Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhalation of an antigen, ovalbumin (OVA), in the absence of adjuvant has been demonstrated to induce an immune response that is associated with increased airway responsiveness. Determination of OVA-specific serum IgE and IgG antibody responses revealed an early increase in antibody titers that were initially restricted to the IgE class. Subsequently, IgG antibody titers increased and IgE antibody plateaued. Furthermore, we observed a tenfold increase in the number of lymphocytes caused by a predominant expansion of CD3+ T cells in the peribronchial-associated lymph modes (PBLNs) of sensitized animals compared with the numbers of cells in control animals or in the gut-associated lymphoid tissue. The sensitized animals demonstrated an increase in airway responsiveness to intravenous methacholine challenge. Analysis of in vitro immunoglobulin production by spleen mononuclear cells revealed increased spontaneous IgE production that was more than fourfold enhanced in the presence of OVA, but IgG production was not increased. Spleen and PBLN lymphocytes, but not lymphocytes from gut-draining lymph nodes, demonstrated a proliferative response to OVA. Control animals exhibited no proliferative response to OVA. Histopathologic examination of the sensitized lung revealed an absence of acute inflammatory cells (e.g., neutrophils and macrophages), lymphocytes, or monocytes at the time of the increased airway hyperresponsiveness. These data indicate that, after sensitization of mice by inhalation of antigen, the animals develop a specific IgE antibody response, expansion of PBLN lymphocyte numbers, and increased airway hyperresponsiveness in the absence of signs of airway inflammation.
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PMID:Aerosolized antigen exposure without adjuvant causes increased IgE production and increased airway responsiveness in the mouse. 160 48

Translocation of enteric bacteria occurs in rats after hemorrhagic shock. A proposed mechanism involves intestinal mucosal injury by hypoperfusion. Recent work suggests that moderate hypovolemia causes gut arteriolar constriction, which is ameliorated by hypertonic saline resuscitation. Bacterial translocation should, therefore, be reduced when hypertonic saline (HS) is used as the resuscitative fluid. Seventy-eight Sprague-Dawley rats were anesthetized and subjected to 30 minutes of hemorrhagic shock (systolic blood pressure 30 to 50 mm Hg) through a modified Wigger's model. Resuscitation was performed with either shed blood (B), 3% HS + 1/2B (1:1), or with 7.5% HS + 1/2B (1:1). Spleen, liver, and mesenteric lymph nodes were sent for quantitative culture 24 hours later. Translocation occurred if enteric organisms were cultured from at least one organ. Statistical analysis used the Fisher exact test. Compared to autotransfusion, hemodilutional resuscitation from hemorrhagic shock with hypertonic saline resulted in a significant reduction in bacterial translocation (p values were 0.03 and 0.04 for 3% and 7.5% hypertonic saline, respectively). The reduction in translocation after hypertonic saline resuscitation may be the consequence of microcirculatory alterations preventing gut hypoperfusion.
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PMID:The effect of hypertonic saline resuscitation on bacterial translocation after hemorrhagic shock in rats. 192 57

Various organs--lung, trachea, liver, kidney, heart, adrenal gland, skin, spleen, thymus, lymph node, gut, thyroid, spinal cord and brain--were removed from 43 seals at dissections performed on the German North sea coast. The specimens were fixed in formalin and routinely processed for light microscopy. The major pathological findings were Lung: acute congestion with interstitial and intra-alveolar oedema; intra-alveolar haemorrhage; suppurative bronchitis and bronchopneumonia; larvae and adult forms of Parafilaroides gymnurus. Liver: acute congestion; granulomatous lesions and infiltrates of eosinophils; intravascular nematodes. Spleen: varying degrees of atrophy of the white pulp; haemosiderosis; acute congestion of the red pulp. Lymph nodes: varying degrees of atrophy of the lymphatic tissue; long-standing sinus histiocytosis with partial fibrotic obliteration of the lumina; parasitic infiltration, sometimes with the Splendore-Hoeppli phenomenon; germinal centre hyperplasia. Thymus: pronounced atrophy of the lymphatic tissue, particularly in the cortical areas. Thyroid: marked reduction in colloid content. The other organs studied were normal or showed only minor histopathological changes. The morphological findings do not allow definite conclusions to be made about the aetiology and pathogenesis of the illness and death of the seals. However, evidence has been published that the seals' illness is probably due to canine distemper virus. The atrophy of the lymphoreticular tissues is consistent with infection by this virus.
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PMID:Histopathological findings in harbour seals (Phoca vitulina) found dead on the German North sea coast. 236 46

