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Biomedical subjects

U Sengupta

Publications and source records attributed to U Sengupta.

At least 37 records · Page 2Linked to original sources
PubMed1993

Serum lactoferrin in lepromatous leprosy patients.

The serum concentrations of lactoferrin were determined by competitive enzyme immunoassay in the sera of 38 lepromatous leprosy patients and 16 healthy volunteers. Of the 38 lepromatous patients, 25 were without any sign of reactions while 13 were suffering from ENL type of reactions. The lactoferrin levels, in both types of patients, were observed to be significantly higher (P < 0.01 and < 0.001, respectively) than in that of healthy volunteers. The rise in lactoferrin level in reactive patients was also higher (P < 0.05) when compared to those without reactions. The serum lactoferrin levels were also found to be associated with bacterial load (r = 0.414; P < 0.01) indicating that in lepromatous leprosy patients, lactoferrin may not be very effective in preventing the growth of Mycobacterium leprae. Further studies to improve the understanding of the role of elevated levels of lactoferrin in pathogenesis of lepromatous leprosy patients and in establishing its possible use in predicting the occurrence of ENL type of reactions would be worthwhile pursuing.

Humans↗
PubMed1992

Analysis of circulating immune complexes from leprosy patients for Mycobacterium leprae antigens.

Circulating immune complexes (CICs) from 31 leprosy patients (16 tuberculoid, 15 lepromatous) and 12 healthy volunteers, precipitated by 3.5% polyethylene glycol, were individually subjected to SDS-PAGE and immunoblotting using a variety of monoclonal and polyclonal antibodies against Mycobacterium leprae. A common mycobacterial antigen of an apparent molecular size of 65 kDa was identified in CICs from about 40% of the patients. No correlation was observed between the positivity for this antigen and any of the following parameters: bacterial index, M. leprae-specific antibody titers, motor nerve involvement, duration of disease or treatment. Nevertheless, patients with a relatively recent and massive infection were more frequently positive for antigen than the others.

Antibodies, Bacterial↗
PubMed1992

Suppressive effect of circulating immune complexes from leprosy patients on the lymphocyte proliferation induced by M. leprae antigens in healthy responders.

The effect of circulating immune complexes, isolated in the form of polyethylene glycol (PEG) precipitates from leprosy patients, on lymphocyte proliferation was studied. The results obtained showed that PEG precipitates obtained from the borderline lepromatous/lepromatous (BL/LL) types of leprosy patients and those undergoing erythema nodosum leprosum (ENL) had significant suppressive effects on the lymphocyte proliferation induced by Mycobacterium leprae antigens in healthy responders. The percent decreases in the mean values of delta cpm in the presence of PEG precipitates from the BL/LL and ENL groups were found to be 46.8 +/- 22.4 and 65.0 +/- 24.3, respectively. However, no significant suppressive effects (except for ENL PEG precipitates) of these PEG precipitates were observed on the lymphocyte proliferation induced by tuberculin (PPD). Further, PEG precipitates alone (in the absence of M. leprae antigen) from the BL/LL and ENL groups were found to have no effect on the lymphocyte proliferation.

Antigen-Antibody Complex↗
PubMed1992

Sensitization potential and reactogenicity of BCG with and without various doses of killed Mycobacterium leprae.

A study was conducted in 997 individuals in two villages in south India to find the acceptability and sensitizing effect of the antileprosy combination vaccine of BCG plus killed Mycobacterium leprae (KML). Three preparations of the combination, BCG 0.1 mg + 6 x 10(8) KML (I), BCG 0.1 mg + 5 x 10(7) KML (II), and BCG 0.1 mg + 5 x 10(6) KML (III), along with BCG 0.1 mg (IV), and normal saline (V), were used in the study. Each individual received one of the above five preparations by random allocation. They were also tested with Rees' M. leprae soluble skin-test antigen (MLSA) and lepromin-A, both at intake and 12 weeks after vaccination. Reactions to Rees' MLSA were measured after 48 hr; those to lepromin-A after 48 hr and 3 weeks. The character and size of the local response at the vaccination site were recorded at 3, 8, 12, 15, and 27 weeks after vaccination. The mean sizes of postvaccination sensitization to both Rees' MLSA and lepromin-A in the vaccine groups were significantly larger than those in the normal saline group, clearly demonstrating the ability of the vaccines to induce sensitization as measured by responses to the two skin tests. The sensitizing effect was the highest following vaccination with vaccine I. It was not significantly different for vaccines II, III, and IV, although, generally, a dose-response effect was observed. The sensitizing effect attributable to the vaccine was more clearly seen in children than in adults. The above conclusions were the same irrespective of which results were considered, reactions to Rees' MLSA or Fernandez or Mitsuda reactions to lepromin-A. A significant finding of the study was that at intake the Mitsuda reactions provided a measure of sensitizing effect due to vaccine. The healing of vaccination lesions was uneventful. In more than 90% of vaccinated individuals, the lesions had healed by the 12th week in vaccine groups II, III, and IV, and by the 15th week in vaccine group I. The results showed that vaccination with BCG or combination vaccines was equally safe in individuals with or without previous BCG scars. Thirteen persons, aged 10 years or older, developed suppurative lymphadenitis around the 8th week (7 in vaccine group I, 3 each in vaccine groups II and III). However, healing was prompt after drainage in these individuals.

