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PubMed2000

Influence of Hyperimmunization on Formation of Plaque Forming Cells in Lymphoid Organs Made with Transplantation of Spleen Stromal Fibroblasts.

When heterotopically transplanted under the renal capsule, the strains of stromal fibroblasts from spleen cultures formed the lymphoid organs, which had no specialized structures, such as red and white pulp and consisted of the accumulations like lymphoid follicles. The purpose of the given work was the study of ability of spleen stromal fibroblast strains, when heterotopically transplanted into the organism, to transfer the specific lymphoid microenvironment. The heterotopic transplantation of spleen fragments and stromal cells, grown in vitro, was made in autologous variant. The spleen fragments were put under a renal capsule. The strains of stromal fibroblasts of 5-7th passages were put into porous frames under a renal capsule of normal or immunized rabbits. The immune response to sheep red blood cells was studied in spleen of normal and hyperimmune rabbits, in regenerating spleens, in heterotopic grafts of spleen and in lymphoid organs, formed by strains of spleen stromal fibroblasts, grown in cultures. The immune response was determined on the 7-8th day after immunization by counting the amount of plaque forming cells (PFC) by Jerne method. In lymphoid organs, formed at the place of transplantation of spleen stromal fibroblasts strains of rabbits, the number of PFC was almost 3 times lower, than in heterotopic transplants of spleen, and 6 times lower, than in normal and regenerating spleens, but hundreds times exceeding the number of spontaneous PFC which could be only found, when 10(7)-10(8) spleen cells of normal non-immunized animals were tested. The concentration of PFC in lymphoid organs, formed at the place of the graft of stromal fibroblasts, was 3 times lower in regenerating spleens of hyperimmunised animals and 5 times higher, than in transplants of stromal fibroblasts of normal spleen. The obtained results give an evidence, that the transplantation of spleen stromal fibroblasts provides the transfer of specific lymphoid microenvironment.

Journal Article↗

PubMedDate not supplied

Inclusion of spleen in pediatric multivisceral transplantation.

Inclusion of the donor spleen may be beneficial for small children who receive multivisceral transplantation (MVT) because asplenia is associated with increased risk of bacterial sepsis. Beginning in 2003, the spleen was transplanted together with multivisceral transplantation in 17 children under daclizumab induction (spleen group). The results were compared to 23 children who received multivisceral transplantation without the spleen (control group) with the same immunosuppression regimen. Median age of 17 patients who received a spleen was 0.80 years (range 0.54-1.66). Platelet counts at 30 and 60 days posttransplant were significantly lower in the spleen group (average values: day 30: 399,000 vs 636,000, P = .015; day 60: 413,000 vs 622,000, P = .0056). WBC counts at 30 and 60 days posttransplant were also decreased in the spleen group but the difference was not statistically significant. Median rejection-free survival was 205 days in the spleen group and 101 days in the control group (P = NS). Median length of hospital stay was 39 days in the spleen group and 61 days in the control group. With a median follow-up of 398 days (spleen group) and 1232 days (control group), 3 of 17 (17%) in the spleen group developed graft versus host disease (GVHD), whereas 1 of 23 (4.5%) in control group did (P = NS). In one patient in each group, GVHD was fatal. No patient developed posttransplant lymphoproliferative disorder (PTLD) in the spleen group, whereas 4 of 23 (17%) in the control group developed PTLD. One-year patient survival was 84% in the spleen group and 86% in the control group. Recipients of the spleen as part of a multivisceral graft had significantly lower platelet counts. Rejection-free survival may be prolonged, but the risk of GVHD may be increased.

Antibodies, Monoclonal↗

PubMed1988

Presence of natural suppressor cells in the chicken embryo spleen and the effect of virus infection of the embryo on suppressor cell activity.

Spleen cells but not the thymus or the bursa cells of chicken embryos suppressed the in vitro mitogenesis of spleen cells of adult syngeneic or allogeneic chickens. The natural suppressor cell activity of embryo spleen was present at embryonation day 16, reached peak levels at embryonation day 18 and disappeared at hatch. The embryo spleen cells did not by themselves respond to phytohemagglutinin stimulation in vitro. The suppressive effect of embryonic spleen cells on adult spleen cells was present when the embryonic cells were added at the time of or after initiation of the adult spleen mitogenic cultures. When the embryonic cells were added to the cultures of adult spleen cells after the blastogenic response of the adult cells had peaked, the embryonic cells inhibited the incorporation of the label into adult spleen cell blasts. The suppressive activity of the embryonic spleen cells was mediated by soluble suppressor product(s) secreted by these cells, and direct cell-to-cell contact between embryonic and adult spleen cells was not necessary for suppression to occur. Infection of embryos with turkey herpesvirus and Marek's disease virus reduced the suppressor cell activity of embryonic spleen, although substantial residual suppressor cell activity remained in virus-infected embryos. Several pathogenic or non-pathogenic isolates of infectious bursal disease virus did not appreciably alter the suppressor cell activity of embryonic spleen cells.

