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Biomedical subjects

A Mathur

Publications and source records attributed to A Mathur.

At least 199 records · Page 11Linked to original sources
PubMed1988

Immunological memory in latent Japanese encephalitis virus infection.

Long term B-cell memory to Japanese encephalitis virus (JEV) in latently infected mice was investigated by adoptive cell transfer. Both IgM and IgG memory were elicited by antigen challenge or cyclophosphamide induced reactivation of virus. A weak antigen-specific IgM response for a brief period and a strong IgG response were detected in Swiss albino mice exposed to secondary infection. A correlation between the secondary IgM antibody and protection against JEV challenge was observed in adoptive transfer experiments. This was abrogated by pretreatment of the serum with 2-mercaptoethanol. Similarly secondary immune splenic T-cells up to day 5 post-reactivation provided protection. These results suggest that a long term antigen-specific IgM and IgG memory was induced by JEV challenge in latently infected mice. Further, the role of IgM antibody and T-cells in the response of mice to secondary JEV infection has been shown.

Animals↗
PubMed1988

Immunopathological study of spleen during Japanese encephalitis virus infection in mice.

Following intraperitoneal inoculation, Japanese encephalitis virus replicated in peritoneal macrophages, appeared on day 3 in the splenic macrophages of the perifollicular region and later in cells of the periarteriolar lymphoid sheath (PALS) as shown by indirect immunofluorescence. Productive JEV infection was observed both in macrophages and T-cells. Morphological study of spleen during JEV infection revealed proliferative changes, with increased number of macrophages from day 3 p.i. in the perifollicular region followed by accumulation of polymorphonuclear leucocytes which reached a maximum on day 9 p.i. The T dependent areas were considerably enlarged by day 9 and gradually reduced in size by week 3. At later periods germinal centres appeared in the T independent area and were prominent by day 15. The cells containing virus antigen disappeared with the appearance of germinal centres, thus indicating the role of the latter also in virus clearance.

Animals↗
PubMed1987

Thymus-dependent in vivo suppression of IgE synthesis in a murine IgE-secreting hybridoma.

In previous studies we demonstrated that BALB/c mice bearing ascitic tumors of the IgE-secreting hybridoma B53 (epsilon, kappa, anti-dinitrophenyl) developed large numbers of Lyt-1-2+ Fc epsilon R(+) T lymphocytes (T cells with membrane Fc receptors) in response to the elevated serum IgE concentration. The development of Fc epsilon R(+) T lymphocytes was followed by a progressive decrease in the levels of serum IgE in spite of continued proliferation of the hybridoma cells. This sequence of events suggested that the IgE-secreting hybridoma triggered a suppressive immunoregulatory circuit of the host that inhibited IgE expression by the hybridoma cells. The present studies were undertaken to investigate the basis for the subsequent decline in serum IgE levels in mice with B53 tumors and to identify host factors that might be involved in this process. We observed that ascitic B53 cells recovered at increasing time points from BALB/c mice exhibited a selective decline in steady state levels and rates of synthesis of epsilon-heavy chain protein and mRNA. The expression of kappa-light chain protein and mRNA appeared relatively unchanged. The decrease in epsilon-heavy chain gene expression did not occur when B53 tumors were passaged in nu+/nu+ mice or in BALB/c mice depleted of Lyt-2+ cells (suppressor/cytotoxic cell lineage), but did occur in nu+/nu+ mice reconstituted with neonatal BALB/c thymus and in BALB/c mice depleted of L3T4+ cells (helper/inducer cell lineage). That Fc epsilon R(+) T lymphocytes were directly involved in the inhibition of IgE expression was supported by the earlier and more pronounced inhibition of B53 IgE in mice infused with Fc epsilon R(+) T lymphocytes. We conclude from these findings that: 1) the decline in serum IgE levels that occurs toward the end of each generation of in vivo passage of the B53 hybridoma is due to decreased production of IgE by the hybridoma cells, 2) the decreased production of IgE is due to a selective loss of epsilon mRNA expression, 3) the decrease production of IgE by B53 cells is dependent on the presence of Lyt-2+ cells, and 4) Fc epsilon R(+) T lymphocytes participate in the mechanism by which IgE production is suppressed.