A protocol was elaborated for the adoptive transfer of lymphocytes from mice which were orally immunized with cholera toxin (CT) to enable the study of long-term gut mucosal immunological memory at the single-cell level. Mesenteric lymph node (MLN) cells were transferred 1 year after priming immunizations, and recipient animals were challenged perorally on days 1 and 2 with CT before sacrifice on day 6 to 7 following transfer of cells. Strong antitoxin ELISPOT spot-forming cell (SFC) responses were recorded in spleens, MLN, and laminae propriae (LP) of recipient mice. In contrast, no SFC were found in Peyer's patches. The magnitude of the response equaled that of the acute response seen after optimal oral CT immunization and was directly dependent on the number of transferred cells. The memory antitoxin response in MLN and LP required oral challenge with CT as opposed to the spleen SFC response, which could also be triggered by intravenous challenge with antigen. Spleen cells from mice immunized perorally with CT were as effective as MLN cells in transferring immunological memory detectable in the gut immune system. Irrespective of the tissue source of transferring immunological memory detectable in the gut immune system. Irrespective of the tissue source of the memory cells, the isotype distribution of the antitoxin SFC response in recipient mice was similar with predominantly immunoglobulin A (96%) in LP and immunoglobulin G (66%) in MLN and spleen. Transfer of antitoxic memory was completely abrogated by treatment of the cells with J11d monoclonal antibody and complement prior to their injection into recipient mice by was unaffected by treatment with anti-Thy-1.2 antibody and complement, suggesting that long-term gut mucosal memory is carried by B cells. Antitoxin B memory cells might help explain the long-term protection against recurrent disease seen in convalescents from cholera in cholera-endemic areas.
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PMID:Adoptive transfer of gut mucosal antitoxin memory by isolated B cells 1 year after oral immunization with cholera toxin. 278 16

Molecular forms of immunoglobulin A (IgA) produced by cultured cells from various human lymphoid tissues were analyzed using high speed liquid chromatography (HLC). IgA secreted into culture media was easily separated into polymeric and monomeric forms by HLC. HLC has the advantages of high resolution, reproducibility, rapidity and technical simplicity in the separation of polymeric and monomeric IgA. Peripheral blood lymphocytes and cells from gut-associated lymphoid tissues, such as mesenteric lymph nodes or large bowel mucosa, secreted predominantly polymeric IgA, whereas lymphoid cells from bone marrow produced mainly monomeric IgA. Spleen cells and tonsillar cells produced nearly equal proportions of polymeric and monomeric IgA. These results suggest that with regard to IgA in serum, the polymer may originate from the gut-associated lymphoid tissues and the monomer may mostly derive from the bone marrow.
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PMID:Molecular forms of IgA produced by various lymphoid tissues--analysis using high speed liquid chromatography. 344 52

A highly reproducible paired immunofluorescence staining method was used to map the relative distribution of IgA1- and IgA2-producing cells in peripheral lymphoid organs and various secretory tissues. Spleen, peripheral lymph nodes, and tonsils all contained a marked predominance (91 to 95%) of IgA1 immunocytes. However, striking variations were demonstrated among the secretory tissues with regard to the median proportion of IgA1-producing cells: nasal mucosa, 96%; lacrimal glands, 81%; major salivary glands, 66%; mammary glands, 63%; gastric and proximal small intestinal mucosa, 84 to 77%; ileum, 55%; and large bowel, 41%. Thus, IgA2 production is relatively enhanced mainly in the distal gut and in mammary and salivary glands, in that order.
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PMID:Different subclass distribution of IgA-producing cells in human lymphoid organs and various secretory tissues. 351 60

Peyer's patch (PP) and mesenteric lymph node (MLN) cell cultures from young adult X-linked immunodeficient (xid) CBA/N and (CBA/N X DBA/2) F1 male mice support primary anti-sheep erythrocyte (SRBC) plaque-forming cell (PFC) responses, which suggests that gut-associated lymphoreticular tissue (GALT) contains a normal B lymphocyte subpopulation. Further support for this was provided by the observation that PP cells from xid mice gave responses to both TI-1 and TI-2 antigens that were similar to the responses of PP cell cultures from normal mice. Spleen cell cultures from xid mice were unresponsive to SRBC and TI-2 antigens. Proof that GALT of xid mice contain mature B lymphocytes was provided by the demonstration of PP B cells that bear a low density of surface immunoglobulin M. When these cells were separated by flow cytometry and immunized with trinitrophenyl (TNP)-Ficoll in vitro, good anti-TNP PFC responses were observed. These results suggest that GALT of young adult xid mice contain mature B cells and may represent the origin for the mature B cell responses seen in aged xid mice.
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PMID:Evidence for a mature B cell subpopulation in Peyer's patches of young adult xid mice. 660 Apr 93

