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Biomedical subjects

K Saha

Publications and source records attributed to K Saha.

At least 19 recordsLinked to original sources
PubMed1992

Protective role of cytotoxic lymphocytes against murine leukemia virus-induced neurologic disease and immunodeficiency is enhanced by the presence of helper T cells.

We examined the role of T cells and their separated subsets in providing immunity against ts1 (a mutant of the Moloney murine leukemia virus) induced paralysis and immunodeficiency. Adoptive transfer of syngeneic total T cells from immunized mice protected newborn mice, at least partially, from ts1-induced disease syndrome. In infected mice who received total immune T cells, virus replication was reduced and the mice survived longer. When only separated immune CD8+ T cells were transferred to infected mice, similar protection, albeit to a lesser extent, was observed. Transfer of separated immune CD4+ T cells alone gave no protection. However, when recombined CD4+ and CD8+ cells were transferred together, an immune response similar to that when total T cells were transferred was observed. Cytotoxic assays from ts1-immunized mice revealed the presence of virus-specific CD8+ cytotoxic T lymphocytes that could lyse virus-expressing cells at a high effector/target ratio. We conclude that CD8+ T cells alone can provide immunity against ts1-induced paralysis and immunodeficiency and that the simultaneous presence of CD4+ T cells can also significantly enhance the immune response.

Animals↗
PubMed1992

In vivo effects of anti-leprosy drugs on the rat peritoneal macrophages and lymphocyte subpopulations.

The present study describes the in vivo effects of anti-leprosy drugs on rat peritoneal macrophages and T-cell homeostasis. It was observed that BCG-elicited rat peritoneal macrophages produced more H2O2 and expressed more Ia antigen on their cell surfaces compared with resident peritoneal macrophages. Furthermore, elicited macrophages isolated from rats administered multidrug therapy (MDT), consisting of dapsone, clofazimine and rifampicin in high dose (10 x MDT) released more O2-. On the contrary, there was a significant decrease in the Ia antigen expression on these macrophages. Anti-leprosy drug treatment in high dose (10 x MDT) decreased the total number of blood T-helper (W3/25+) cells and increased the total number of blood T-suppressor (OX-8+) cells which resulted in a significant decrease in a W3/25: OX-8 ratio. Electron microscopy of elicited macrophages isolated from 10 x MDT treated rats showed development of many filipodia compared with control macrophages. These data show that 10 x MDT treatment in rats for 1 month alters the homeostasis of blood T-cell subpopulations which perhaps decreases the Ia expression on macrophages. However, the increase in O2- production and the appearance of filipodia on the macrophages is due to a direct effect of drugs on the macrophages. MDT treatment for 1 month in a therapeutic dose has no effect on the above-mentioned parameters.

Animals↗
PubMed1992

Retrovirus-induced immunodeficiency in mice exacerbates gastrointestinal candidiasis.

Dysfunction of neutrophils in patients infected with human immunodeficiency virus is at least partly responsible for secondary microbial diseases in these individuals, including invasive gastrointestinal (GI) candidiasis. Immunoregulatory disturbances associated with the development of AIDS in human immunodeficiency virus-infected patients exacerbates Candida albicans infection of the upper GI tract and frequently leads to oropharyngeal and esophageal candidiasis. In this article, we present the first report of a murine model of invasive GI candidiasis associated with an AIDS-related murine immunodeficiency syndrome that results from infection of C57BL/6 mice with a previously described retrovirus complex (LP-BM5). Mice of the inbred strain were infected with C. albicans by oral-intragastric inoculation as infants and with the retrovirus by the intraperitoneal route 30 days later. Control mice of the same strain were infected with C. albicans as above and subsequently infected with the avirulent, ecotropic helper virus (MBI-5). Animals were killed 90 days after retroviral challenge. Total and differential blood cell counts, CD4+ T-cell counts in the spleen, and the histopathology of the gastric mucosa of experimental and control animals were determined. The virulent LP-BM5-infected animals developed murine AIDS and showed eruptive and suppurative lesions, with associated C. albicans mainly in regions of the cardial-atrium fold of the stomach. Well-defined abscesses with entrapped C. albicans hyphae were observed in the region of the cardial-atrium fold of control mice. A significant increase in the number of C. albicans CFU in homogenized and plated segments of the GI tract was recognized in mice with murine AIDS versus the control animals. The murine model of GI candidiasis reported here permits examination of the nature of C. albicans interaction with the gastric mucosa both in the immunocompetent host under conditions in which the yeast exists predominantly as a commensal organism and in the immunosuppressed host during progressive stages of AIDS induced by a retroviral infection.

