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Biomedical subjects

I Gigli

Publications and source records attributed to I Gigli.

At least 55 records · Page 3Linked to original sources
PubMed1987

Langerhans cells in connective tissue diseases.

We have conducted a quantitative analysis of Langerhans cells (LC) in skin biopsies of 20 patients with various connective tissue diseases. Clinically normal skin of SLE patients as well as lesional skin of DLE showed consistently normal LC densities as assessed using ATPase staining, anti-DR and anti-OKT6. Examination of LC in clinically involved skin of patients with scleroderma revealed an absolute or relative decrease in ATPase and OKT6 expression, while staining with anti-DR gave inconclusive results. Clinically normal skin of the same individuals showed basically normal LC density. These findings suggest that the perturbation of the LC population is probably an expression of a secondary local phenomenon, and does not reflect a more widespread derangement of the accessory cells in the skin.

Adenosine Triphosphatases↗
PubMed1987

Langerhans' cells in paracoccidioidomycosis.

Langerhans' cells (LCs) appear to be altered in diseases that express a depressed cellular immune response. We measured the density of LCs in the skin of patients with the disseminated form of paracoccidioidomycosis. The study was performed using adenosine triphosphatase staining of epidermal sheets. Sixteen patients with paracoccidioidomycosis were evaluated. They had a highly significant reduction in LCs (LCs, 323 +/- 135/mm2) when compared with the number (LCs, 689 +/- 204/mm2) found in the control subjects. Morphological alterations of these cells were noted in patients with low numbers of LCs. These findings may reflect the depressed cellular immunity secondary to the infection with Paracoccidioides brasiliensis.

Adult↗
PubMed1986

Activation of complement by pathogenic and nonpathogenic Entamoeba histolytica.

Previous studies had demonstrated that strains of Entamoeba histolytica isolated from patients with colitis or amebic liver abscess were resistant to complement-mediated killing, whereas strains from asymptomatic patients were readily lysed by non-immune serum. Both serum-sensitive and serum-resistant strains of E. histolytica depleted complement rapidly as assessed by CH50, C3, and C7, and C5-9 hemolytic activities. Activation of the alternative pathway was important in lysis of nonpathogenic strains, as demonstrated by lysis by NHS (60.9 +/- 15.6%) and NHS + 5 mM EGTA (59.3 +/- 4.5%) as well as by C4-deficient guinea pig serum (72.8 +/- 7.1%) and C2-deficient human serum (64.4 +/- 11.1%), but not by NHS + 5 mM EDTA. Classical pathway activation also occurs as both pathogenic and nonpathogenic strains deplete greater than 98% of C4 activity, although it is not necessary for lysis. Pathogenic strains are not lysed by either the classical or the alternative pathway. These results suggest that pathogenic strains of E. histolytica activate complement but are able to evade an important host defense, complement-mediated lysis.

Animals↗
PubMed1986

The effect of fibronectin on the processing of C1q- and C3b/bi-coated immune complexes by peripheral blood monocytes.

In the past several years, it has been demonstrated that plasma fibronectin (Fn) binds to the C1q subunit of the complement system. The effect of Fn on the processing of immune complexes containing C1q and C3b by human peripheral blood monocytes was investigated. Preincubation of monocytes with Fn causes a significant increase in attachment of sheep erythrocytes coated with IgM and C1q (EIg-MC1q), but does not mediate their ingestion. EIg-MC1q attach to the Fn-treated monocytes via the C1q receptor because Fab anti-Fn antibodies do not inhibit their attachment to the monocytes. In addition, Fn-treated monocytes exhibit no change in C1q receptor number or affinity compared with monocytes treated with buffer. Fn mediates the phagocytosis of C3b/bi-coated particles, and C1q can enhance this process in two ways. First, phagocytosis of particles bearing C3b/bi and Fn is enhanced by the presence of C1q on the immune complex. Second, monocytes on Fn-coated surfaces ingest more particles if they are coated with both C3b/bi and C1q, compared with particles coated with either C3b/bi or C1q alone.