Animals↗
PubMed1987

Memory suppressor T cells in latent Japanese encephalitis virus infection.

The generation of secondary suppressor T (Ts) cells has been studied during latent Japanese encephalitis virus (JEV) infection of mice. The mice infected with JEV 27 weeks earlier, on challenge with the homologous virus, showed accelerated generation of secondary Ts cells; these appeared on Day 6, with peak activity on Day 8, and lasted for 27 days. The secondary Ts cells were Thy1.2+, Ly1-2+, antigen-specific, and acted in a dose-dependent manner. The secondary Ts cells could also be generated by reactivation of the JEV in latently infected mice. The findings thus show the presence of memory suppressor T cells in mice latently infected with JEV that can be stimulated to produce secondary Ts cells by exogenous or endogenous virus challenge. This phenomenon could help to persistence of the virus.

Animals↗
PubMed1987

Induction of secondary immune response by reactivated Japanese encephalitis virus in latently infected mice.

Development of secondary immune response has been studied following reactivation of latent Japanese encephalitis virus (JEV) infection in mice. The virus could be reactivated in 43% of the latently infected mice at 27 weeks p.i. by treatment with cyclophosphamide. The reactivated virus induced delayed-type hypersensitivity (DTH) and leucocyte migration inhibition (LMI) responses in mice, with peak activity on Day 5 post-reactivation (p.r.). The DTH persisted at low levels for long periods. Humoral immunity measured by haemagglutination-inhibiting antibody showed a four-fold rise in antibody titres. DTH was transferable by immune spleen cells for 5 days p.r. only. It is, therefore, concluded that JEV reactivation generates a quick and short-lived secondary immune response.

Animals↗
PubMed1987

Variable effects of dengue virus-induced cytotoxic factors on different subpopulations of macrophages.

Dengue virus (DV) induces T lymphocytes of the spleen to produce a cytotoxic factor (CF) that induces a subpopulation of macrophages (M phi) to produce a soluble cytotoxin (CF2). Both these factors kill normal lymphoid cells and M phi. The present study was undertaken to investigate the effects of these factors on the I-A-positive and I-A-negative subpopulations of mouse peritoneal M phi. It was observed that CF kills I-A-negative M phi and induces I-A-positive M phi to produce the CF2 that kills both types of cells. However, even when combined together, CF and CF2 do not kill 100% of the M phi. The two-step mechanism involving co-operation between T cells and M phi appears to be biologically economical for maintaining the cytotoxic pathway.

Animals↗
PubMed1987

Macrophage functions during dengue virus infection: antigenic stimulation of B cells.

This study was undertaken to investigate the function of dengue type 2 virus (DV)-infected mouse peritoneal macrophages (M phi) regarding the antigenic stimulation of B lymphocytes of the spleen. It was observed that a variable proportion of M luminal diameter show DV-specific immunofluorescent antigen, which depended upon the route of administration of the virus, being higher in i.p.-inoculated mice and in vitro-infected M luminal diameter monolayers. The DV-infected M luminal diameter presented the DV antigen to B cells in vitro and in vivo, leading to their clonal expansion as shown by counting the virus-specific IgM antibody plaque-forming cells (PFC). The PFC response depended upon the number of DV-infected M luminal diameter. The antigen was presented equally well both by I-A-negative and I-A-positive M luminal diameter. Superimposition of a heterologous antigen (Coxsackie B4 virus) in a Mackaness type of experiment depressed the capacity of M luminal diameter to present both the homologous as well as heterologous antigen.

Animals↗
PubMed1986

Increased T epsilon cells in BALB/c mice with an IgE-secreting hybridoma.