Animals↗

PubMed2003

A type of rat hepatosplenic gamma-delta (gammadalta) T-cell lymphoma developed after injections with hepatocyte growth factor (HGF) oligonucleotides, which was rejected by surviving syngeneic spleen graft.

The transduction of exogenous hepatocyte growth factor (HGF) genes to spleen T lymphocytes and the immune effects of syngeneic spleen graft on spleen lymphoma cells were studied in LEW/Sea rats. Three different systems were designed. (1) Six female rats and six male rats received irradiated spleen graft and were followed for 7 months. (2) Five female rats and six male rats received intra-peritoneal (i.p.) injections of the Lewis red cells incorporated 20-bp HGF genes and anti-interleukin-6 (IL-6) antibody (Ab) with spleen graft and were followed for 5.5 months. (3) Four females and five males received i.p. injections of the Lewis red cells incorporated 20-bp HGF genes and anti-IL-6 Ab without spleen graft and were followed for 5.5 months. Hemato-pathological analyses, flow cytometer analyses of gamma-delta (gammadelta) T-cell receptor (TCR)-positive lymphocytes and reverse-transcription-polymerase chain reaction (RT-PCR) of TCRgamma gene, TCRValpha3 gene and apoptotic genes were performed. Results showed that one of the six females received irradiated spleen graft developed nodal gamma-delta (gammadelta) T-cell pre-lymphoma with 100% of gammadelta TCR+ lymphocytes in the mesenteric lymph nodes. One female injected with the HGF genes and anti-IL-6 Ab and grafted spleen died of advanced hepatosplenic gammadelta T-cell lymphoma at 3.5 month observation. All the five males injected with the HGF genes and anti-IL-6 Ab without spleen graft developed early hepatosplenic gammadelta T-cell lymphoma at 5.5 month observation. In two rats with spleen graft and the two rats without spleen graft, which were injected with the HGF genes and anti-IL-6 Ab, the lymphoma was suspected uncertainly with activated TCRValpha3 mRNA. The i.p. injections of HGF genes, which were incorporated in the red blood cells, triggered hapatosplenic gammadelta T-cell lymphoma. Surviving spleen graft rejected the lymphoma cells, but not in rats rejected the graft. Spleen graft was a good organ transplantation to expect graft versus lymphoma effects.

Animals↗

PubMed1981

Spleen changes in animals inhaling ambient levels of nitrogen dioxide.

The effects of ambient levels of NO2 on the spleens of adult and newborn Swiss Webster (S/W) mice were determined. Spleens were evaluated by the following criteria: (1) spleen weight, expressed as a percent of the body weight (% spleen weight), (2) size of the spleen lymphoid nodules as determined by computed image analysis, (3) spleen cell counts, and (4) histopathologic evaluation. Data for NO2-exposed animals were compared with data for control animals that inhaled filtered air. Totals of 217 control and 217 NO2-exposed animals were studied. After 6 wk of exposure to NO2 at ambient levels (0.35 +/- 0.05 ppm), the following significant changes were observed in the spleens of exposed mice: (1) increase in % spleen weight (p less than 0.0025), (2) increase in size of spleen lymphoid nodules (p less than 0.01), (3) smaller increase in spleen cell number per given weight increment of spleen as determined by correlation coefficients (p less than 0.0125) and linear regression analysis of spleen cell counts, and (4) an apparently greater predominance of red cells in the red pulp. It is concluded that inhalation of NO2 is associated with quantifiable spleen changes, which may prove to be useful indicators for assessing effects of inhaled NO2.

Air↗

PubMed1987

Specific inhibition of hybrid resistance in F1 hybrid mice pretreated with parent strain spleen cells. I. Induction of a nylon-adherent, Thy-1+Lyt-1+2- suppressor cell.