Adolescent↗
PubMed1992

A study on viability of mycobacteria after treating them with complement system.

The effect of complement system on viability of mycobacteria (Mycobacterium vaccae and Mycobacterium bovis-BCG, as models) was studied by using 3H-uracil uptake method. The results showed no killing effect on these mycobacteria. Pretreatment of these mycobacteria with antimycobacterial antibodies also did not result in making them susceptible to complement. These observations were confirmed electronmicroscopically where no ultrastructural changes indicative of cell destruction were seen after treatment with complement in the presence and absence of antibody.

Antibodies, Bacterial↗
PubMed1991

Association of mycobacterial-specific and Mycobacterium leprae specific antibody levels with clinical activity in tuberculoid leprosy: a comparative study of three serological enzyme-immunoassays.

The ELISAs for polyclonal antibodies against Mycobacterium leprae (ML-ELISA) and specific antibodies against epitopes on 35 kDa protein (SACT-ELISA) and phenolic glycolipid I (PG-ELISA) of M. leprae were evaluated comparatively in a group of 88 tuberculoid leprosy patients. The overall seropositivity rate with a battery of 3 tests (68%) was not significantly higher than that obtained with ML-ELISA alone (55%) for IgG class of antibodies. Seropositivities for SACT-ELISA and PG-ELISA were, respectively, 38% and 26%. ML-ELISA for IgM class of antibodies was least sensitive, showing only 8% positivity. A significant correlation was noted between individual values of the three assays, but the positive proportions overlapped maximally in the case of ML-ELISA (IgG) and SACT-ELISA. Further, positivity for the latter two assays, particularly SACT-ELISA, showed significant associations with the extent of 'active' (largely untreated) infection. Immunoblotting revealed that the main antibody response was directed towards M. leprae antigens in the molecular weight range of 20-40 kDa and the densitometry results of this zone correlated significantly with corresponding SACT-ELISA and ML-ELISA (IgG) values.

Antibodies, Bacterial↗
PubMed1991

Survival of Mycobacterium leprae in mononuclear phagocytes: a possible role of complement system.

Mycobacterium leprae, the causative agent of leprosy, is an obligate intracellular pathogen that is ingested primarily by the host mononuclear cells. Upon ingestion, it is able to reside and multiply within these microbicidal cells. The reason for survival of these organisms in such cells is supposed to be their failure in induction of oxidation burst. In the present communication, we have proposed that most probably complement mediated entry of M. leprae into the monocytes does not result in induction of oxidative burst in the monocytes. As a result thereof these organisms are not killed rather they might grow in such phagocytes.

Complement Activation↗
PubMed1991

A method for the detection of M. leprae antigens in urine of leprosy patients by gel diffusion and gel electrophoretic techniques and significance in diagnosis.

A simple and novel method has been developed for the first time to detect M. leprae antigens in the urine of leprosy patients by treating the urine samples with sodium dodecyl sulphate (SDS). The antigens thus released can be demonstrated by simpler techniques like gel diffusion. By this method about 86% antigen positivity is observed in the urine of TT/BT and 83% positivity in BB patients. In BL/LL patients the antigen positivity is observed in 87% of the subjects. The high rate of M. leprae antigen positivity by the present method in the urine of patients with early leprosy may prove to be of diagnostic significance.

Adult↗
PubMed1991

A clinical, immunological, and histological study of neuritic leprosy patients.

An assessment has been made of 108 neuritic leprosy patients to find out if the number of affected nerves and the clinical presentations of these patients give any indication of the underlying severity (classification) of the disease. Detailed clinical recordings, skin smears, lepromin testing with Dharmendra antigen, and a leukocyte migration inhibition test (LMIT) using sonicated Mycobacterium leprae antigens were done in these patients. Nerve biopsies of available affected nerves were taken in 39 patients. The results show that neuritic leprosy patients also have a spectrum. However, none of the clinical parameters, including the number and distribution of affected nerves, the immune response and the nerve histology, were found to be inter-related. Further, even though all of the patients were skin-smear negative, a significant proportion showed lepromatous histology and nearly two thirds had a moderate-to-heavy bacterial load within the nerves.

Adolescent↗
PubMed1991

On the value of sequential serology with a Mycobacterium leprae-specific antibody competition ELISA in monitoring leprosy chemotherapy.