Animals↗
PubMed1986

Deficiency of erythrocyte C3b receptor (CR1) in AIDS and AIDS-related syndromes.

The expression of C3b receptors (CR1) on erythrocytes of gay men at various levels of risk for AIDS was studied. Fourty-nine heterosexual male controls had a mean (X) +/- standard deviation of 516 +/- 136 CR1 per erythrocyte (CR1-3); 17 asymptomatic gay men had X = 423 +/- 156, 16 gay men with one AIDS-related complex (ARC) symptom or sign had X = 342 +/- 154, 9 patients with ARC had X = 252 +/- 76, and 14 gay men with AIDS had X = 173 +/- 76 CR1-E. The patients with ARC and AIDS had a highly significant decrease in CR1-E when compared with normal individuals (p = less than 0.001) and studies of families of 4 AIDS patients suggest that this defect is acquired.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Fibronectin binding to C1q associated with antigen-antibody complexes in EDTA-treated plasma.

In this report we have investigated the association of fibronectin with antigen-antibody-C1q complexes incubated in fibronectin-depleted and C1q-depleted plasma. When BSA--anti-BSA immune aggregates are incubated in plasma depleted of both fibronectin and C1q to which 125I-fibronectin has been reconstituted, little radio-activity is bound to the immune complexes. However, pre-incubation of immune complexes with purified C1q prior to incubation in the plasma causes an approximately 10-fold increase in the amount of radioactivity bound. The binding of 125I-fibronectin to preformed antigen-antibody-C1q complexes is specific, since the reaction is inhibited by the addition of unlabelled fibronectin but not by ovalbumin. When antigen-antibody-C1q complexes are incubated in C1q-depleted plasma containing physiological concentrations of fibronectin, and analysed by immunoblotting, fibronectin antigens are detected on the immune complexes. Identical results are obtained using immune complexes composed of sheep erythrocyte rabbit anti-sheep erythrocyte C1q (EAC1q) cells. There is no specific requirement for preformed antigen-antibody-C1q complexes, since fibronectin can be detected on antigen-antibody complexes after incubation in normal human serum or in C1q-depleted ethylenediamineteraacetic acid (EDTA) serum reconstituted with purified C1q prior to incubation with the complexes. Finally, we also demonstrate that in the presence of C1q, 125I-fibronectin will associate with soluble antigen-antibody complexes.

Animals↗
PubMed1986

Altered erythrocyte C3b receptor expression, immune complexes, and complement activation in homosexual men in varying risk groups for acquired immune deficiency syndrome.

We studied levels of erythrocyte C3b receptors (E-CR1) and correlated them to the level of circulating immune complexes (CIC) and complement activation in patients with or at risk for acquired immunodeficiency syndrome (AIDS). A significant reduction was found in patients with AIDS (185 +/- 93 CR1/cell), AIDS-related complex, and generalized lymphadenopathy, whereas healthy male homosexuals or normal controls had 434 +/- 193 and 509 +/- 140 CR1/cell, respectively (P less than 0.001). Family studies indicate that this defect is acquired. Reduction in E-CR1 was associated with increased levels of CIC when assayed by binding to Raji cells, but not when tested by C1q binding. Complement activation was assessed by levels of C3bi/C3d-g in plasma, measured with a monoclonal antibody specific for a neoantigen in C3d. AIDS patients had increased C3 activation (2.68 +/- 1.67%) when compared with normal controls (0.9 +/- 0.22%) (P less than 0.01). The decreased E-CR1, the presence of CIC, and C3 activation suggest that complement activation by immune complexes may play a role in the clinical expression of the disease.

AIDS-Related Complex↗
PubMed1985

Fibronectin binding to complement subcomponent C1q. Localization of their respective binding sites.