Hybrid resistance, which is observed in certain strain combinations when parent-strain bone marrow cells are grafted into lethally irradiated F1 hybrids, can be specifically overcome by the i.v. injection, 1 wk before the graft, of spleen cells syngeneic with the bone marrow graft. This phenomenon is due to a suppressor mechanism, induced in the spleen of the F1 hybrid by the injection of parent-strain spleen cells and mediated by a nylon-adherent Thy-1+Lyt-1+2- cell population of hybrid origin, because hybrid resistance can be inhibited by the transfer into a normal B6D2F1 of nylon-adherent Thy-1+Lyt-1+2- spleen cells from B6D2F1 mice pretreated with B6 spleen cells 1 wk earlier (B6-pretreated B6D2F1); spleen cells from B6-pretreated B6D2F1 mice not depleted of their nylon-adherent subpopulation cannot restore hybrid resistance when they are injected into a B6D2F1 rendered nonresistant by split-dose irradiation; and spleen cells from normal B6D2F1 mice cannot restore hybrid resistance when they are injected into B6-pretreated B6D2F1 hybrids. The suppressor cells specifically inhibit resistance against bone marrow cells syngeneic with the spleen cells used for pretreatment, because transfer of nylon-adherent B6-pretreated B6D2F1 spleen cells into a normal B6D2F1 does not enhance syngeneic B6D2F1 or parent-strain D2 bone marrow growth, and when injected into normal B6D2F1 hybrids, nylon-adherent spleen cells from B6D2F1 mice pretreated with D2 spleen cells 1 wk earlier (D2-pretreated B6D2F1) are not able to transfer the inhibition of hybrid resistance against B6 bone marrow cells. Moreover, the activity of the suppressor cells depends on the genetic environment of the hybrid host mice, because nylon-adherent B6-pretreated B6D2F1 spleen cells injected into normal B6C3F1 hybrids do not transfer an inhibition of hybrid resistance, and when injected into B6C3F1 hosts previously rendered nonresistant by split-dose irradiation, spleen cells from B6-pretreated B6D2F1 mice can, in contrast, transfer hybrid resistance.

Animals↗

PubMed2004

Study on the pathological basis of classification of spleen deficiency in chronic gastritis.

BACKGROUND: Spleen in Traditional Chinese Medicine (TCM) is not actually the spleen in the anatomic sense designated in western medicine because its functions basically belong to the physiological category of digestive system in modern medicine, and it represents a macroscopic concept of digestion, absorption and nutrition metabolism. Spleen deficiency syndrome refers to the clinical phenomena such as hypofunction of digestion, absorption and nutrition metabolism. By integrating TCM with modern medicine, this paper is intended to explore the pathological basis of classification of spleen deficiency in chronic gastritis. METHOD: By means of optical microscope, scanning electron microscope (SEM), transmission electron microscope (TEM) and histochemical staining, we conducted histopathological and subcellular ultrastructural (nuclei and mitochondrial) analysis of gastric mucosa of 188 patients of spleen deficiency, and that of 42 voluntary blood donors without clinical symptoms. RESULTS: The gastric mucosa of patients with spleen Qi deficiency (SQD) and spleen yang deficiency (SyangD) could either be affected by organic lesion (type G-occurring on the basis of chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG)) or unaffected (type F-chiefly belonging to functional indigestion); spleen yin deficiency (SyinD) and spleen deficiency with Qi stagnation (SDQS) both occurred on the basis of CSG and CAG; and the degree of mucosa inflammatory cells infiltration, the degree of decrease in glands propria, and the incidence of IMIIb in CSG and CAG were more serious than those of G-SQD and G-SyangD, P < 0.05 - 0.01. CONCLUSION: Spleen deficiency syndrome is likely to occur on the basis of organic lesion of gastric mucosa (disease with symptoms of both CSG or CAG and spleen deficiency symptoms), as well as on the basis of inorganic lesion of gastric mucosa (nondisease with symptoms, which is, despite spleen deficiency symptoms, there is no CSG or CAG). Besides, the clinical phenomenon of disease without symptoms (despite CSG or CAG, there is no spleen deficiency symptoms) occurres because of such factors as genetic diathesis and compensation. The lesion degree of CSG or CAG and the incidence of IMIIb of SyinD and SDQS are more serious than those CSG and CAG of G-SQD and G-SyangD.

