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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathogenic Yersinia have a pronounced tropism for lymphatic tissues and harbor a virulence plasmid that encodes a type III secretion system, pTTSS, that transports Yops into host cells. Yops are critical virulence factors that prevent phagocytosis by macrophages and neutrophils and Yersinia mutants lacking one or more Yops are defective for survival in lymphatic tissues, liver, and gastrointestinal tract. However, here we demonstrate that Y. pseudotuberculosis (Yptb) mutants lacking the pTTSS survived as well as or better than wild-type (WT) Yptb in the mesenteric lymph nodes (MLN). Infection with pTTSS mutants caused lymphadenitis with little necrosis, whereas infection with WT Yptb provoked lymphadenitis with multiple necrotic suppurative foci. Gentamicin protection assays and microscopic examination of the MLN revealed that pTTSS mutants resided extracellularly adjacent to B and T lymphocytes in the cortex and paracortex. WT Yptb was found extracellularly adjacent to neutrophils and macrophages in necrotic areas and adjacent to B and T lymphocytes in less-inflamed areas. To determine whether lymphocytes protected pTTSS mutants from phagocytic cells, Rag1(-/-) mice were infected with pTTSS mutants or WT Yptb. pTTSS mutants but not WT, were impaired for survival in MLN of Rag1(-/-) mice, suggesting that lymphocyte-rich regions constitute a protective niche for pTTSS mutants. Finally, we show that invasin and the chromosomally encoded TTSS were not required for Yptb survival in MLN. In summary, chromosomally encoded factors are sufficient for Yptb replication in the cortex and paracortex of MLN; the pTTSS enables Yersinia to survive within phagocyte-rich areas of lymph nodes, and spread to other tissues.
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PMID:Yersinia has a tropism for B and T cell zones of lymph nodes that is independent of the type III secretion system. 1694 31

Yersinia enterocolitica (Ye) targets mouse dendritic cells (DCs) and inhibits their ability to trigger T cell activation. Here we have investigated whether Ye might interfere with antigen presentation in DCs. Infection of DCs with the Ye wild-type strain reduced OVA uptake by DCs as demonstrated by flow cytometry and confocal laser scan microscopy. In contrast, DCs infected with Yersinia outer protein P (YopP)-deficient mutant strain rapidly internalized OVA. Furthermore, transfection of DCs with YopP, but not with a cysteine protease deficient YopP-C172A mutant, reduced uptake of OVA. This finding suggests that YopP, a virulence factor of Ye, inhibits OVA uptake by DCs. By the use of MAPK inhibitors we provide evidence that YopP mediates reduction of OVA uptake by its ability to block MAPK signalling pathways in host cells. Using transferrin (Tf) as specific marker for clathrin-mediated endocytosis (CME) and lucifer yellow (LY) as specific marker for macropinocytosis (MP) we could show that YopP inhibits CME, whereas other Yops inhibit MP. In keeping with these data, activation and proliferation of OVA-specific T cells was reduced when DCs were treated with MAPK inhibitors. Together, our data demonstrate that (i) MAPK play an important role in antigen uptake by CME in DCs, and (ii) that YopP inhibits this pathway of antigen uptake in DCs, which might contribute to evasion of adaptive immunity.
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PMID:Yersinia enterocolitica YopP inhibits MAP kinase-mediated antigen uptake in dendritic cells. 1695 1

Live attenuated Shigella vaccines elicit protective immune responses, but involve a potential risk of inducing a strong inflammatory reaction. The bacterial invasiveness that is crucial for Ag delivery causes inflammatory destruction of infected epithelial cells and proinflammatory cell death of infected macrophages. In this study, the noninvasive Shigella mutant DeltaipaB was equipped with Yersinia invasin protein, which has been shown to mediate bacterial invasion and targeting to M cells located in follicle-associated epithelium. Invasin-expressing DeltaipaB (DeltaipaB/inv) was internalized into epithelial cells and retained in the intraphagosomal space. DeltaipaB/inv did not induce necrotic cell death of infected macrophages nor cause symptomatic damage after intranasal vaccination of mice. DeltaipaB/inv was safer and more effective than the conventional live vaccine, DeltavirG. Infection by DeltaipaB/inv caused polymorphonuclear neutrophil infiltration in the lung, but did not induce production of large amounts of proinflammatory cytokines. We concluded that the low experimental morbidity and high vaccine efficacy of DeltaipaB/inv are primarily based on high protective immune responses, which may be enhanced by the polymorphonuclear neutrophil infiltration unaccompanied by tissue injury.
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PMID:High vaccine efficacy against shigellosis of recombinant noninvasive Shigella mutant that expresses Yersinia invasin. 1698 10

