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T K Mondal

Publications and source records attributed to T K Mondal.

4 recordsLinked to original sources
PubMed2006

Effects of murine endotoxemia on lymphocyte subsets and clearance of staphylococcal pulmonary infection.

In a model of staphylococcal pneumonia initiated during systemic endotoxemia in BALB/c mice, a significant reduction of the number of circulating CD4+ and CD8+ T-lymphocytes, B-lymphocytes, and NK cells, as well as lung-resident total T- and CD4+ T-lymphocytes was demonstrated. Staphylococcus aureus exposure only induced a similar decrease of lymphocyte subsets in the blood. However, the number of lung-resident total T- and CD4+ T-lymphocytes was increased. More viable bacteria were recovered from the lungs of S. aureus-infected mice than from those animals previously treated with lipopolysaccharide (LPS) followed by a staphylococcal challenge. These results indicate that LPS-induced reduction in the number of circulating lymphocyte subsets and lung-resident total T- and CD4+ T-lymphocytes do not increase susceptibility to staphylococcal respiratory infection. Moreover, LPS challenge prior to S. aureus exposure significantly improves clearance of the bacteria in the lung.

Animals↗
PubMed2005

The dietary supplement ephedrine induces beta-adrenergic mediated exacerbation of systemic lupus erythematosus in NZM391 mice.

The dietary supplement and adrenergic receptor agonist ephedrine has been a controversial topic as its safety has been questioned. Beta-adrenergic receptor (beta-AR) activation causes immunomodulation, which may contribute to promotion of autoimmune pathology. This report investigated the ability of ephedrine to exacerbate processes associated with autoimmune disease in a lupus-prone mouse model. To mimic human supplementation, ephedrine was administered to NZM391 (lupus-prone) and BALB/c (nonlupus prone) mice orally twice a day for three months at a dose of 50 and 100 microg/day. Some ephedrine-treated NZM391 mice also were preadministered the beta-AR antagonist propranolol to investigate beta-AR involvement. Mice were bled monthly, and sera were assayed for a variety of lupus manifestations and immunological measurements. In NZM391 males and females, both doses of ephedrine significantly increased lupus manifestations, including IgG production and organ-directed autoantibody titers, and significantly lowered the ratio of IgG2a/IgG1 compared to controls. Ephedrine significantly decreased female lifespan and significantly increased circulating populations of plasma cells (CD38(hi) CD19(lo) cytoplasmic IgG+) and CD40+ B1a cells, while preventing an age-related decrease in the B1a cell population expressing a high level of CD5. While ephedrine induced gender-specific immunomodulation in BALB/c mice, increases in the lupus manifestations of anti-dsDNA titers and serum urea nitrogen were not detected. Preadministration of propranolol decreased lupus manifestations and serum levels of IgG and IgE in ephedrine-treated mice, but did not block the shift towards IgG1 production. These findings indicate that ephedrine via beta-AR can exacerbate lupus symptoms in NZM391 mice and that blockade of the beta-ARs on B cells, and not T cells, apparently was of greater importance as the inhibition of lupus symptoms corresponded to an inhibition of immunoglobulin levels, not a change of Th1/Th2 balance.

Adrenergic beta-Agonists↗
PubMed2001

Synergistic immunopotentiating effects induced by T-cell and B-cell superantigen in mice.

Staphylococcal Enterotoxin-A(SEA), a 27kDa monomeric protein, produced by some strains of Staphylococcus aureus, is a prototype T-cell superantigen which causes proliferation of cytotoxic T-lymphocytes and produces cytokines like TNF-alpha and IFN-gamma. Recently Protein A (PA), a 42 kDa membrane protein of the Staphylococcus aureus Cowan-I strain, has been termed a B-cell super antigen. It has been shown to cause multiple immunological responses. In the present study we examined the effect of these two superantigens used separately as well as combination in a normal mouse system. It has been shown that combination treatment of PA and SEA is more effective than that of each individual one. FACS analyses of cell cycles showed that a finely turned cellular collaboration occurred in various phases of cell growth and proliferative response compared with controls (P<0.01). It has also been shown that the percentage of various cell types bearing different clusters of differentiation markers, e.g., CD8+, CD34+ increases considerably due to the combined effect of PA and SEA. We also observed that co-administration of both the elicits different soluble mediators like cytokines (TNF-alpha, INF-gamma, IL-1beta). No apoptotic phenomenon was observed (from the cell cycle analysis) for the dose of PA and SEA, used for the experiments, suggesting that these doses of PA and SEA should be non-toxic.

Animals↗