Adult↗

PubMed1986

Clonal analysis of T lymphocytes in spleens from patients with Hodgkin's disease. Frequent occurrence of unusual T4-positive cells which co-express cytolytic activity and production of interleukin-2.

T-lymphocyte populations isolated from spleens of untreated patients with Hodgkin's disease (HD) were grown by combining limiting dilution techniques and an assay system that allows clonal proliferation of virtually all human T cells. Under these conditions, high proportions of splenic T lymphocytes (50-80%) underwent clonal expansion, so that the set of clones obtained could be considered representative of the starting T-cell population. A total number of 229 clones from 6 HD spleens (3 uninvolved and 3 histologically involved by the disease) and 133 clones from 3 control spleens (obtained from otherwise healthy individuals, who underwent post-traumatic splenectomy) were examined for surface markers and tested in functional assays. One hundred and seventy-five clones from HD spleens and 75 clones from control spleens expressed the "helper/inducer" (T3+ T4+ T8-)phenotype, whereas as 54 clones from HD spleens and 58 control clones expressed the "cytotoxic/suppressor" (T3+T4-T8+) phenotype. As assessed by a non-specific lectin-dependent lytic assay, the proportion of HD clones displaying cytolytic activity was higher than that of cytolytic clones derived from control spleens. The majority of T4+ clones obtained from HD spleens (either uninvolved or histologically involved by the disease) were cytolytic, whereas only a small proportion (less than 10%) of T4+ clones derived from normal peripheral blood or spleens displayed cytolytic activity. The cytolytic potential of T4+ clones obtained from HD spleens did not reflect the activity of natural killer (NK) cells, since a minority of these clones exerted NK activity on K562 target cells. In addition, most of the T4+ cytolytic clones derived from HD spleens produced particularly high amounts of interleukin-2 (IL-2). These data indicate that T lymphocytes which concentrate in spleens of patients with HD consist at least in part of an infrequent T4+ cell subset co-expressing cytolytic activity and production of IL-2. These cells may reflect a cytotoxic reaction against unknown antigens associated with self class-II histocompatibility antigens.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1993

Two tumor models of curative adoptive chemoimmunotherapy using tumor-infiltrated spleen cells with potent antitumor cytotoxicity stimulated by antigen-sharing tumors.

Previously we have established curative protocols for adoptive chemoimmunotherapy (ACIT) of mice bearing different plasmacytomas that are known to bear cross-reacting antigens: (a) the cure of mice bearing an early-stage, nonpalpable MOPC-315 tumor by a very low dose of cyclophosphamide (10 mg/kg) and cultured MOPC-315-tumor-infiltrated (TI) spleen cells (25 x 10(6)) and (b) the cure of mice bearing a late-stage, relatively drug-resistant, highly metastatic RPC-5 tumor with cyclophosphamide (100 mg/kg) and cultured RPC-5 TI spleen cells (25 x 10(6) - 50 x 10(6)). In both models, the spleen cells were obtained from mice bearing a late-stage tumor and were cultured for 5 days in the presence of polyethyleneglycol 6000 and autochthonous tumor cells as a source of tumor antigen. Here we show that RPC-5 tumor cells could substitute for MOPC-315 tumor cells in the 5-day culture of MOPC-315 TI spleen cells so that they became curative in ACIT for mice bearing an early-stage MOPC-315 tumor. Similarly, MOPC-315 tumor cells could substitute for RPC-5 tumor cells in the 5-day culture of RPC-5 TI spleen cells so that they became curative in ACIT of mice bearing a late-stage RPC-5 tumor. In addition, RPC-5 TI spleen cells cultured with either MOPC-315 or RPC-5 tumor cells were effective in curing all mice bearing an early-stage MOPC-315 tumor by ACIT. However, MOPC-315 TI spleen cells whether cultured with MOPC-315 or RPC-5 tumor cells, were much less effective than cultured RPC-5 TI spleen cells in curing mice bearing a late-stage RPC-5 tumor by ACIT (although the survival of these mice was extended significantly). Interestingly, whereas RPC-5 TI spleen cells cultured with either MOPC-315 or RPC-5 tumor cells were as effective as MOPC-315 TI spleen cells cultured under the same conditions in lysing MOPC-315 tumor cells in vitro, MOPC-315 TI spleen cells that had been cultured with either MOPC-315 or RPC-5 tumor cells exerted a much weaker in vitro cytotoxic T lymphocyte activity against RPC-5 tumor cells than did RPC-5 TI spleen cells that had been cultured under the same conditions.