The interaction of purified human plasma fibronectin with the C1q subcomponent of complement was investigated by using a solid-phase radiobinding assay. 125I-fibronectin binding to native C1q, purified collagen domain (C1q-c) or globular domain (C1q-g) was compared. When the purified domains were insolubilized by binding to plastic, the C1q-c exhibited 59% of the binding demonstrated with intact C1q, whereas the C1q-g exhibited 35% of the binding. N-Terminal sequencing of the globular domain showed that a sequence of seven collagen-like amino acids was retained on each chain of the C1q-g fragment. 125I-fibronectin binding to C1q could be inhibited equally well by fluid-phase C1q and C1q-c, but not by fluid-phase C1q-g, implying that the collagen-like region retained on the C1q-g is masked in the fluid phase. In addition, studies were performed to determine which subunit(s) of C1q bind(s) fibronectin. The percentages of fibronectin bound by the A, B, and C chain of C1q were found to be 38, 21 and 41% respectively. Inhibition studies with purified 200-180 kDa, 50 kDa or 29 kDa fragments of fibronectin show that the binding site on fibronectin for C1q is the 50 kDa gelatin-binding domain.

Amino Acid Sequence↗
PubMed1985

Delayed phase of hematoporphyrin-induced phototoxicity: modulation by complement, leukocytes, and antihistamines.

We have investigated the role of complement, leukocytes, and histamine in the delayed phase of hematoporphyrin-induced phototoxicity in guinea pigs. The phototoxic response was quantified by the accumulation of intravenously injected [125I]bovine serum albumin in the skin. There was a greater than 6-fold increase in the vascular response at the completion of irradiation, which subsided partially to reach a plateau of twice the preirradiation level between 0.5 h and 12 h. At 18 h, the vascular responsiveness returned to the baseline value. The 7 h timepoint was selected in this study to evaluate the modulation of the delayed phase. In complement-depleted guinea pigs, as well as in leukopenic animals, the enhancement in the vascular response was significantly suppressed (p vs control, less than 0.0001 and 0.0022, respectively). Cimetidine, when administered prior to irradiation, significantly suppressed the phototoxic response (p vs control, 0.0365). The combination of diphenhydramine and cimetidine, administered 6 h after the induction of phototoxicity, also suppressed the vascular response (p vs control, less than 0.0001). These data indicate that the expression of the delayed phase of hematoporphyrin-induced phototoxicity, similar to the early phase, requires the presence of an intact complement system, leukocytes, and histamine.

Animals↗
PubMed1985

Leprosy: altered complement receptors in disseminated disease.

We have studied the expression of the C3b receptor (CR1) on erythrocytes of 55 patients with Hansen's disease. We developed a radioimmunoassay utilizing a monoclonal antibody that recognized an epitope different from the C3b binding site, which therefore enabled us to measure total number of CR1 regardless of receptor occupancy. We observed that patients in the lepromatous pole of the disease had a mean of 310 CR1/erythrocyte, whereas the ones in the tuberculoid pole showed a mean of 577 CR1/erythrocyte; 77 normal controls had a mean of 512 CR1/erythrocyte. The number of C3b receptors on the cells of lepromatous patients was significantly decreased (p less than .001) when compared to the normal population or tuberculoid patients. The presence of receptors for the C3b fragment of complement (CR1) on the surface of human erythrocytes enables these cells to participate in a number of immune functions including the clearance of circulating immune complexes. These findings could bear importance in the ability of the host to clear immune complexes from the circulation in patients with lepromatous leprosy.

Adult↗
PubMed1985

Effect of captopril on the vascular permeability changes induced by C5a, histamine and compound 48/80.

The modulating effect of captopril, an inhibitor of angiotensin-converting enzyme, on the vascular permeability changes induced by intradermal injections of C5a, histamine and compound 48/80, was evaluated in guinea-pigs. Cutaneous vascular permeability changes were measured by the extravasation of intravenously injected 125I-bovine serum albumin. Intraperitoneal injection of 12.5, 25, or 50 mg/kg of captopril 30 min prior to the injection of C5a (10(-11) mol) significantly enhanced the increase in vascular permeability induced by this agent (P less than 0.02). This may be explained by the known property of captopril as an inhibitor of carboxypeptidase. No effect was observed when captopril was injected either 2 or 4 h before the injection of C5a. In contrast, the same doses of captopril, when injected intraperitoneally 2 h before the injection of histamine (10(-8) mol) or compound 48/80 (10 micrograms), significantly suppressed the increase in vascular permeability induced by these agents (P less than 0.02). This suppressive effect occurred in a captopril dose-dependent manner. The ability of captopril to modulate the vascular permeability response induced by vasoactive agents indicates that it is a potentially useful tool to dissect the relative roles of mediators involved in inflammatory processes.

