitors, increased fragmentation and increased chemotactic activity were noted. In addition, chemotactically active small m.w. fragments arose from high m.w. fragments or from intact fibronectin as demonstrated by rechromatography experiments over Sephadex G-150. These findings suggest that proteolytic cleavage of fibronectin during inflammatory processes produces fragments that selectively augment the recruitment of monocytes into tissue sites of inflammation.

Cells, Cultured↗

Nevoid basal cell carcinoma syndrome. Multiple basal cell carcinomas of the palms after radiation therapy.

A patient with the nevoid basal cell carcinoma syndrome had been treated with radiation therapy to the hands at 5 years of age. Multiple basal cell carcinomas of the palms and dorsa of the hands developed when the patient was 28 years of age. It is proposed that the radiation therapy induced tumors in palmar pits that seem to represent a forme fruste of basal cell carcinoma. Radiation therapy should be avoided in individuals with the nevoid basal cell carcinoma syndrome.

Adult↗

ADCC effector function in patients with atopic dermatitis. A possible mechanism of susceptibility to severe cutaneous viral infections.

Peripheral blood mononuclear cells from patients with chronic atopic dermatitis were evaluated as effectors of antibody-dependent cellular cytotoxicity (ADCC) to determine if faulty effector function might explain the susceptibility of atopics to severe cutaneous viral infections in spite of adequate specific antibody titers. Eleven atopic patients whose dermatitis was well controlled and who were not infected or on immunosuppressive therapy were studied using sensitized human and chicken erythrocyte targets at three different effector:target ratios. No significant differences in mean ADCC were seen between atopics and controls. However, the function of peripheral blood mononuclear cells from atopic patients who had a previous history of severe cutaneous viral infection was significantly depressed against sensitized chicken, but not human targets. This suggests that atopic patients who develop severe cutaneous viral infections may represent a subset of atopics with an intrinsic or variable defect in K lymphocyte--mediated ADCC which might render them susceptible to persistent, extensive viral infections.

Adult↗

Cryoglobulinemia and decreased monocyte chemotaxis is malignant melanoma.

The sera fromm 13 patients with malignant melanoma were evaluated for immune complexes by cryoprecipitation and the 125I Clq binding assay. Cryoprecipitates were identified in 12/13 patients (92%) and cryoimmunoglobulins in 7/13 patients (54%). Either cryoimmunoglobulin or elevated Clq binding was identified in 8/13 patients (62%). Incubation of normal monocytes with the resuspended cryoimmunoglobulin of 7 melanoma patients produced greater than 50% reduction in the ability of th monocytes to respond to chemotactic stimuli (p < .01). Similar inhibition was seen with cryoimmunoglobulin from erythema multiforme patients, but not with 'medium alone, albumin, heat aggregated albumin or heat aggregated-IgG in similar concentrations. No soluble factors produced in vitro could be demonstrated to produce this inhibition. Inhibition of monocyte function by immune complexes may be an important component of impaired host response to malignant melanoma, or alternatively may represent an important mechanism for the accumulation of monocytes at sites of inflammation, analogous to migration inhibition factor.

Adolescent↗

Monocyte chemotaxis in leukemia patients.

Monocyte chemotaxis was studied in 35 patients with ALL, six with CLL, six with AML, and 10 with CML before beginning chemotherapy. Function was contrasted to age-matched control groups. Significant inhibition of chemotaxis was seen in patients with ALL (p less than 0.001) and CLL (p less than 0.01), whereas function in CML and AML patients was not significantly depressed. The deficient monocyte chemotaxis was not due merely to decreased percentages of peripheral blood monocytes. Thus, in addition to numerical deficiencies in monocyte numbers, qualitative deficiencies in monocyte function exist in patients with ALL and CLL.

Acute Disease↗

Defective monocyte chemotaxis in mycosis fungoides: lack of essential helper lymphocytes.