Since it has been proposed that T cells with receptors for the Fc portion of IgE (T epsilon) in rats, mice and humans are IgE-specific regulatory cells, it was investigated whether mice with an IgE-secreting hybridoma might be a source of large numbers of T epsilon cells. BALB/c mice with ascitic tumors of the IgE hybridoma B53 (epsilon, kappa, anti-DNP) developed high serum concns of monoclonal IgE which was followed by the appearance of large numbers of Lyt1-2+ L3T4- T epsilon cells. In contrast, mice bearing a non-IgE producing variant of B53 failed to develop T epsilon cells. Mice infused with cell-free ascites fluid (containing high levels of monoclonal IgE) from the IgE-secreting B53 hybridoma developed high serum IgE levels and also developed high numbers of T epsilon cells. Mice infused with cell-free ascites obtained from the non-IgE-secreting variant ENP-1 (containing very low amounts of IgE) did not develop either high serum IgE levels or T epsilon cells. These findings suggest that high serum IgE concns induce large numbers of T cells that express phenotypic markers of suppressor cells and have surface IgE-Fc receptors. These studies extend to IgE the principle that hybridomas and plasmacytomas induce large numbers of immunoregulatory T cells that express Fc receptors specific for the heavy chain class of the secreted monoclonal immunoglobulin. Since T epsilon cells are normally present only in small numbers, their marked increase in mice with IgE-secreting hybridomas identifies a ready source of large numbers of T epsilon cells that can be used to investigate their regulatory properties.

Animals↗
PubMed1986

The effect of clofazimine on the pharmacokinetics of rifampicin and dapsone in leprosy.

Fifteen untreated leprosy patients were given rifampicin and dapsone for seven days, and then rifampicin, dapsone and clofazimine for seven days. Concentrations of rifampicin and dapsone were estimated in timed plasma specimens and in 24 h urine specimens on days 7 and 14. No significant differences in the pharmacokinetics of rifampicin and dapsone were observed between the two occasions of sampling.

Clofazimine↗
PubMed1986

Microcirculation in muscle.

The microvascular architecture in muscle is reviewed herein. The intrinsic vasculature is similar in different muscles. There are numerous arterioarterial (100 microns diameter) and venovenous (150 microns) anastomoses creating a large microscopical network. End-arterioles (30 microns), end-venules (50 microns), and capillaries (6 microns) form a smaller microscopical network. There are no arteriovenous shunts. Precapillary arterial vessels larger than 10 microns have one or several layers of smooth muscle cells. There are no precapillary sphincters. Postcapillary vessels larger than 15 microns have one continuous layer of smooth muscle cells. Calculations show that the cross-sectional area is the smallest and hence resistance the greatest in arterioles of 22 microns and venules of 40 microns. There is better physiological support for giving plasma expanders, such as dextran, rather than vasodilators in low flow situations.

Animals↗
PubMed1986

Persistence, latency and reactivation of Japanese encephalitis virus infection in mice.

Persistent and latent Japanese encephalitis virus (JEV) infection was studied in pregnant and non-pregnant mice. Following intraperitoneal inoculation into pregnant mice JEV persisted for 16 weeks in contrast to 4 weeks in non-pregnant mice. This was followed by a higher frequency of latent infection in pregnant mice. The virus could be reactivated during pregnancy or by cyclophosphamide treatment, the latter being more effective.

Animals↗
PubMed1986

Japanese encephalitis virus latency following congenital infection in mice.

Latent Japanese encephalitis virus (JEV) infection was shown in inapparently congenitally infected Swiss albino mice after their mothers had been given JEV intraperitoneally during pregnancy. Only one of 37 (2.7%) of the baby mice showed persistence of infectious virus at 5 weeks of age. Reactivation of JEV in Swiss albino mice was demonstrated by stimulation with allogeneic spleen cells from Parks strain mice at 21 weeks of age; reactivation was demonstrated in 41% of the inapparently infected mice. The spleen cells of congenitally infected mice had depressed [3H]thymidine uptake following stimulation with concanavalin A, and depressed ability to induce a graft-versus-host response.

Animals↗