Animals↗

PubMed1999

Laparoscopic management of accessory spleens in immune thrombocytopenic purpura.

BACKGROUND: A disparity exists between the incidence of accessory spleens reported in the open (15-30%) versus the laparoscopic (0-12%) literature. This disparity implies that a percentage of laparoscopic patients will require a reoperation for accessory splenectomy. We present our experience with the laparoscopic management of accessory spleens discovered after primary splenectomy for idiopathic thrombocytopenic purpura (ITP). METHODS: Seventeen patients who underwent primary splenectomy for ITP were reviewed (1 open, 16 laparoscopic). In the laparoscopic group, the incidence of accessory spleens was 3 in 16 (19%). In 1 of these 3 patients, the accessory spleen was found and removed at the initial operation, whereas in 2 of the 16 patients (13%), the accessory spleens were missed. A third patient, whose initial operation was open, presented with recurrent thrombocytopenia after primary splenectomy. After recurrent thrombocytopenia developed, radio nuclide spleen scans were performed showing accessory spleens in all three patients. These three patients underwent accessory splenectomy using a four-port laparoscopic approach. RESULTS: Laparoscopic accessory splenectomy was successfully performed in all three patients. Location of accessory spleens correlated with the spleen scan in each case. Mean operation time was 180 min. There were no conversions to open surgery and no complications. All patients were discharged from the hospital on postoperation day 1. The three patients had a good clinical response and were weaned effectively from their steroid medications. CONCLUSIONS: Patients undergoing a laparoscopic splenectomy for chronic ITP have a higher probability of requiring a reoperation for a missed accessory spleen. To minimize missing an accessory spleen, a systematic search should be made at the beginning of the laparoscopic operation. We have found that preoperation imaging with heat-treated erythrocyte scans is valuable for locating accessory spleens before reoperation. When reoperation for accessory splenectomy is necessary, a laparoscopic approach is safe and effective.

Adolescent↗

PubMed1991

GM-CSF augments the immunosuppressive capacity of neonatal spleen cells in vitro.

Addition of exogenous granulocyte-macrophage colony stimulating factor (GM-CSF) to cultures of adult murine spleen cells with sheep red blood cells (SRBC) results in an augmented plaque forming cell (PFC) response. The influence of GM-CSF on the ability of neonatal spleen cells to suppress the anti-SRBC plaque forming response of adult spleen cells was tested by adding GM-CSF to cultures of neonatal and adult spleen cells. The suppressive capacity of the neonatal spleen cells was augmented by exogenous GM-CSF. The augmented suppression of the neonatal spleen cells was dependent on a G-10 adherent population since the addition of GM-CSF to cultures containing G-10 passed neonatal spleen cells resulted in an augmented PFC response and not suppression. Neonatal splenic glass adherent cells were also capable of suppressing the response. Neonatal spleen cells or purified neonatal glass adherent spleen cells cultured in the presence of GM-CSF had markedly increased levels of PGE2 in the culture supernatant. Neonatal spleen cells cultured with GM-CSF had increased numbers of morphologically identifiable macrophages after 48 hr of culture. Both irradiation and G-10 passage of the neonatal spleen diminished the numbers of macrophages formed in response to GM-CSF, and both of these manipulations resulted in reversal of suppression in response to GM-CSF. Thus, the augmented suppressive capacity of neonatal spleen cells in response to GM-CSF is probably mediated by its ability to drive monocyte to macrophage differentiation as well as increase the suppressive capacity of the existing neonatal splenic macrophages by increasing their production of PGE2.

Animals↗

PubMed2006

Primitive hematopoietic cell populations reside in the spleen: Studies in the pig, baboon, and human.

