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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with Trypanosoma cruzi decreases the ability of spleen cells from mice to respond to either T cell, concanavalin A (Con A), or B cell, lipopolysaccharide (LPS), mitogens. The effect of infection on the mitogenic response depends on the elapsed time between the day of infection and the time of mitogen presentation. Responses early in infection are normal, whereas later responses to either mitogen are depressed. Spleen cells from late trypanosome-infected mice inhibit the ability of normal spleen cells to respond to Con A or LPS. The cell in the T. cruzi-infected spleen cells responsible for this effect is nonadherent, sensitive to treatment with anti-mouse thymus serum plus complement, but insensitive to treatment with anti-immunoglobulin plus complement. These data indicate that infection with T. cruzi elicits over time the generation of T cells suppressive to T and B cell mitogenic responses.
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PMID:Suppressor cells present in the spleens of Trypanosoma cruzi-infected mice. 10 8

Infection of chickens with a myeloblastosis-associated virus which induced a high incidence of osteopetrosis was accompanied by immunosuppression. The immunosuppression was manifested in the following ways. The weight of the bursa, spleen, and thymus was depressed in infected chickens. Infected animals had a diminished capacity to form hemolytic plaques in a direct assay. Spleen cells from osteopetrotic animals did not respond to phytohemagglutinin, and the spleen and bursa had a decreased proportion of cells possessing surface immunoglobulin. Osteopetrotic animals failed to show an age-dependent increase in the proportion of cells demonstrating surface immunoglobulin that was observed in normal animals. However, several individual chickens with heavy osteopetrosis responded to antigenic stimulation in a normal fashion, indicating that although immunosuppression usually accompanies avian osteopetrosis, it may not contribute directly to abnormal bone proliferation.
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PMID:Characterization of the immunosuppression accompanying virus-induced avian osteopetrosis. 73 Mar 67

Infection of adult CBA mice with Rauscher or Moloney leukaemia virus concomitantly with caseination significantly accelerated spleen amyloid development in irradiated, bone-marrow protected mice, but had no effect on untreated, adult thymectomized or thymectomized irradiated mice. Spleen tissue of mice infected with Moloney virus had the highest titre in the mice with accelerated amyloid development.
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PMID:The effect of Rauscher and Moloney leukaemia virus on amyloid development in casein-treated CBA mice. 116 70

A 15-year study of perioperative complications was carried out in 142 adults who underwent splenectomy for hematologic disease at the University of Alberta Hospital in order to obtain recent statistics on morbidity and mortality. The patients were grouped into four diagnostic categories: idiopathic thrombocytopenic purpura (71 patients), lymphoproliferative disorders (34 patients), myeloproliferative disorders (12 patients) and miscellaneous disorders (25 patients). Splenectomy was carried out for therapeutic reasons in 93% of patients and to establish a diagnosis in 7%. The overall complication rate was 22% (31 of 142) and the death rate was 6% (7 of 142). Infection accounted for 42% of the complications. Steroid or antibiotic therapy preoperatively did not significantly affect the infection rate. Drains, if removed within the first week, also did not affect the postoperative infection rate. Spleen size and the interaction between diagnosis and the presence of thrombocytopenia were predictors of the need for intraoperative transfusion.
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PMID:Perioperative complications of splenectomy for hematologic disease. 149 46

Infection with Trypanosoma cruzi is accompanied by a profound suppression of immune responses including the production of IL-2. Previous experiments have confirmed a correlated decrease in IL-2 mRNA levels in lymphoid cells from infected mice. To further define the molecular basis of this regulation, we have examined the production and degradation of mRNA for IL-2 and other T cell activation genes in cells from T. cruzi-infected mice. Spleen cells from C57BL/6J mice infected with the Brazil strain of T. cruzi were analyzed for the kinetic expression of IL-2, IL-2R alpha, c-myc, and c-fos genes in response to Con A and PMA costimulation. Cells from infected mice exhibited a selective reduction of c-myc and c-fos mRNA in association with the severe suppression of the IL-2 gene, but a less severe to comparable production of IL-2R alpha mRNA compared with normal spleen cells. The similar patterns of the suppression of c-myc and IL-2 mRNA suggest a common mechanism of down-regulation of these two genes in T. cruzi infection. Actinomycin D treatment was used to demonstrate that decreased steady state levels of IL-2, c-myc, and c-fos mRNA in cells from infected mice were not due to an increased rate of degradation of these mRNA. Cycloheximide treatment enhanced the expression of IL-2, IL-2R alpha, c-myc, and c-fos mRNA in spleen cells from both normal and infected mice. Although a larger percentage of induction was observed in cells from infected mice, the mRNA levels for IL-2, c-myc, and c-fos in cells from infected mice were still lower than those of normal cells. Spleen cells from infected mice precultured for 24 to 72 h before the addition of mitogens showed significant enhancement of IL-2 and c-myc gene expression; however, this recovery was inhibited if fixed T. cruzi was present in the preculture medium. These data suggest that the reduction of IL-2 mRNA in infected mice is not the result of an increased degradation of its mRNA but to down-regulation of transcription of the IL-2 gene in T cells from T. cruzi-infected mice. Preculture-induced recovery of IL-2 production appears to result from release from this regulation and full expression of the IL-2 gene.
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PMID:Selective suppressive effects of Trypanosoma cruzi infection on IL-2, c-myc, and c-fos gene expression. 151 73