The effect of lymphocytes on monocytes chemotaxis in vitro was studied using lymphocyte fractions prepared by glass bead column separation and mononuclear cell fractions prepared by Ficoll-Hypaque separation. The diminished monocyte chemotaxis in ten patients with mycosis fungoides was corrected in vitro by the addition of normal lymphocytes. This helper effect was not mediated by soluble factors. Lymphocytes from mycosis fungoides patients did not inhibit chemotaxis by monocytes from mycosis fungoides patients did not inhibit chemotaxis by monocytes from normal donors. No cell directed chemotactic inhibitor, differences in LDCF production in vitro or differences in circulating chemattractants were found. These data support the conclusion that the abnormal monocyte chemotaxis seen in mycosis fungoides is due to lack of essential helper lymphocyte function and represents an abnormal mononuclear cell interaction which may be important in the establishment of the mononuclear cell infiltrate in mycosis fungoides.

Adult↗

Human monocyte chemotaxis: a quantitative in vivo technique.

This report describes a new quantitative technique for evaluating monocyte chemotaxis to a site of superficial epidermal abrasion. Micro-acrylic chambers containing 50% Zymosan activated autologous serum were separated from a 5-mm diameter epidermal abrasion by 2 Nucleopore filters which entrapped migrating monocytes but allowed free neutrophil migration. Monocytes were specifically identified by alpha napthyl acetate esterase activity. Monocytes accumulated within the filters by 4 hr and maximized at 16 and 20 hr. This technique is superior to previous skin chamber techniques in the high yield of monocytes and in specific histochemical identification of monocytes. In contrast to the Rebuck window, it does not generate attractants and has greater reproducibility. This technique will be useful in the study of diseases characterized by monocytic infiltrates, in contrasting the function of peripheral blood monocytes to those available in the skin, and in testing the effects of drugs, immunodeficiency and infection on monocyte function in vivo.

Chemotaxis, Leukocyte↗

Isolation of functional subsets of human peripheral blood monocytes.

Monocytes were isolated by counterflow centrifugation of Ficoll-Hypaque separated peripheral blood mononuclear cells. The monocytes formed a bimodal volume distribution of "large" and "small" phagocytic esterase-positive, peroxidase-positive cells with peaks at 470 and 410 mu3, respectively. The large monocytes were predominately Fc receptor positive, and were able to lyse both sensitized human and chicken erythrocyte targets in ADCC assays, whereas the small monocytes were largely FcR negative and were inactive against sensitized human erythrocyte targets. However, ADCC against chicken erythrocyte targets was seen in some fractions containing small monocytes and was probably due to FcR+ lymphocytes (K cells) in those fractions. These experiments establish that monocytes are effectors of ADCC against both human and chicken erythrocyte targets and that the peripheral blood monocyte is heterogeneous in size, function, and surface receptor distribution.

Animals↗

Pyoderma gangrenosum. Abnormal monocyte function corrected in vitro with hydrocortisone.

A 34-year-old man with chronic active hepatitis and pyoderma gangrenosum demonstrated abnormalities in neutrophil and monocyte function. Monocytes from this man had diminished chemotaxis and bacterial phagocytosis. These functions were significantly improved in vitro after one hour of incubation of monocytes with 10(-5) hydrocortisone. Neutrophil function was nornal for bactericidal activity and phagocytosis, but neutrophil chemotaxis was diminished. A plasma inhibitor was not found to explain these phagocyte alterations.

Adult↗

Monocyte cellular function in asthmatic patients on alternate-day steroid therapy.

Monocyte cellular function in 15 asthmatics on alternate-day steroid therapy (mean dose of prednisone, 45.4 +/- 17.45 mg qod) was studied at 8 A.M. and noon after receiving an 8 A.M. steroid dose and at 8 A.M. the following day, and was contrasted to function in 16 healthy controls. Monocyte chemotaxis, bacterial killing and phagocytosis, and oil phagocytosis were not significantly altered by the steroid dose. On the other hand, all the patients experienced monocytopenia, lymphopenia, and neutrophilia 4 hr following the administration of steroid. The lack of functional impairment on this clinically relevant steroid regimen is consistent with the lack of serious infections seen in patients on such regimens. This study re-enforces the need to differentiate the effect of even small doses of steroid on circulating cell populations from direct effects on cell function which occur only with very high or frequent steroid dose regimens.

Asthma↗

An evaluation of Brass mortality estimates under conditions of declining mortality.