OBJECTIVE: We previously observed high levels (>40%) of multilineage hematopoietic cell chimerism following spleen transplantation across full MHC barriers in immunosuppressed miniature swine. We therefore investigated the spleen as a source of hematopoietic progenitor cells (HPCs). MATERIALS AND METHODS: Specific cell-surface markers were used to identify HPCs in the spleen and bone marrow (BM) of young adult (n = 15) and fetal (n = 9) miniature swine by flow cytometry. Hoechst dye-effluxing side population (SP) cells were analyzed in adult spleen, BM, and blood for their expression of c-kit. Functional HPC activity of varying repopulation potential in vitro was investigated by the ability of spleens and BM to give rise to colony-forming units (CFUs) and cobblestone area-forming cells (CAFCs) in long-term stromal cultures. Studies were also carried out on baboon and human spleens and BM. RESULTS: Spleen c-kit+ cells co-expressed more lymphoid markers, but equal myeloid markers, when compared with BM c-kit+ cells. BM and spleen both contained significant percentages of c-kit+ SP cells. Although the frequency of early-forming CFUs in the spleen was only 0.1 to 1.3% of that in the BM, the frequency of CAFCs developing after 8 weeks in culture was comparable to that of BM. Secondary CFUs in long-term culture-initiating cell assays confirmed the presence of long-term repopulating cells at comparable frequencies in spleen and BM. Similar findings were found with regard to baboon and human spleen cells. CONCLUSION: The adult spleen is a relatively rich source of very primitive HPCs, possibly hematopoietic stem cells (HSCs), and may be of therapeutic value.

Adult↗

PubMedDate not supplied

Congenital anomalies of the spleen mimicking hematological disorders and solid tumors: a single-center experience of 2650 consecutive diagnostic laparoscopies.

Congenital anomalies of the spleen range from splenic lobulation, to accessory spleen to polysplenia. Though most of these anatomical variants have no clinical significance, an accessory spleen may simulate a tumor in the adrenal gland, pancreas, stomach or intestine. Alternatively, a missed accessory spleen may be the site of the relapse of a hematological disorder. We, therefore, assessed retrospectively: (i) the frequency of congenital anomalies of the spleen observed during 2650 consecutive laparoscopies and (ii) looked for possible misdiagnoses of the accessory spleen as hematological disorders or solid tumors located in the left upper quadrant of the abdomen. Congenital anomalies of the spleen were detected in 55 cases, accounting for 2.07%. Accessory spleens were observed in 44 patients (1.6%) and spleen lobulation in 11 (0.47%). An accessory spleen was the most common of the splenic anomalies. Among the 44 patients in whom an accessory spleen was discovered laparoscopically, the recognition of this anomaly prevented a relapse of a hematological disease in one case and avoided a useless exploratory laparotomy in the second, where the radiologist had interpreted this malformation as a space-occupying lesion. In the third case, the accessory spleen was initially misdiagnosed as a solid tumor of the pancreas, but was eventually recognized as a congenital anomaly by a second laparoscopy.

Abdominal Neoplasms↗

PubMed1988

Lectin-induced cytotoxic activity in spleen cells from young and old mice. Age-related changes in types of effector cells, lymphokine production and response.

Concanavalin A (Con A)-induced cytotoxic activity, interferon (IFN) and interleukin-2 (IL-2) levels in cultures of spleen cells from young (2-3 months) and old (22-24 months) C57BL/6 female mice were studied. Con A-activated spleen cells from old mice attained significantly higher cytotoxic activity compared with activated spleen cells from young mice. Activated spleen cells from old and young mice showed differences in their ability to lyse different types of target cells. Both could lyse P-815 cells, neither could lyse K562 cells, and only activated cells from old mice could lyse EL-4 cells. Cytotoxic spleen cells from the old mice were more sensitive to anti-asialo-GM-1 and anti-Lyt-2.2 plus complement (C) treatment. While levels of IL-2 produced by spleen cells from young mice were higher, the addition of exogenous IL-2 had no effect on cytotoxic activity of the spleen cells from old mice. Exogenous IL-2, however, could lower cytotoxic activity of Con A-activated spleen cells from young mice. Activated spleen cells from old mice generated higher levels of IFN-gamma while the addition of an anti-IFN-gamma antibody boosted the level of cytotoxicity by Con A-activated spleen cells from young mice. These results suggest that IFN-gamma may act as a feedback inhibitory signal regulating the levels of cytotoxicity induced in spleen cells from young mice in response to Con A. The cytotoxic activity generated in Con A-activated spleen cells from old mice reflects a defect in this feed-back regulation.

Aging↗

PubMed2005

Study on the pathophysiologic basis of classification of 'spleen' deficiency in chronic gastritis.

