concanavalin-a and Pancytopenia

concanavalin-a has been researched along with Pancytopenia* in 1 studies

Other Studies

1 other study(ies) available for concanavalin-a and Pancytopenia

Article	Year
Oral treatment with trimethoprim-sulfamethoxazole and zidovudine suppresses murine accessory cell-dependent immune responses. Toxicological sciences : an official journal of the Society of Toxicology, 2000, Volume: 55, Issue:2 Trimethoprim-sulfamethoxazole (TMP-SMX), commonly used for prophylaxis of Pneumocystis carinii pneumonia (PCP) in AIDS patients, often produces a high incidence of treatment-limiting reactions. We investigated the effect of oral administration of TMP-SMX alone or in combination with the antiretroviral drug zidovudine (ZDV) on hematopoiesis and cellular immunity in BALB/c mice. Daily treatment for 28 days with TMP-SMX (160:800 mg/kg) had no effect on hematopoiesis or the ex vivo proliferative response of splenic T lymphocytes to allogeneic tumor cells (EL-4) or to concanavalin A (ConA), or that of splenic B cells to lipopolysaccharide (LPS). ZDV at 240 mg/kg/day was not immunosuppressive but caused a mild macrocytic anemia. Combined treatment produced severe pancytopenia, a significant drop in splenic cellularity, and a 61% decrease in the percentage of splenic macrophages. The percentage of splenic CD3+ lymphocytes increased 150% in the TMP-SMX + ZDV group, but the ratios of T-cell subsets and the frequency of B cells remained unchanged. Combined drug treatment did not impair the proliferative response of B cells to LPS or that of T cells to EL-4 cells. In concert with the reduction in the percentage of macrophages, the proliferative response of T lymphocytes to ConA decreased significantly. Optimal ConA-induced T-cell proliferation requires the participation of accessory cells (AC) (e.g., macrophages); EL-4 cells are able to function as AC. These data indicate that ZDV synergizes with TMP-SMX, causing severe hematotoxicity and suppressing AC-dependent immune function, and suggest that this therapeutic regimen may contribute to the immune deterioration in AIDS patients. Topics: Administration, Oral; Anemia, Macrocytic; Animals; Anti-HIV Agents; Anti-Infective Agents; Antigen-Presenting Cells; Concanavalin A; Drug Combinations; Female; Hematopoiesis; Immunity, Cellular; Immunosuppression Therapy; Lipopolysaccharides; Lymphocyte Activation; Lymphocyte Count; Mice; Mice, Inbred BALB C; Pancytopenia; Spleen; T-Lymphocytes; Trimethoprim, Sulfamethoxazole Drug Combination; Tumor Cells, Cultured; Zidovudine	2000

Article

Year

Oral treatment with trimethoprim-sulfamethoxazole and zidovudine suppresses murine accessory cell-dependent immune responses.

Toxicological sciences : an official journal of the Society of Toxicology, 2000, Volume: 55, Issue:2

Trimethoprim-sulfamethoxazole (TMP-SMX), commonly used for prophylaxis of Pneumocystis carinii pneumonia (PCP) in AIDS patients, often produces a high incidence of treatment-limiting reactions. We investigated the effect of oral administration of TMP-SMX alone or in combination with the antiretroviral drug zidovudine (ZDV) on hematopoiesis and cellular immunity in BALB/c mice. Daily treatment for 28 days with TMP-SMX (160:800 mg/kg) had no effect on hematopoiesis or the ex vivo proliferative response of splenic T lymphocytes to allogeneic tumor cells (EL-4) or to concanavalin A (ConA), or that of splenic B cells to lipopolysaccharide (LPS). ZDV at 240 mg/kg/day was not immunosuppressive but caused a mild macrocytic anemia. Combined treatment produced severe pancytopenia, a significant drop in splenic cellularity, and a 61% decrease in the percentage of splenic macrophages. The percentage of splenic CD3+ lymphocytes increased 150% in the TMP-SMX + ZDV group, but the ratios of T-cell subsets and the frequency of B cells remained unchanged. Combined drug treatment did not impair the proliferative response of B cells to LPS or that of T cells to EL-4 cells. In concert with the reduction in the percentage of macrophages, the proliferative response of T lymphocytes to ConA decreased significantly. Optimal ConA-induced T-cell proliferation requires the participation of accessory cells (AC) (e.g., macrophages); EL-4 cells are able to function as AC. These data indicate that ZDV synergizes with TMP-SMX, causing severe hematotoxicity and suppressing AC-dependent immune function, and suggest that this therapeutic regimen may contribute to the immune deterioration in AIDS patients.

Topics: Administration, Oral; Anemia, Macrocytic; Animals; Anti-HIV Agents; Anti-Infective Agents; Antigen-Presenting Cells; Concanavalin A; Drug Combinations; Female; Hematopoiesis; Immunity, Cellular; Immunosuppression Therapy; Lipopolysaccharides; Lymphocyte Activation; Lymphocyte Count; Mice; Mice, Inbred BALB C; Pancytopenia; Spleen; T-Lymphocytes; Trimethoprim, Sulfamethoxazole Drug Combination; Tumor Cells, Cultured; Zidovudine

2000