Animals↗
PubMed1985

Regulation and deregulation of the fluid-phase classical pathway C3 convertase.

Three mechanisms that regulate the formation and function of the fluid-phase classical pathway C3 convertase (C4b2a) have been elucidated: a) a temperature-mediated intrinsic decay of the enzyme; b) an extrinsic accelerated decay mediated by the effect of the serum protein C4b-binding protein (C4-bp); and c) the inactivation of C4b in the C4b-C4b-p complex by the proteolytic action of C3b/C4b inactivator (I), which cleaves the alpha 1-chain of C4b yielding C4d (alpha 2-chain), and C4c (alpha 3-, alpha 4-, beta-, gamma-chains). A fourth mechanism is described based on the observation that the IgG fraction of the serum of certain patients with glomerulonephritis contains a protein that prevents the intrinsic and C4-bp-mediated decay of surface-bound C4b2a. This protein prolongs the half-life of fluid-phase C4b2a from 10 min to more than 5 hr, increasing the utilization of C3. It also inhibits the decay mediated by C4-bp by preventing the dissociation of C2a from the C4b, 2a complex. In addition, I alone or in the presence of C4-bp fails to cleave the alpha 1-chain of C4b in the stabilized C4b, 2a complex. This protective property of the stabilizing factor (NFc) requires the presence of C2a because C4b was not protected unless it was bound to C2a. Therefore, NFc provides a mechanism by which the serum regulatory proteins are bypassed.

Carrier Proteins↗
PubMed1984

Effect of glucocorticoids and gamma radiation on epidermal Langerhans cells.

The effect of 750 rads of gamma radiation on the rate of return of epidermal Langerhans cells (LC) following suppressive doses of topical glucorticoids was studied in guinea pigs. Gamma radiation alone had no effect on the LC as assessed by staining for cell membrane ATPase activity and Ia antigen. It did, however, delay the expected return of Ia but not ATPase surface markers on the LC after perturbation with glucocorticoids. The delayed return of surface Ia antigen is possibly related to a radiation-induced defect in the production of a required lymphokine and/or in intracellular Ia transport. Although our data do not rule out a cytolytic effect of steroids on the LC, they do strongly suggest that, at least in part, glucocorticoids act on the LC by altering cell surface characteristics.

Adenosine Triphosphatases↗
PubMed1984

Participation of mast cells and complement in the immediate phase of hematoporphyrin-induced phototoxicity.

We have investigated the roles of mast cells and the complement system in the immediate phase of hematoporphyrin-induced phototoxicity in guinea pigs. Clinically, i.v. injection of hematoporphyrin, followed by irradiation with a light source containing 400-405 nm wavelength, resulted in the immediate onset of erythema and edema, which subsided partially in 30-60 min. This was followed by the appearance of delayed erythema and edema, which peaked at 6-12 h after irradiation. Histologic examination of the response of the immediate phase, using a 1 micron-thick section, revealed eosinophil infiltration and mast cell degranulation. The immediate phase of the clinical response was further quantitated by the extravasation of intravenously injected [125I]bovine serum albumin. Pretreatment of the guinea pig skin with the intradermal injection of compound 48/80 significantly suppressed the increase in vascular permeability induced by hematoporphyrin and irradiation (p less than 0.05). This hematoporphyrin-induced alteration in vascular permeability was also significantly inhibited by antihistamines, either H1 receptor antagonist alone (p less than 0.05) or a combination of H1 and H2 receptor antagonists (p less than 0.05). Guinea pigs depleted of complement also showed significantly less vascular permeability changes (p less than 0.05). These results indicate that functionally intact mast cells, and the complement system, are required for the full development of the immediate phase of phototoxicity induced by hematoporphyrin.

Animals↗