Biomedical subjects
S R Sengupta
Publications and source records attributed to S R Sengupta.
Seasonal intensity of Angiostrongylus cantonensis in the intermediate host, Laevicaulis alte.
The slug, Laevicaulis alte, is a vector of Angiostrongylus cantonensis in the Greater Bombay area. The seasonal prevalence of A. cantonensis was investigated to determine the maximum intensity of the parasite in a field population occupying an area of approximately 400 m2. The maximum intensity of larvae was observed in the rainy months, June-November. Investigations showed that individual L. alte could tolerate an infecting dose of 150 first-stage A. cantonensis larvae before mortalities occurred.
Bordetella pertussis extract induces increase in the activities of glycolytic enzymes in mouse liver.
The hypoglycemic effect of Bordetella pertussis (Challenge strain No.18323) purified cell extract (protein with traces of carbohydrates, 2 mg%) administered (0.1 mg/100 g body wt. i.v.) into mice on the activities of the key regulatory enzymes, viz. glucokinase, phosphofructokinase, pyruvate kinase, glyceraldehyde phosphodehydrogenase, glucose-6-phosphate dehydrogenase (G-6-PD) and lactate dehydrogenase, of glycolytic pathway in liver has been studied at varying intervals after injection. The maximum hypoglycaemic effect was observed at the end of 12 hr, while activities of all the enzymes studied showed significant enhancement after 18 hr, thus suggesting increased glucose utilization towards the formation of pyruvate. Actinomycin D is found to inhibit stimulation of G-6-PD activity in B. pertussis treated animals, thereby indicating the role of B. pertussis in synthesis of this enzyme.
Effect of tissue culture media on multiplication of Plasmodium falciparum in vitro.
To date RPMI-1640 has been the best medium for cultivation of Plasmodium falciparum in vitro. In addition to this medium, several alternative media, essentially the ones used in animal and plant tissue culture, were employed for the cultivation of P. falciparum. Only the media rich in glucose content, viz. Nitsch medium and White's medium S-3, supported the parasite multiplication.
Major histocompatibility complex restriction of T-cell suppression of immune response to mycobacteria.
In earlier work, intraperitoneal (i.p.) immunization with Mycobacterium vaccae was shown to generate a T-suppressor (Ts) response but intradermal (i.d.) immunization did not. We have now studied the major histocompatibility complex (MHC) restriction of this Ts response. The ability of C57BL/6 (H-2b), BALB/c (H-2d), and the (C57BL/6 x BALB/c) F1 mice to generate suppression after i.p. immunization with 10(8) killed M. vaccae was investigated. The BALB/c and the F1 mice generated suppression, but the C57BL/6 mice failed to do so. The suppression could be ascribed to Lyt-2+, L3T4- antigen-specific T cells. The F1 suppressors generated after i.p. immunization could suppress the generation of T-cell responses to i.d. immunization with M. vaccae in the parental BALB/c but not in the C57BL/6 mice. Monoclonal anti-I-A antibody could suppress the antigen-induced proliferative response of mice primed i.d. with M. vaccae. In contrast, monoclonal anti-I-E antibody enhanced antigen-specific proliferation of spleen cells primed i.p. with M. vaccae. The suppressors generated by i.p. priming of mice with M. vaccae could also suppress the in vitro antigen-induced proliferative response of i.d.-primed spleen cells; the suppression could be blocked by anti-I-E antibody. Thus, the T-cell-mediated suppression in the above experimental model was I-E restricted. The inability of the C57BL/6 mice to generate suppression after i.p. immunization with M. vaccae was ascribed to the lack of I-E expression by mice of H-2b strain.
Sero-diagnosis of schistosomiasis by ELISA test in an endemic area of Gimvi village, India.
Enzyme-linked immunosorbent assay (ELISA) was carried out in Gimvi village, India, using antigens derived from S. haematobium and S. mansoni adult worms. Patients excreting schistosome ova in urine elicited positive ELISA titres, whereas patients who were previously positive but are no longer passing viable eggs were negative for ELISA.
Emergence of drug resistance in salmonellosis.
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Role of antigen-presenting cells in variation in immunogenicity of mycobacteria.
The route of immunization was observed to play a significant role in deciding the outcome of immunization with killed mycobacterial vaccines. Whereas the slow growers were immunogenic by both intraperitoneal and intradermal routes, the rapid growers were immunogenic only by intradermal route. The non-responder state of mice to Mycobacterium vaccae by i.p. route of immunization could be corrected by prior treatment with poly I:poly C, an interferon inducer, or indomethacin, a prostaglandin inhibitor. Antigen-presenting efficiency of peritoneal and spleen cells were compared employing M. vaccae and M. tuberculosis H37Rv primed T cells and corresponding sonicates as antigens in an in vitro lymphocyte transformation test. Irradiated spleen cells presented both the antigens efficiently. However, with peritoneal cells as antigen-presenting cells, proliferative response against only M. tuberculosis was observed; proliferation of M. vaccae primed T cells was very poor. Peritoneal cells of poly I:poly C treated mice showed distinct improvement in their efficiency of presentation; even paraformaldehyde-fixed peritoneal cells gave an efficient stimulation with M. vaccae. The percentage of Ia-positive fraction in peritoneal cells was very low (5.95%) in comparison with spleen cells (38.37%). Poly I:poly C treatment resulted in increase in the Ia-positive cell fraction of the peritoneal cells to 24.5%.
Route-related variation in immunogenicity of mycobacteria.