Yersinia pestis has been found in human body lice during plague outbreaks. To evaluate the role that the human body louse plays as a vector of plague, we allowed lice to feed on rabbits made bacteremic by intravenous inoculation of 10(9) colony-forming units of 3 strains of Y. pestis. High mortality rates were observed in all lice 2 and 3 days after infection. The lice remained infected with the strains for their life span and excreted viable organisms in their feces from day 1, although they were unable to lay eggs. The lice infected with 2 virulent strains of Y. pestis transmitted the organisms during feeding to uninfected rabbits, which became septicemic and died of plague (with 1 exception) 1 day later. Infections were transmitted to naive lice that were fed on these rabbits, showing that lice can be vectors of Y. pestis in an experimental model.
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PMID:Experimental model to evaluate the human body louse as a vector of plague. 1708 45

Previous epidemiological studies have demonstrated a potential link between the serotypes of Yersinia enterocolitica recovered from cattle, sheep and pigs and those isolated from human disease cases. Further studies utilizing amplified fragment length polymorphisms have shown a relationship at the genetic level between strains of biotypes 3 and 4 from humans and livestock, and also suggested that some biotype 1A isolates, classically defined as non-pathogenic, are closely related to biotype 3 and 4 isolates. This study sought to understand further the pathogenic potential of Y. enterocolitica isolates from livestock in Great Britain. A range of surrogate in vitro models, such as invasion of epithelial tissue cultures, survival in cultured macrophages and cytokine secretion response, was employed to assess the pathogenicity of 88 strains. The results suggested that all isolates examined were capable of adhering to and invading epithelial cells and of surviving within macrophages. However, the inflammatory response of the infected macrophages differed with the infecting Y. enterocolitica subtype, with the response to pathogenic biotype 3 and 4 isolates different to that observed with biotype 1A isolates, and with the biotype 3 O : 5,27 isolates recovered exclusively from animals. Infections of porcine tissue also suggested the possibility of host-tissue tropism within Y. enterocolitica subtypes.
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PMID:Yersinia enterocolitica isolates of differing biotypes from humans and animals are adherent, invasive and persist in macrophages, but differ in cytokine secretion profiles in vitro. 1710 78

Bacteriological analysis of water that accumulates at the bottom of freezers in restaurants when the power was cut in Calabar, southeastern Nigeria, was carried out using standard procedures. Mean heterotrophic bacterial counts and Escherichia coli counts ranged from 3.1 +/- 0.02 to 7.1 +/- 0.30 x 10(4) cfu/ml and 0.2 +/- 0.10 to 0.6 +/- 0.50 x 10(4) cfu/ml, respectively, indicating heavy bacterial contamination whose source was mostly fecal. There was no significant difference (p > 0.05, 0.01) in bacterial counts between freezers. Some biochemically identified enteric bacterial pathogens were Salmonella typhi, Shigella sp, enteropathogenic E. coli, Yersinia sp, Klebsiella pneumoniae, Vibrio cholerae O1 and Vibrio parahaemolyticus. This reveals that the hygienic quality of the food items stored in the freezers and the hygienic status of the restaurants are in doubt. Infection could be going on unnoticed and thus endemicity maintained in the area. The pathogens showed alarming antibiotic resistance. The water in the freezers was a "soup" in which different species of the enteric pathogens were close to each other and could transfer drug resistance among themselves. Public health education of restaurant operators in southeastern Nigeria is recommended.
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PMID:Incidence of enteric bacterial pathogens in water found at the bottom of commercial freezers in calabar, southeastern Nigeria. 1712 5