Investigations with animals demonstrate that dietary nucleotides influence immune function. Restriction of dietary nucleotides in mice decreases several indices of cell-mediated immunity as well as resistance to challenge with Staphylococcus aureus or Candida albicans. Spleen cells of mice maintained on nucleotide-free diet produce less interleukin-2 and have lower natural killer cell cytotoxicity and macrophage activation than those of animals fed nucleotide-supplemented diets. In vivo lymphoproliferative response, macrophage phagocytic activity and expression of interleukin-2 receptor and lyt1 surface marker are also lower in animals fed nucleotide-free diets. At 2 mo of age, infants fed breast milk or nucleotide-supplemented infant formula exhibit increased natural killer cell activity compared with infants fed unsupplemented formula. Dietary nucleotide restriction in animals may also result in hepatic lipid accumulation and decreased mucosal height and gut wall thickness. Adenosine monophosphate, a mediator of hepatic and small bowel blood flow, may play a unique role among the nucleotides studied. In conclusion, de novo synthesis and salvage of nucleotides is a metabolically costly process. An exogenous source of nucleotides from the diet may optimize the function of rapidly dividing tissues, particularly when growth is rapid and the diet is low in nucleotides.
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PMID:Dietary nucleotides: cellular immune, intestinal and hepatic system effects. 828 5

We have previously shown that following oral administration of myelin basic protein (MBP), regulatory T cells are generated from gut-associated lymphoid tissue and that these cells suppress experimental allergic encephalomyelitis (EAE). These regulatory T cells produce transforming growth factor-beta (TGF-beta) with various amounts of IL-4 and IL-10 and these TGF-beta-secreting T cells have been termed Th3 cells. T cells in lymphoid organs drained by mucosal sites secrete IL-4 as a primary T cell growth factor. In the present study, we examined the role of IL-4 on oral tolerance and in the generation of TGF-beta secreting cells. Treatment of (PLJ x SJL)F1 mice with intraperitoneal (i. p.) IL-4 and low-dose oral MBP (0.5 mg) given three times reduced the severity of EAE, whereas i.p. injection of IL-4 alone or oral MBP alone given in these suboptimal doses, showed no protection. Spleen cells from protected mice produced increased amounts of TGF-beta and reduced IFN-gamma upon stimulation with MBP in vitro. Mucosal MBP-specific IgA production was significantly increased in IL-4 plus MBP fed animals. Moreover, oral administration of IL-4 (1 microg per feeding) also enhanced the suppression of EAE by oral MBP and this protective effect was reversed by administration of anti-TGF-beta antibody in vivo. Reverse transcription-PCR showed enhanced suppression of IFN-gamma in Peyer's patch in animals fed MBP and IL-4 versus those fed MBP alone. We then investigated the role of IL-4 in the generation of TGF-beta-secreting cells using MBP Ac1-11 TCR transgenic animals. Cells were cultured with IL-2, IL-4, or IFN-gamma in the presence of MBP and limiting dilution analysis for cytokine-secreting cells performed. We found that IL-4, but not IL-2 or IFN-gamma, generated TGF-beta-secreting T cells from naive splenic T cells and that these cells provided help for IgA production. These findings demonstrate that IL-4 is a differentiation factor for TGF-beta-secreting Th3 cells and oral IL-4 has a synergistic effect on low-dose oral tolerance that is associated with increased TGF-beta secretion.
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PMID:IL-4 is a differentiation factor for transforming growth factor-beta secreting Th3 cells and oral administration of IL-4 enhances oral tolerance in experimental allergic encephalomyelitis. 975 65

Localization of eosinophil granule major basic protein by immunofluorescence permits recognition of both eosinophil infiltration and degranulation. Over the past decade and a half, our laboratory has shown that eosinophil infiltration and degranulation occur in many diseased tissues in humans; among normal tissues studied as controls, only the gut showed striking eosinophil infiltration and degranulation. Using an indirect immunofluorescence procedure for the detection of major basic protein, we extended our analyses of normal human tissues to include tissues from essentially all body organs; a total of 117 biopsy/autopsy specimens were analyzed. To determine whether the method of tissue procurement affected the level of eosinophil degranulation in the normal gastrointestinal tract, normal proximal jejunum from six patients was biopsied using either an endoscopic forceps or a scalpel at the time of elective surgery and examined by immunofluorescence. Spleen, lymph node, and thymus tissues showed eosinophil infiltration with scant evidence of degranulation, but the only organ showing both eosinophil infiltration and remarkable degranulation was the gastrointestinal tract. Eosinophil degranulation was significantly increased in specimens obtained by endoscopic forceps compared to those obtained by scalpel (P = 0.021). These results indicate that tissue procurement methods affect the degree of eosinophil degranulation in the gut. Thus, among normal human body organs, both eosinophil infiltration and appreciable degranulation consistently occur only in the gut.
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PMID:Eosinophil infiltration and degranulation in normal human tissue. 981 Dec 20


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