Neonatal mice (CR:NIH:S) were infected with a cloned human isolate of Giardia lamblia (GS/M-83-H7) and the surface antigens of the intestinal trophozoites, as well as the cellular and humoral immune responses, were analysed during the course of infection. Infections in mice peaked 2-3 weeks after inoculation and were self-cured by day 42 post-infection (p.i.). The proportion of trophozoites expressing the Mr 72,000 surface antigen of the initial inoculum had decreased by day 12 and approached zero by day 22 p.i., similar to infections in humans. The predominant parasite-specific humoral response was an IgM- and IgG-isotype directed to the original Mr 72,000 surface antigen as well as other antigens. T-lymphocytes (predominantly LY4(CD4)+) isolated from Peyer's patches 12 days p.i. and later showed a significant proliferative response to Giardia lamblia antigens. Spleen and lymph node cells showed no lymphoproliferative response. T-cell blot analysis revealed the presence of dominant T-cell epitopes in the areas of Mr 200,000-75,000 and less than 50,000 polypeptides. No response was demonstrated in the Mr 72,000 region (migration site of the major surface antigen), suggesting T-cell dependent mechanisms are most likely not responsible for the surface antigen switch which occurred during the course of infection. This model infection can be used to study the role of immunological mechanisms in Giardia lamblia variant antigen switching and in the control of infections.
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PMID:Antigenic variation in Giardia lamblia: cellular and humoral immune response in a mouse model. 170 8

Macrophages are important regulatory cells that can both stimulate and down-regulate various immune functions. During syphilitic infection, these cells phagocytize, kill, and lyse Treponema pallidum. They also modulate early T cell activation by decreasing IL-2 production through secretion of PG. This report focuses on additional complexities of macrophage regulation. Non-adherent splenic cells were stimulated with Con A to induce IFN-gamma synthesis. High levels were detected in preparations from normal rabbits and much lower levels in preparations from infected rabbits. The organisms also readily stimulated IL-1 synthesis by adherent spleen preparations from normal but not from infected rabbits. When indomethacin was added to these latter preparations, this IL-1 defect was reversed, implicating PG in this down-regulation. Spleen cells were obtained from normal rabbits and from rabbits infected testicularly for 9 to 12 days. Infection elevated basal levels of class II Ia Ag on adherent cells. In addition, macrophage Ia expression was increased during 4 days of in vitro incubation with treponemes. Non-adherent spleen cells from infected animals inhibited two different macrophage functions. First, culture filtrates obtained after 48 h of incubation contained a soluble factor that subsequently decreased LPS-induced IL-1 synthesis. Second, when macrophages were co-incubated with non-adherent cells, treponemal stimulation of macrophage Ia expression was inhibited; this inhibition was reversed by indomethacin implicating prostaglandins in this down-regulation. In further experiments an exogenous source of IFN-gamma was incubated with adherent cells from infected rabbits. This stimulated macrophage function as shown by increased IL-1 synthesis and Ia expression and decreased PGE2 secretion. Results are discussed in terms of the complexities of immunoregulation by macrophages during syphilitic infection.
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PMID:Splenic macrophage function in early syphilitic infection is complex. Stimulation versus down-regulation. 190 94