BACKGROUND: Most of the studies on traditional Chinese medicine (TCM) 'spleen' deficiency syndrome in the recent 30 years were conducted only on the basis of single functional index, neglecting the study on the pathophysiologic internal relationship between spleen deficiency syndrome and gastric diseases in modern medicine. But it was at the subcellular molecular biological level that we explored the pathophysiologic basis of classification of spleen deficiency in chronic gastritis by detecting the bioactive substances in gastric mucosa nuclei and mitochondria. METHODS: By means of optical microscope, scanning electron microscope (SEM), transmission electron microscopy (TEM) and histochemical staining, we conducted histopathological, subcellular ultrastructural analysis and nuclei and mitochondrial ultrastructural analysis of gastric mucosa of 188 spleen deficiency patients and of 42 voluntary blood donors. At the same time, bioactive substances were measured by means of X-ray energy dispersive analysis system (EDAX) image analysis system, radioimmunoassay method and chemiluminescence method. RESULTS: The content of cAMP, superoxide dismutase (SOD), Zn and Cu in gastric mucosa, and the content of Zn and Cu in mitochondria decreased progressively in order of groups: healthy control (HC), spleen Qi deficiency without organic lesion (F-SQD), spleen Yang deficiency without organic lesion (F-SyangD), disease without symptoms group, spleen Qi deficiency with organic lesion (G-SQD), spleen Yang deficiency with organic lesion (G-SyangD), spleen Yin deficiency (SyinD) and spleen deficiency with Qi stagnation (SDQS), chronic spleen deficiency gastritis (CSG) and chronic atrophic gastritis (CAG); decreased in order of HC, intestinal metaplasia (IM)Ia, IMIb, IMIIa and IMIIb, P < 0.05. The content of DNA, Zn and Cu in nuclei progressively increased in order mentioned above, P < 0.05. CONCLUSIONS: The quantitative changes of gastric mucosal cAMP, SOD, Zn, Cu, of mitochondrial Zn, Cu and of nuclear DNA, Zn and Cu are not only the substance base on which the lesion of gastric mucosa tissue structure occurs, but also the substance base on which spleen deficiency is classified. G-SQD and G-SyangD were more likely to be found in low-grade or middle-grade CSG and CAG, while SyinD and SDQS in middle-grade or high-grade CSG, CAG and IMIIb.

Adult↗

PubMed1984

Immunotherapy of murine leukemia. XI. differential susceptibility of spleen cells from serum-protected mice to the in vitro immunosuppressive effects of Friend leukemia virus-infected splenocytes.

It has previously been shown that DBA/2 mice protected against the development of Friend leukemia virus (FLV)4-induced disease by the passive administration of heterologous antisera directed against disrupted virions or the major viral envelope glycoprotein (gp71) fail to undergo the generalized immunosuppression which characterizes FLV leukemogenesis. In the present studies, the susceptibility of spleen cells from serum-protected mice to the immunosuppressive effects of FLV-infected spleen cells has been examined by means of in vitro assays of antibody production and of natural killing (NK). In contrast to the parallel suppression of both functions in FLV-infected mice and their lack of suppression in serum-protected animals, a dichotomy was observed in the in vitro susceptibility of these activities of spleen cells from serum-protected mice to the suppressive effects of virus-infected splenocytes, implying that more than one mechanism of suppression is operative. Thus, the antibody-producing capability of serum-protected splenocytes was not suppressed by FLV-infected spleen cells, this suppression reflecting the activity of infectious virus, while the NK effector function of serum-protected spleen cells was as susceptible as that of normal splenocytes to suppression by virus-infected spleen cells. This suppression of NK activity is mediated by virus-induced suppressor cells and does not involve free infectious virus, in contrast to suppression of antibody production. These results thus indicate that, while serum therapy inhibits the development of the virus-induced NK suppressor cells found in the spleens of progressively infected mice, splenic NK effectors, which are present, demonstrate full susceptibility to the suppressive effects of such independently generated virus-induced suppressor cells. Preliminary attempts at characterizing these NK suppressors in the spleens of FLV-infected mice indicate that they are not eliminated by treatment with antisera directed against T cells, B cells, macrophages or FLV gp71. However, Percoll fractionation of spleen cells from infected mice has revealed the presence of an expanded (as compared to normal spleen cells) population of cells of density 1.077 which demonstrates high in vitro NK suppressor activity, presumably representing the virus-induced suppressor cells measured in this assay. At the present time, the mechanism of the resistance of serum-protected spleen cells' antibody production to suppression by FLV-infected splenocytes (i.e., by FLV itself) remains undefined.