The detailed composition and structure of the Caenorhabditis elegans surface are unknown. Previous genetic studies used antibody or lectin binding to identify srf genes that play roles in surface determination. Infection by Microbacterium nematophilum identified bus (bacterially unswollen) genes that also affect surface characteristics. We report that biofilms produced by Yersinia pestis and Y. pseudotuberculosis, which bind the C. elegans surface predominantly on the head, can be used to identify additional surface-determining genes. A screen for C. elegans mutants with a biofilm absent on the head (Bah) phenotype identified three novel genes: bah-1, bah-2, and bah-3. The bah-1 and bah-2 mutants have slightly fragile cuticles but are neither Srf nor Bus, suggesting that they are specific for surface components involved in biofilm attachment. A bah-3 mutant has normal cuticle integrity, but shows a stage-specific Srf phenotype. The screen produced alleles of five known surface genes: srf-2, srf-3, bus-4, bus-12, and bus-17. For the X-linked bus-17, a paternal effect was observed in biofilm assays.
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PMID:Caenorhabditis elegans mutants resistant to attachment of Yersinia biofilms. 1733 4

Foodborne illnesses are a substantial health burden in the United States. The Foodborne Diseases Active Surveillance Network (FoodNet) of CDC's Emerging Infections Program collects data from 10 U.S. states regarding diseases caused by enteric pathogens transmitted commonly through food. FoodNet quantifies and monitors the incidence of these infections by conducting active, population-based surveillance for laboratory-confirmed illnesses. This report describes preliminary surveillance data for 2006 and compares them with baseline data from the period 1996-1998. Incidence of infections caused by Campylobacter, Listeria, Shigella, and Yersinia has declined since the baseline period. Incidence of infections caused by Shiga toxin-producing Escherichia coli O157 (STEC O157) and Salmonella, however, did not decrease significantly, and Vibrio infections have increased, indicating that further measures are needed to prevent foodborne illness and achieve national health objectives.
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PMID:Preliminary FoodNet data on the incidence of infection with pathogens transmitted commonly through food--10 states, 2006. 1743 79

Yersinia ruckeri is the causative agent of yersiniosis or enteric redmouth disease leading to significant economic losses in salmonid aquaculture worldwide. Infection may result in a septicaemic condition with haemorrhages on the body surface and in the internal organs. Despite the significance of the disease, very little information is available on the pathogenesis, hampering the development of preventive measures to efficiently combat this bacterial agent. This review discusses the agent and the disease it causes. The possibility of the presence of similar virulence markers and/or pathogenic mechanisms between the Yersinia species which elicit disease in humans and Y. ruckeri is also examined.
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PMID:Yersinia ruckeri infections in salmonid fish. 1750 36

Yersinia outer protein P (YopP) is injected by Y. enterocolitica into host cells thereby inducing apoptotic and necrosis-like cell death in dendritic cells (DC). Here we show the pathways involved in DC death caused by the catalytic activity of YopP. Infection with Yersinia enterocolitica, translocating catalytically active YopP into DC, triggered procaspase-8 cleavage and c-FLIPL degradation. YopP-dependent caspase-8 activation was, however, not mediated by tumor necrosis factor (TNF) receptor family members since the expression of both CD95/Fas/APO-1 and TRAIL-R2 on DC was low, and DC were resistant to apoptosis induced by agonistic anti-CD95 antibodies or TNF-related apoptosis-inducing ligand (TRAIL). Moreover, DC from TNF-Rp55-/- mice were not protected against YopP-induced cell death demonstrating that TNF-R1 is also not involved in this process. Activation of caspase-8 was further investigated by coimmunoprecitation of FADD from Yersinia-infected DC. We found that both cleaved caspase-8 and receptor interacting protein 1 (RIP1) were associated with the Fas-associated death domain (FADD) indicating the formation of an atypical death-inducing signaling complex (DISC). Furthermore, degradation of RIP mediated by the Hsp90 inhibitor geldanamycin significantly impaired YopP-induced cell death. Altogether our findings indicate that Yersinia-induced DC death is independent of death domain containing receptors, but mediated by RIP and caspase-8 at the level of DISC.
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PMID:Catalytically active Yersinia outer protein P induces cleavage of RIP and caspase-8 at the level of the DISC independently of death receptors in dendritic cells. 1762 95


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