Concentrations of IgM and IgG isotypes were determined by capture ELISA in plasma of Swiss, BALB/c and C58/M mice. Plasma IgG isotype concentrations, especially of IgM, IgG1 and IgG2a, varied considerably between mouse strains, batches of mice of the same strain and individual mice and as a function of age. Infection of the mice with LDV, which is known to replicate primarily in a subpopulation of macrophages, consistently resulted in a rapid elevation of plasma IgG2a (or of IgG2b in some Swiss nu/+ mice), but no plasma IgG increases were observed in mice immunized with inactivated LDV. Plasma IgG2a elevation after LDV infection was greatly delayed and reduced by depletion of the mice of CD4+, but not of CD8+, T cells by administration of protein-G-purified anti-CD4 or anti-CD8 mAbs, and completely inhibited by repeated treatment of the mice with cyclophosphamide. Treatment with anti-CD4 mAbs, or cyclophosphamide also greatly reduced the production of anti-LDV antibodies, while not significantly affecting the replication of LDV in these mice. Nude Swiss mice also failed to produce anti-LDV antibodies, though supporting normal LDV replication. Plasma IgM, IgG1, IgG2a and IgG2b levels increased in LDV-infected nu/nu mice, but similar changes were observed in uninfected mice. The results indicate that the LDV-induced polyclonal activation of B cells requires productive LDV infection of mice and is, at least partly, dependent on functioning CD4+ cells. They suggest that productive infection of the LDV-permissive subpopulation of macrophages leads to the activation of CD4+ T lymphocytes of subset 1 and their Spleen cells from 5-day LDV-infected BALB/c mice incorporated [3H]thymidine 2-3 times more rapidly in vitro than spleen cells from companion uninfected mice, whereas their responses to concanavalin A and lipopolysaccharide were reduced 60-70%.
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PMID:Polyclonal B cell activation of IgG2a and IgG2b production by infection of mice with lactate dehydrogenase-elevating virus is partly dependent on CD4+ lymphocytes. 207 77

Infection of animals with retroviruses frequently leads to immunosuppressed states. The immune status of chickens injected with the replication-defective avian erythroblastosis virus (AEV), with its naturally occurring subgroup B helper virus (avian erythroblastosis-associated virus; AEAV), was evaluated daily and compared to the immune status of age-matched uninfected control chickens. Spleen cells from AEV-infected chickens gave depressed responses to concanavalin A, phytohemagglutinin, and pokeweed mitogen beginning 3 days after injection of the virus and continuing until death. Spleen cells from AEV-infected chickens suppressed the T-cell mitogen-induced blastogenic responses of spleen cells from uninfected chickens. The ability of spleen cells from infected chickens to suppress mitogen-induced blastogenic responses of spleen cells from normal chickens in coculture was transient beginning 4 days following viral inoculation, reaching peak levels of suppression on day 7 and disappearing by day 12. Cytolysis of splenic cells from AEV-infected chickens with polyclonal anti-T-cell-serum removed the suppressor activity. Addition of conditioned medium rich in T-cell growth factor resulted in a partial restoration of the blastogenic responsiveness of splenic cells from 6-day post-AEV-infected chickens. Addition of exogenous T-cell growth factor had no effect on the suppressed blastogenic responsiveness of spleen cells from 12-day post-AEV-infected chickens, and it had no effect on coculture suppression. In addition to suppressed T-cell responses to polyclonal mitogen-induced proliferation in vitro and transiently expressed T-suppressor cells, thymic atrophy and structural disruption was observed in AEV-infected chickens.
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PMID:Immune abnormalities in avian erythroblastosis virus-infected chickens. 214 45

Previous reports have shown that Bacteroides fragilis may enhance the pathogenicity of coinfecting enterobacteriaceae by interfering with the host's immune response. With the present study, we have investigated the possible role of interferons (IFN) in mediating these effects. Mice injected with B. fragilis developed moderate serum levels of IFN that appeared just prior to alterations of the animals' immunity described earlier. The IFN was neutralized by treatment with anti-IFN-alpha/beta-antibodies or hydrochloric acid; hence it displayed the same "atypical" characteristics as IFN found in patients with immuno-compromising diseases such as AIDS, systemic lupus erythematosus or rheumatoid arthritis. Escherichia coli displayed the same induction patterns as B. fragilis, while gram-positive bacteria induced "regular" IFN alpha/beta and gamma. Spleen cells, peritoneal macrophages, or liver leukocytes taken from B. fragilis or E. coli-injected animals 6 h post infection were refractory to IFN induction by E. coli lipopolysaccharide in vitro; cells from mice infected with gram-positive organisms showed normal or enhanced responsiveness.
Infection
PMID:Induction of an atypical interferon by bacteroides fragilis and Escherichia coli in experimental infections and in leukocyte cultures. 243 31


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