Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A live, avirulent strain of Salmonella typhimurium, SL3235, was previously shown to afford protection against virulent Salmonella challenge in three mouse strains of the C3H lineage, C3H/HeJ, C3HeB/FeJ, and C3H/HeNCrlBR, which differ in their innate susceptibility to Salmonella infection, as well as in their responsiveness to lipopolysaccharide (LPS). Concurrent with protection, however, SL3235 was found to induce greater than 90% reduction in proliferative responses of splenocytes from immunized mice to a panel of B and T cell mitogens. Suppression appeared to be independent of susceptibility to Salmonella infection, since the mitogenic responses of hypersusceptible C3H/HeJ and C3HeB/FeJ, as well as resistant C3H/HeNCrlBR mice, were suppressed. The suppressor cell population in immunized C3HeB/FeJ mice was recently shown to be of monocytic lineage. Using transwell plates, co-culture studies indicated that suppression was mediated by soluble factors. In the present study, the effect of LPS responsiveness on susceptibility to SL3235-induced suppression was evaluated in C3H mice by studying their ability to mount plaque-forming cell (PFC) responses to sheep red blood cells (SRBC) and in vivo antibody responses to tetanus toxoid. Comparison of PFC responses as a function of SL3235 dose in C3HeB/FeJ and C3H/HeJ mice, revealed that the latter strain was markedly more resistant to the development of suppression, as evidenced by the significantly higher (10-35-fold) SL3235 doses needed to achieve comparable suppression to those seen in C3HeB/FeJ mice. In contrast to C3HeB/FeJ mice, suppression in C3H/HeJ mice required direct cell-cell contact. In both mouse strains, suppression was alleviated by pre-treatment of immune splenocytes with either mitomycin C or x-irradiation, indicating that actively proliferating cells are required for suppressor function. Resistance of C3H/HeJ mice to SL3235-induced suppression was not due to a lesser bacterial load in vivo, since a higher number of SL3235 organisms were seen in C3H/HeJ spleens compared to C3HeB/FeJ mice. Rather, resistance of C3H/HeJ mice correlated with their reduced ability to recruit macrophages and other inflammatory cells into the spleen, as evidenced by the significantly smaller degree of splenomegaly induced in these mice following immunization with SL3235.
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PMID:Immunosuppression induced by attenuated Salmonella: effect of LPS responsiveness on development of suppression. 163 Feb 97

32 cases (21 acute severe malaria and 11 chronic malaria syndrome), who developed unusual complications and/or manifestations are reported. The acute manifestations were unexplained tachypnoea 4, pulmonary oedema 5 and shock due to multiple organ dysfunction syndrome 3, melena 2 and E coli septicaemia in one. The other features were concomitant salmonellosis 2, meningitis 1, renal failure 3, hepatorenal syndrome 2, hepatitis like illness 7, neck stiffness with normal CSF 3, urticaria and subconiunctival haemorrhage 2 each, apyrexial spell with anaemia 4, thromocytopenia 3, and hypoglycaemia 3 (two pretreatment and one while on quinine in 5% glucose drip). The chronic syndrome noted were hyperreactive malaria syndrome (Tropical splenomegaly) 3, repeated haemolysis 2, chronic simple malaria with positive parasitaemia and normal Igm levels 4, and cerebellar ataxia with tremors 3. Bone marrow in these cases was hypercullular with increase plasma cells. Liver biopsy revealed lymphocytic infiltration. There was no case with permanent neurogical deficit. All patients with pulmonary oedema and multiple organ dysfunction died but chronic syndrome patients recovered fully. Early recoginition of atypical manifestation and prompt treatment will decrease the mortality and morbidity due to malaria.
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PMID:Unusual acute and chronic complications of malaria. 928 1

Our laboratory has previously shown that after immunization with a strain of Salmonella typhimurium, SL3235, made avirulent by a blockage in the pathway of aromatic synthesis, murine splenocytes were profoundly suppressed in their capacity to mount an in vitro antibody plaque-forming cell (PFC) response to sheep erythrocytes. Evidence indicated that suppression was mediated by nitric oxide (NO), since the in vitro addition of NG-monomethyl-L-arginine blocked suppression. The present studies examined the effect of blocking NO production on Salmonella-induced immunosuppression by in vivo administration of aminoguanidine hemisulfate (AG). AG was administered to C3HeB/FeJ mice in their drinking water (2.5% solution) for 7 days prior to intraperitoneal inoculation with SL3235. AG treatment inhibited the increase in nitrate and nitrite levels in plasma and nitrite levels in the spleen seen in immunized mice. Importantly, AG treatment completely blocked suppression of the splenic PFC response and markedly attenuated the suppression of the response to concanavalin A in immunized mice, providing further evidence that Salmonella-induced immunosuppression is mediated by NO. AG treatment also alleviated the majority of the splenomegaly associated with SL3235 inoculation, which correlated with a blockage of influx of neutrophils and macrophages into spleens, as assessed by flow cytometry. AG treatment unexpectedly resulted in 90% mortality in mice injected with the highly attenuated vaccine strain of Salmonella, SL3235. Increased mortality in AG-treated mice correlated with inability to clear organisms from the spleen by day 15 postinoculation and with persistent bacteremia, compared with control mice. Collectively, these in vivo results underscore the dual biological consequences of NO production following Salmonella infection, with NO being necessary for host defense, but also having the potentially adverse effect of immunosuppression. A unifying hypothesis to explain how these seemingly paradoxical effects could both result from NO production is presented.
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PMID:In vivo blockage of nitric oxide with aminoguanidine inhibits immunosuppression induced by an attenuated strain of Salmonella typhimurium, potentiates Salmonella infection, and inhibits macrophage and polymorphonuclear leukocyte influx into the spleen. 991 5

