concanavalin-a and Pyelonephritis

Blast transformation of peripheral blood lymphocytes stimulated with phytohemagglutinin and concanavalin A was studied in children with pyelonephritis and glomerulonephritis. Activity of natural killer cells from children with pyelonephritis was estimated before and after treatment with 50% autologous plasma. The autologous plasma modulated blast transformation of lymphocytes and activity of natural killer cells, which depended on the stage of diseases.

Topics: Adolescent; Child; Child, Preschool; Concanavalin A; Glomerulonephritis; Humans; Immune Tolerance; Immunotherapy; K562 Cells; Killer Cells, Natural; Lymphocyte Activation; Lymphocytes; Phytohemagglutinins; Pyelonephritis

Splenic lymphocytes and peritoneal macrophages from BALB/c mice with Escherichia coli pyelonephritis were obtained at various intervals after infection. These cells were stimulated in vitro with different antigens and cytokine release was assayed in the supernate of the cultured cells. It was observed that both specific antigens such as outer-membrane proteins (OMPs), porins and heat-shock protein-65 (hsp-65), as well as non-specific mitogens such as phytohaemagglutinin (PHA), were able to induce cytokine production by splenic cells from infected mice. Of all these antigens, hsp-65 was found to be the best inducer of cytokine release. In the acute stage of pyelonephritis, the release of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) was found to increase with time; both reached their peak values on the seventh day after infection. The TH1 pattern of cytokine secretion by splenic cells was observed, i.e., IL-2 and IFN-gamma, whereas there was complete absence of IL-4 secretion. In the chronic stage of pyelonephritis, i.e., 150 days after infection, a decrease in the level of IL-2 and IFN-gamma was observed. Peritoneal macrophages released IL-1 on stimulation with hsp-65, which increased with the progression of disease. The possible implications of this study for the disease process are discussed.

Topics: Acute Disease; Animals; Antigens, Bacterial; Bacterial Outer Membrane Proteins; Bacterial Proteins; Cell Line; Cells, Cultured; Chaperonin 60; Chaperonins; Chronic Disease; Concanavalin A; Cytokines; Escherichia coli; Escherichia coli Infections; Female; Interferon-gamma; Interleukin-1; Interleukin-2; Interleukin-4; Macrophages, Peritoneal; Mice; Mice, Inbred BALB C; Phytohemagglutinins; Porins; Pyelonephritis; Spleen; Th1 Cells; Thymus Gland

Cell-mediated immunity (CMI) was studied in a group of 48 children with urinary tract infections (UTI) using a whole blood micromethod for lymphocyte stimulation in vitro. The patients were subdivided into pyelonephritis group (27 cases) and lower urinary tract infection (LUTI) group (21 cases) on the basis of fever, erythrocyte sedimentation rate, C-reative protein and renal concentration capacity. At the acute stage of infection the lymphocyte responsiveness to leucoagglutinin (LA) and concanavalin A (Con A) was suppressed in both groups, but the suppression was much greater in those with pyelonephritis. By 6 weeks after infection the lymphocyte responses were normal in most but not all cases. We conclude that an acute pyelonephritis is associated with marked suppression of CMI and that the latter can be used as an additional criterion for establishing the level of infection. Patients with UTI did not generally appear to have any primary defect of CMI but when suppression of CMI was present, it seemed secondary to an ongoing infection.

Topics: Agglutinins; Blood Sedimentation; C-Reactive Protein; Child; Child, Preschool; Concanavalin A; Female; Fever; Humans; Kidney Concentrating Ability; Lymphocyte Activation; Male; Pyelonephritis; Urinary Tract Infections

A marked suppression of the thymusderived (T)-lymphocyte response to concanavalin A has been demonstrated in vitro during renal infection. Suppression of the T-lymphocyte response in vitro was seen as early as 2 h after the induction of renal infection, but maximum suppression was found 24-72 h later. A population of suppressor cells in the splenic lymphocyte population, generated during the host's response to infection, contributed to the depressed lymphocyte response. Removal of suppressor cells restored the mitogenic responsiveness of the remaining splenic lymphocytes. Conversely, in co-culture experiments, a suppressor cell present in the splenic lymphocyte population of pyelonephritic animals was shown to be capable of suppressing the mitogenic responsiveness of normal splenic lymphocytes. Significantly reduced host vs. graft responses by the pyelonephritic animals confirmed, in vivo, the depression of cell-mediated immune mechanisms. An additional suppressive factor was found in the serum of pyelonephritic animals which depressed in vitro the mitogenic responsiveness of splenic lymphocytes from normal animals. Support for the suppressive role of this serum factor was found when splenic lymphocytes from pyelonephritic animals were tested in vivo in the absence of homolgous serum (graft vs. host). Under these conditions, the lymphocytes showed an enhanced reaction compared with lymphocytes from normal animals. The presence of a suppressor cell population and a serum factor, both capable of depressing cell-mediated mechanisms, may be major factors contributing to the establishment of infection in the kidney.

Topics: Animals; Blood; Concanavalin A; Escherichia coli; Female; Host vs Graft Reaction; Immunity, Cellular; Immunosuppression Therapy; Lymphocyte Activation; Pyelonephritis; Rats; Spleen; T-Lymphocytes

Topics: Animals; Cell Division; Concanavalin A; Escherichia coli Infections; Immunity, Cellular; Lymphocytes; Male; Proteus Infections; Proteus mirabilis; Pyelonephritis; Rats; Spleen