Animals↗

PubMed1993

Acetylcholinesterase staining and choline acetyltransferase activity in the young adult rat spleen: lack of evidence for cholinergic innervation.

Acetylcholinesterase (AChE) staining in spleens from young adult Sprague-Dawley rats was examined following several denervation paradigms to determine the source of splenic AChE+ nerve fibers. In spleens from all control groups, AChE+ neural-like profiles were present along the vasculature and in the trabeculae. AChE+ reactivity also was present in lymphoid and reticular cells in the spleen, and in neuronal cell bodies in the superior mesenteric-coeliac ganglion (SM-CG). Neurochemical analysis revealed no significant choline acetyltransferase activity in spleens from control animals. Surgical removal of the SM-CG resulted in a total loss of both noradrenergic (NA) and AChE+ nerve profiles, as well as a loss of AChE staining in nonneural compartment in the spleen. On Days 1 and 3 after treatment, chemical sympathectomy with 6-hydroxydopamine also resulted in a loss of both NA and AChE nerve profiles in the spleen, except for a few resistant fibers in the hilar region. AChE reactivity in nonneural compartments also was diminished in chemically denervated regions of the spleen. AChE staining in both neural and nonneural profiles progressively increased from 10 to 56 days after chemical sympathectomy, with a time course and distribution pattern similar to NA fibers reinnervating the spleen. AChE+ staining was preserved following bilateral vagal nerve transection. The miniscule splenic levels of choline acetyltransferase suggest that at best, only a small density of cholinergic nerves distribute to the rat spleen. Further, what cholinergic innervation is present does not arise from the vagus nerve as suggested in the earlier literature. Collectively, the overlapping distribution of AChE+ and NA nerve profiles in spleen and parallel loss of both population of nerve fibers following surgical and chemical sympathectomy support the presence of AChE in NA nerves colocalized with norepinephrine, and thus make AChE+ staining an inappropriate marker for cholinergic innervation in the rat spleen.

Acetylcholinesterase↗

PubMed1998

Spleen cells of non-obese diabetic mice fed with pig splenocytes display modified proliferation and reduced aggressiveness in vitro against pig islet cells.

A new means of modifying xenogeneic reaction to pig islet cells, which involves pre-feeding with pig spleen cells, was investigated for the first time in the non-obese diabetic (NOD) mouse. Compared with controls, mice fed with pig spleen cells displayed much higher splenocyte proliferation in response to pig spleen and islet cells (p < 0.0001). This enhanced proliferation was specific for the species providing the fed cells. Positive relationships (p < 0.01) were found between increased splenocyte proliferation in response to pig spleen or islet cells and the number of cells per feeding or the number of daily feedings. Concomitantly, while co-incubation with splenocytes from control mice led to inhibition of both basal and stimulated insulin releases from pig islet cells (p < 0.001), this aggressiveness was abolished (p < 0.001) after co-culture with splenocytes from mice fed with pig spleen cells. The proliferative responses of splenocytes from fed or control mice to pig islet or spleen cells were abolished after removal of plastic-adherent cells, indicating that the major indirect pathway of T-cell activation was unchanged by pig spleen cell feeding. The main T-splenocyte subsets involved were restricted to MHC class II as they did not proliferate in the presence of monoclonal antibodies (mAbs) directed at I-A molecules. In mice fed with pig spleen cells, as well as in control mice, the blocking of CD4 + T cells with mAbs led to abolition of proliferation (p < 0.002), while the blocking of CD8 + led to a less marked effect. However, an increase in the blocking effect of anti-CD8 mAbs was noted in mice fed with pig spleen cells (p < 0.02). In control mice, the main splenocyte subset involved during proliferation in response to pig islet cells was Thl, since interferon gamma (IFNgamma) production increased significantly (p < 0.01) while that of interleukin-10 (IL-10) increased only slightly. The main change observed in mice fed with pig spleen cells was a marked increase in basal IL-10 production (p < 0.01) and the basal IL-10/IFNgamma ratio (p < 0.001). It seems likely that feeding with pig spleen cells shifted the Th1/Th2 balance towards a dominance of Th2-type class II-restricted CD4 + T cells, which may have been conducive to activating CD8 + suppressor T cells. In any event, oral administration of pig cells modified xenogeneic cellular response, which may have implications for xenografts of pig islets. In a more general sense, physiological feeding of cells from xenogeneic species would appear to have certain effects on the immune system.

Administration, Oral↗