The route of immunization was observed to play a significant role in deciding the T-cell response to immunization with killed mycobacterial vaccines. Slow-growing mycobacteria were found to be immunogenic by both the intraperitoneal (i.p.) and intradermal (i.d.) routes; rapid-growing mycobacteria were immunogenic by the i.d. route only. The nonresponder state following i.p. immunization with Mycobacterium vaccae could be corrected by treatment of the mice with poly I:poly C or indomethacin prior to immunization. Both poly I:poly C, an interferon inducer, and indomethacin, a prostaglandin inhibitor, are known to enhance the expression of major histocompatibility complex glycoproteins. Since they are so important in antigen preparation, it was concluded that the inability of mice to respond to M. vaccae by the i.p. route is likely due to defective presentation of the bacterial antigens by the antigen-presenting cells at the site, namely, the peritoneal macrophages. These findings are significant because M. leprae has been reported to be antigenically similar to M. vaccae, and the response of mice to i.p. immunization with both of these mycobacteria is very similar.
Pathogenesis of route-related variation in T-suppressor response on immunization with mycobacteria.
The route of immunization was observed to play a significant role in deciding the outcome of immunization with killed mycobacterial vaccines. Earlier we reported that the slow growers were immunogenic by both the intraperitoneal (i.p.) and intradermal (i.d.) routes. In contrast, the rapid growers were immunogenic by the i.d. route only. Both rapid and slow growers generated the classical, antigen-specific Lyt-2 positive, T-cell-mediated suppression after i.p. immunization but not after i.d. immunization. Thus, in the case of the slow growers, T-cell-mediated suppression was only a component of the immune response generated after i.p. immunization. In contrast, in the case of Mycobacterium vaccae and the other rapid growers, the T-cell-mediated suppression was the predominant response with i.p. immunization. The T-cell-mediated suppression generated by i.p. immunization exhibited crossreactivity, the spectrum of which was dependent upon the dose of the immunization.
Variation in immunogenicity of mycobacteria: role of antigen-presenting cells.
The antigen-presenting efficiency of peritoneal cells and irradiated spleen cells was compared using Mycobacterium tuberculosis- and M. vaccae-primed T cells and corresponding sonicates as antigens in an in vitro lymphocyte transformation test. The presentation efficiency of irradiated spleen cells was reasonably good for both antigens. However, with peritoneal cells as the antigen-presenting cells, the proliferative response against only M. tuberculosis sonicate was good. Proliferation of M. vaccae-primed T cells was very poor when the antigen was presented by peritoneal cells. Poly I:poly C treatment of mice prior to harvesting the peritoneal cells resulted in distinct improvement in their efficiency to present M. vaccae sonicate; maximal proliferative response was obtained with peritoneal cells from mice receiving two and three doses of poly I:poly C 24 hr apart. Even paraformaldehyde-fixed peritoneal cells from poly I:poly C-treated mice gave an efficient M. vaccae-specific stimulation to primed T cells. Based on these data, it was concluded that failure of mice to respond to M. vaccae by intraperitoneal immunization is the result of the poor efficiency of presentation of M. vaccae antigen.
Route-related variation in the immunogenicity of killed Salmonella enteritidis vaccine: role of antigen presenting cells.
In order to assess the role of the route of immunization on the immunogenicity of killed Salmonella vaccine, mice were immunized with killed S. enteritidis by intraperitoneal (i.p.) and intradermal (i.d.) routes. Whereas the former was non-immunogenic, the i.d. immunization generated an excellent delayed-type hypersensitivity response; further, i.p. immunization could even suppress the subsequent i.d. immunization. Since the peritoneal macrophages (MO) are known to be particularly low in Ia or MHC-class II antigens, so essential for antigen presentation, the non-immunogenicity by i.p. route was thought to be due to their poor presentation efficiency. Poly I: poly C, an interferon inducer, is known to enhance the MHC-class II expression; hence effect of poly I: poly C treatment on the immunogenicity of the killed vaccine by i.p. route was tested and indeed the non-immunogenicity was corrected. Poor efficiency of presentation of S. enteritidis antigen by peritoneal cells and its improvement by prior poly I: poly C treatment was further confirmed by in vitro lymphocyte transformation test using primed T cells and peritoneal cells from normal and poly I: poly C treated mice. Poly I: poly C treatment also enhanced expression of Ia antigens on peritoneal cells.
Alpha-1-antitrypsin in pulmonary tuberculosis.
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Serial estimation of alpha-1-antitrypsin in active pulmonary tuberculosis.
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Bacterial adherence to periurethral epithelial cells in women with urinary tract infection.
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Serogrouping of clinical isolates of beta haemolytic streptococci-comparison of two methods.
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Lymphocyte transformation test in lepromatous leprosy patients and their healthy siblings.
Lymphoproliferative response to M. leprae, PHA, PPD and mixed leucocyte culture (MLC) were measured in 20 cases of lepromatous leprosy, 17 of their normal healthy siblings and 15 healthy controls. 7 siblings of LL patients were HLA-D identical, which was identified by doing MLC reaction. All healthy siblings including HLA-D identical responded normal to all stimulating agents including M. leprae antigen. In contrast 20 cases of LL responded very poorly to M. leprae antigen and almost near normal to other stimulating agents. The specific unresponsiveness of LL patients to M. leprae antigen does not result from an HLA linked genetic defect and the defective CMI response to M. leprae antigen seems to be acquired and not genetically determined.
Protease inhibitors activity in lepromatous leprosy and lepra reaction.
Serum alpha one antitrypsin levels were measured in 50 healthy age and sex matched controls with 45 lepromatous leprosy cases and 5 cases of lepra reaction. It was noted that the mean level in healthy controls was 281.00 mg%, while the mean levels in LL patients was 421.00 mg% and in LR 570.00 mg%. The elevation of Alpha one antitrypsin was statistically significant in LL patients. It is possible that the rise is a reaction to release of proteases and or higher complement activity, which are the results of a high bacillary loading to formation of immune complexes.