Animals↗
PubMed1992

ts1, a temperature-sensitive mutant of Moloney murine leukemia virus TB, can infect both CD4+ and CD8+ T cells but requires CD4+ T cells in order to cause paralysis and immunodeficiency.

When neonatal FVB/N mice were inoculated with ts1, a temperature-sensitive mutant of Moloney murine leukemia virus TB, they developed a progressive bilateral hindlimb paralysis and immunodeficiency leading to death 4 to 6 weeks after inoculation. T lymphocytes have been shown to be primarily responsible for this ts1-induced syndrome. Here we compare the role played by each subset of T lymphocytes, i.e., CD4+ and CD8+ T cells, in disease development. Mice were depleted of a specific subset for the first 10 days of their lives by using either anti-CD4 or anti-CD8 monoclonal antibodies in vivo. Disease development in these mice was then monitored. Depletion of CD4+ T cells significantly attenuated the ts1-induced syndrome: virus replication was decreased, disease latency was extended, and death was prevented in 60% of the mice. Similar treatment with anti-CD8 antibody had almost no effect on disease progression. However, when depletion was begun 2 weeks after neonatal ts1 inoculation, CD4+ T cell depletion did not affect disease development. ts1 infected CD4+ and CD8+ T lymphocytes equally well in vivo, as shown by flow cytometric analysis, but virus replication was restricted primarily to the CD4+ subset of T cells, as found by in vitro assay. Hence, CD4+ T lymphocytes play an important role in the development of ts1-induced paralysis and immunodeficiency. The mechanism of this CD4+ T-cell-mediated disease production by ts1 is not clear; however, increased replication of ts1 in the CD4+ T cells, especially in the early stages of the disease, seems to play a crucial role.

Animals↗
PubMed1992

Colonic immunity in patients and amoebic liver abscess.

Secretory immunoglobulin A (S-IgA), coproantibody titre (antiamoebic) and IgA, IgG, IgM immunocytes in rectal mucosa were studied in 13 patients with amoebic liver abscess (ALA) prior to and 4-6 weeks after completion of antiamoebic therapy. Ten asymptomatic Entamoeba histolytica cyst passers and 17 healthy age and sex matched volunteers served as controls. Fecal S-IgA levels and counts of IgA bearing immunocytes in mucosa were significantly higher in patients with ALA and cyst passers as compared to healthy controls and showed a significant fall after treatment. Fecal antiamoebic antibodies were high in cyst passers and in cases of ALA after treatment. Raised levels of S-IgA and IgA class immunocyte counts probably indicate a local mucosal immune response directed at containing the infection.

Antibodies, Protozoan↗
PubMed1979

Impairment of Jones-Mote hypersensitivity and specific antibody response against depolymerized flagellin in lepromatous leprosy.

Cutaneous hypersensitivity and antibody-producing capacity were assessed in patients with lepromatous leprosy with defective immunity, by immunizing them with monomeric flagellin from Salmonella adelaide. Results were compared with those of controls, matched for age and sex, derived from similar socioeconomic stratum, but without any defect of the immunological system. In contrast to the normal individuals, who showed Jones-Mote type of hypersensitivity, no lepromatous patient could mount any 'delayed-in-time' cutaneous hypersensivivity reaction against an intradermal challenge of monomeric flagellin. However, when immunized through the subcutaneous route, both groups could produce adequate amounts of specific serum antibody. In addition to this unique split tolerance found in all lepromatous patients, some patients showed low levels of 'natural' IgM antibody, reduced formation of specific antibody when immunized through the subcutaneous route, and incomplete maturation of IgG class of anti-flagellin antibody. When immunized by the intradermal route, however, production of both anti-flagellin antibody and maturation of IgG antibody was significantly inhibited in normal adults but not in lepromatous patients. Thus, contrary to the earlier concept of hyperactivity of the humoral immune apparatus in lepromatous leprosy, the present study detected B-cell hypofunction in some patients.

Adult↗
PubMed1979

Immune deficit in patients with lepromatous leprosy: its nature and relation to genetic factors, spectrum, and duration of the illness.

Cell-mediated immunity or hypersensitivity to M. leprae and other unrelated antigens, such as tuberculin and dinitrochlorobenzene, was studied in 73 leprosy patients of different histopathologic types. It was found that specific as well as nonspecific anergy intensified as the disease spectrum shifted from the tuberculoid toward the lepromatous immunologic pole. Within the lepromatous group, the impairment of cellular immunity became more pronounced as the bacillary load increased. It was found that the impairment of the cell-mediated immunity towards antigens other than M. leprae became more severe as the duration of the illness increased. Late lepromin responsiveness, which is the hallmark of resistance of an individual to M. leprae, may be absent even before the onset of clinical illness. Its deficit seems to be primary and has a genetic predisposition.

Adult↗