Lymphocyte trafficking in the gastrointestinal tract is primarily mediated by interactions with the mucosal addressin cell adhesion molecule 1 and its lymphocyte ligand, alpha(4)beta(7), and partly by L-selectin (L-Sel) interactions with peripheral node addressin coexpressed on some mucosal addressin cell adhesion molecule 1. We inquired whether intestinal responses in mice lacking L-Sel would be enhanced. L-Sel-deficient (L-Sel(-/-)) mice were orally immunized with either Salmonella vaccine vector or Salmonella vector-expressing colonization factor Ag I (CFA/I) from enterotoxigenic Escherichia coli. In L-Sel(-/-) mice, mucosal IgA anti-CFA/I fimbrial responses were greatly reduced, and systemic IgG2a anti-CFA/I fimbrial responses were 26-fold greater compared with C57BL/6 (L-Sel(+/+)) mice. L-Sel(-/-) Peyer's patch (PP) CD4(+) Th cells revealed IFN-gamma-dominated responses and an unprecedented absence of IL-4, whereas the expected mixed Th cell phenotype developed in L-Sel(+/+) mice. PP CD4(+) Th cell anti-Salmonella responses were nearly nonexistent in L-Sel(-/-) mice immunized with either Salmonella vaccine. Splenic CD4(+) Th cell anti-Salmonella responses were reduced but did show cytokine production in Ag restimulation assays. Increased colonization of PP and spleen was noted only with the Salmonella vector in L-Sel(-/-) mice, resulting in increased splenomegaly, suggesting that the Salmonella-CFA/I vaccine was not as infectious or that the presence of the fimbriae improved clearance, possibly because of reduced neutrophil recruitment. However, sufficient anti-Salmonella immunity was induced, because Salmonella vector-immunized L-Sel(-/-) mice showed complete protection against wild-type Salmonella challenge, unlike L-Sel(+/+) mice. This evidence shows that L-Sel is important for development of mucosal immunity, and absence of L-Sel is protective against salmonellosis.
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PMID:Impaired mucosal immunity in L-selectin-deficient mice orally immunized with a Salmonella vaccine vector. 1141 77

Septicemic salmonellosis caused by Salmonella Typhimurium 4, 12: i:1, 2 was diagnosed in 94 (64.8%) of 145 small passerines comprising nine species, examined in Norway during 1999-2000. The birds were found dead at private feeding places throughout the country. The bullfinch (Pyrrhula pyrrhula), Eurasian siskin (Carduelis spinus), common redpoll (Carduelis flammea), and Eurasian greenfinch (Carduelis chloris) were the most frequently affected species. Pathologic findings in 94 carcasses included poor body condition (84%), enlarged spleen (73%), and necrosis of crop/esophagus (78%), liver (53%), spleen (46%), proventriculus (13%), and intestine (5.3%). Histologically, necrosis consisted of debris, fibrin, inflammatory cells, and aggregates of Gram-negative bacteria and occasionally giant cells. Based on information from questionnaires sick and dead birds were observed at feeding places from December to June, with a distinct peak during February and March. The duration of recorded outbreaks varied from less than 1 wk to 4 mo. In a separate study, 1,990 apparently healthy passerines caught at feeding places established for bird-ringing purposes were surveyed for cloacal carriage of Salmonella spp. Forty (2.0%) of the birds examined, representing sampling sites both in southern and northern parts of the country, harbored S. Typhimurium 4, 12: i:1, 2 in their intestines. The carrier species largely reflected the species most often suffering from fatal infection.
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PMID:Epidemiologic and pathologic aspects of Salmonella typhimurium infection in passerine birds in Norway. 1268 69