The Mycobacterium leprae-specific antibody assays--a serum antibody competition test (SACT-ELISA) for the epitope on the 35-kDa protein, and an enzyme immunoassay for the disaccharide epitope of phenolic glycolipid-I (PGDS-ELISA)--were evaluated as tools for the serological monitoring of chemotherapy in 20 lepromatous and 6 tuberculoid leprosy patients. In addition to estimates for M. leprae-specific antibodies, assessments of the bacterial index (BI) and clinical activity of the disease were also carried out prospectively in these patients on two to four occasions over a period of 19 months. In most cases, a decline in the BI, clinical scores, and antibody levels was observed during the course of treatment. The relative rate of decline was steepest and least variable with the SACT-ELISA, followed by the PGDS-ELISA and the BI. In some patients who showed a static or even an increased BI, despite marked clinical improvement, the antibody levels decreased. These data indicate that, unlike the BI, there is a greater dependence of specific antibody levels on the viability of M. leprae. This, combined with the fact that antibody titers would reflect the antigen load in the whole body, makes M. leprae-specific serology a promising tool for monitoring chemotherapy in leprosy patients.

Antibodies, Bacterial↗
PubMed1991

Persistent reduced solubilization of immune complexes in lepromatous leprosy patients with reactions.

It is held that immune complexes (IC) play a vital role in the pathogenesis of some of the reactions in leprosy. The complement system is known to solubilize and render IC innocuous. We have previously shown that patients undergoing lepra reactions had lowered complement-mediated IC solubilization (CMS). We, therefore, undertook a prospective study of untreated multibacillary leprosy patients and monitored their CMS levels sequentially while on therapy. In addition, the concentrations of the complement component C3d, immunoglobulins G, A and M, and circulating immune complexes (CIC) were also estimated. A total of 26 patients were included in the study and were investigated at 3-month intervals for 3 years. Thirteen of the 14 patients who did not develop reactions at all had normal CMS values, although all of them showed elevated CIC. From the inception of treatment, 10 of the 12 patients who developed lepra reactions had low CMS values which remained below normal levels even after evidence of complement activation disappeared and long after the subsidence of reaction. It is suggested that this defective CMS acts as a predisposing cause of lepra reactions.

Adult↗
PubMed1991

Antigens of Mycobacterium leprae in the cerebrospinal fluid of leprosy patients: detection by monoclonal-antibody-based sandwich immunoradiometric assay and avidin/biotin immunoblotting.

Mycobacterium leprae antigens could be detected in the cerebrospinal fluid (CSF) of patients with leprosy, using a monoclonal-antibody-based sandwich immunoradiometric assay (SIRMA). Antigens of 12 kD, 35 kD and 30-40 kD were detected using ML06, ML04, and ML34 monoclonal antibodies, respectively. The 30-40-kD polysaccharide antigen, although present in larger amounts in M. leprae than the 12-kD and 35-kD protein antigens, was found in the CSF of comparatively fewer subjects. The antigen capture assay has been found sensitive to the level of nanograms. Avidin-biotin-based immunoblotting using pooled leprosy sera detected a larger number of antigens than using anti-M. leprae antisera raised in rabbits. The immunoblotting of CSF samples revealed about three antigens in the region of 100-160 kD and three more in the region of 45-60 kD as probed by leprosy sera. This study has for the first time revealed the presence of M. leprae antigens in the CSF of leprosy patients and the probable involvement of the central nervous system in leprosy.

Antibodies, Monoclonal↗
PubMed1990

In situ demonstration of Mycobacterium leprae antigens in leprosy lesions using monoclonal antibodies.

Cryostat sections of skin and nerve lesions of leprosy were stained with monoclonal antibodies recognising Mycobacterium leprae antigens and indirect immunofluorescence. In both the tuberculoid and lepromatous lesions, PGL1, 55-65-kDa, 17-kDa protein antigens and cross-reactive non-protein antigens were present. 65-kDa antigens were seen mainly in the skin lesions of lepromatous leprosy. The infiltrates in both the skin and nerve granulomas of tuberculoid and lepromatous leprosy showed membranous staining with monoclonal antibodies recognising PGL1 and 55-65-kDa antigens. Bacilli in the lesions and the cells in the lymph node granulomas of patients with tuberculosis or the infiltrates in the lesions of tinea corporis or sections of normal skin did not show any staining with these monoclonal antibodies. These results confirm that M. leprae antigens are present and are expressed on the infiltrating cells of leprosy lesions.

Antibodies, Bacterial↗
PubMed1990

Activation of the human complement system by phenolic glycolipid 1 of Mycobacterium leprae.

The activation of the complement system by phenolic glycolipid 1 (PGL) from Mycobacterium leprae was studied. It was found that PGL consumed haemolytic complement through both the classical and the alternative pathways. This was further studied at the level of C3. Although the activation was independent of anti-PGL antibodies present in normal human serum, the addition of antibody augmented the activation of complement by PGL. The uptake of C3 through the classical pathway was enhanced predominantly by IgM antibody whereas, IgG antibody against PGL was responsible for the augmentation of the alternative pathway activation. Furthermore, it was found that both the disaccharide and trisaccharide components of PGL were able to activate the complement system.

Antigens, Bacterial↗