An evaluation of the Brass childhood mortality estimates under conditions of declining mortality shows them to overestimate current mortality. Error increases as the rate of mortality decline increases, as the childhood age up to which cumulative mortality is being estimated increases, and as age at onset of childbearing decreases. We use the results to develop a method for correcting the Brass estimates for the effects of quasistability. The method requires an estimate of the rate of mortality decline within the population in addition to information on the pattern of childbearing in the population.

Birth Rate↗

The sequelae of group B beta-hemolytic streptococcal meningitis in early infancy.

The group B beta-hemolytic streptococcus is responsible for an escalating frequency of neonatal meningitis. Of the 18 consecutive cases we report in this study, the mortality was 17%. Among the 15 survivors, there were two children with extensive neurological and psychological impairment. There were no major differences between the survivors and controls in tests of hearing and language function, social skills, and psychological testing. There was a greater number of minor neurological signs among the study group. The mortality and morbidity of group B beta-hemolytic streptococcal meningitis is apparently substantially less than that of all other types of neonatal bacterial meningitis.

Bender-Gestalt Test↗

The effect of immunosuppressive and anti-inflammatory drugs on monocyte function in vitro.

MNL cellular chemotaxis, bacterial killing and phagocytosis, and Oil Red O phagocytosis were studied in vitro in the presence of eight anti-inflammatory or immunosuppressive drugs. Inhibition of Boyden Chamber migration of MNL's in a MNL-lymphocyte mixture was achieved after 1/2 hr incubation by 10(-3) and 10(-4) mol/L. concentrations of chloroquine (maximum inhibition 63% +/- 2.8), dexamethasone (58% +/- 8.6), 6-mercaptopurine (62% +/- 4.2), methotrexate (66% +/- 6.4), and vinblastine (100%). Bacterial killing was not significantly affected by any of the drugs studied. Bacterial phagocytosis was improved by vinblastine at 10(-3) and 10(-4)M and by 6-mercaptopurine at 10(-5)M, but there was apparent interference with the assay at high drug concentrations. Modification of the Oil Red O technique showed inhibitions of MNL phagocytosis by vinblastine at 10(-3)M (69% +/- 2.8 inhibition), chloroquine at 10(-3)M (49% +/- 8.5), and mercaptopurine at 10(-3)M (32.5% +/- 0.7). Cyclophosphamide, although reported to require hepatic conversion in vivo, may be partially activated in a lymphocyte-MNL mixture in vitro, producing a decrease in cell viability but no statistically significant impairment of MNL function. These results support direct inhibition of MNL cellular function as one of the mechanisms of the anti-inflammatory action of chloroquine, dexamethasone, methotrexate, 6-mercaptopurine, and vinblastine.

Anti-Inflammatory Agents↗

Pathogenesis of cutaneous lupus erythematosus.

Antibody-dependent mechanisms of tissue damage are the principle mechanism of disease in systemic and cutaneous lupus erythematosus. Antibody-dependent mechanisms of keratinocyte damage appear to be a primary pathogenetic factor in all forms of papulosquamous cutaneous lupus. Photosensitive papulosquamous lupus syndromes, such as subacute cutaneous LE, neonatal LE, "ANA-negative" LE, and complement-deficient LE are all strongly associated with antibodies to the ribonucleoprotein SSA. Evidence is accumulating that antibodies to SSA (and perhaps to SSB) induce antibody-dependent cell-mediated cytotoxicity (ADCC) of basal keratinocytes in all of these lupus syndromes. Evidence is also growing that autoantibodies in cutaneous LE syndromes are directly involved in disease pathogenesis, and are not simply markers of disease subsets. The relationship of the photosensitive anti-SSA-associated LE syndromes to more classical discoid LE or to acute papulosquamous LE in SLE patients remains to be studied. In both discoid LE and acute LE, basal keratinocyte damage can be seen, just as in the anti-SSA-associated photosensitive LE syndromes, but other antigen-antibody systems may be involved in initiating keratinocyte damage, or other cytotoxic mechanisms may produce keratinocyte damage characteristic of these syndromes.

Antibody-Dependent Cell Cytotoxicity↗