Inducible costimulator (ICOS) is expressed on activated T cells and plays a key role in sustaining and enhancing the effector function of CD4 T cells. Given the function of this molecule in sustaining T-cell responses, we reasoned that ICOS might play an important role in a prolonged infection model, such as Salmonella infection of mice. To test this hypothesis, wild-type (WT) and ICOS-deficient (ICOS-/-) mice were infected systemically with a Salmonella enterica serovar Typhimurium strain expressing the chicken ovalbumin gene (Salmonella-OVA). ICOS-/- mice exhibited greater splenomegaly than WT mice and showed delayed bacterial clearance. The acquired immune response in this model was slow to develop. Maximal T-cell responses to Salmonella-OVA were detected at 3 weeks postinfection in both WT and ICOS-/- mice. CD4 T-cell-dependent gamma interferon production and a class switch to immunoglobulin G2a were severely reduced in ICOS-/- mice. ICOS-/- mice also exhibited a substantial defect in antigen-specific CD8 T-cell responses. In vitro, the effect of anti-ICOS on CD8 T-cell division was greater when CD8 T cells rather than CD4 T cells expressed ICOS, suggesting that the in vivo effects of ICOS on CD8 T cells could be direct. Taken together, these studies show that ICOS plays a critical role in control of Salmonella infection in mice, with effects on antibody, Th1, and CD8 T-cell responses.
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PMID:Role for inducible costimulator in control of Salmonella enterica serovar Typhimurium infection in mice. 1642 52

The present study characterizes immune cell populations in mice chronically infected with Salmonella. Mice were characterized as chronically infected based on persistently high titers of Salmonella-reactive immunoglobulins in the serum >6 months after a single oral dose of S. enterica serovar Typhimurium. These mice had a visibly enlarged spleen but not liver, while both organs harbored bacteria and had increased total cellularity up to 11 months post-infection. Flow cytometry analysis revealed significantly elevated numbers of neutrophils, dendritic cells (DC) and macrophages in the spleen of chronically infected mice. In contrast, no significant increase in the absolute number of T and B cells was apparent in the spleen and DX5+ cells, which includes NK cells, some NK T cells and possibly some activated T cells, appears to correlate with chronic Salmonella infection in the liver but not the spleen. In situ analyses revealed that CD8alpha+ DC and Gr-1+ cells (neutrophils) increased in the splenic red pulp of chronically infected mice. In addition, Gr-1+ cells, CD68+ cells and CD11c+ cells (DC), the latter lacking detectable staining for CD8alpha and CD4, accumulated around hepatic blood vessels and in the hepatic network in the liver of mice chronically harboring bacteria. These data provide insight into changes that occur within immune cell populations, most notably within splenic and hepatic phagocytic cell populations, that accompany chronic infection with the intracellular bacterium Salmonella.
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PMID:Elevated neutrophil, macrophage and dendritic cell numbers characterize immune cell populations in mice chronically infected with Salmonella. 1678

We report the case of a 35 year patient from Nigeria who presented with fever and splenomegaly. The initial diagnosis was Salmonellosis. However, relapsing symptoms lead to a re-evaluation and ultimately a diagnosis of Multicentric Castleman's Disease (MCD). There is no gold standard treatment but our patient responded to Rituximab and Highly active anti-retroviral therapy. MCD is a rare, aggressive disease that should be considered in a HIV positive patient presenting with fever and significant lymphadenopathy.
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PMID:Multicentric Castleman's disease & HIV infection. 1990 50

Systemic Salmonella infection commonly induces prolonged splenomegaly in murine or human hosts. Although this increase in splenic cellularity is often assumed to be due to the recruitment and expansion of leukocytes, the actual cause of splenomegaly remains unclear. We monitored spleen cell populations during Salmonella infection and found that the most prominent increase is found in the erythroid compartment. At the peak of infection, the majority of spleen cells are immature CD71(-)Ter119(+) reticulocytes, indicating that massive erythropoiesis occurs in response to Salmonella infection. Indeed, this increase in RBC precursors corresponded with marked elevation of serum erythropoietin (EPO). Furthermore, the increase in RBC precursors and EPO production required innate immune signaling mediated by Myd88/TRIF. Neutralization of EPO substantially reduced the immature RBC population in the spleen and allowed a modest increase in host control of infection. These data indicate that early innate immunity to Salmonella initiates marked splenic erythropoiesis and may hinder bacterial clearance.
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PMID:Innate immune activation during Salmonella infection initiates extramedullary erythropoiesis and splenomegaly. 2095 75

We investigated two mortality events in wintering and migrating Song Thrushes (Turdus philomelos) in Catalonia, northeastern Spain in 2009 and 2010. Both episodes occurred in late February to mid-March during the spring migration. Salmonellosis produced by the serotype Salmonella enterica subsp. enterica serotype Hessarek (S. Hessarek) was identified as the cause of death in both episodes. Poor body condition, marked splenomegaly, and microscopic disseminated intravascular coagulation with numerous intravascular and tissular bacteria were the most consistent findings. Macro-restriction profiling by pulsed-field gel electrophoresis (PFGE) using XbaI was performed for epidemiologic typing of the S. Hessarek isolates. Two clusters were discernible, that are possibly related, with a similarity of 82.8%. Analysis comparing pectoral muscle and subcutaneous fat scores from the Song Thrushes that died from S. Hessarek with those from healthy Song Thrushes from nearby areas during 2009 and 2010 suggest that poor body condition was associated with the S. Hessarek infection.
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PMID:Septicemic salmonellosis caused by Salmonella Hessarek in wintering and migrating Song Thrushes (Turdus philomelos) in Spain. 2224 79


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