The Journal of Infectious Diseases

Publisher: Memorial Institute for Infectious Diseases (Chicago, Ill.); John McCormick Institute for Infectious Diseases; John Rockefeller McCormick Memorial Fund; Infectious Diseases Society of America

Description

  • Impact factor
    5.85
  • 5-year impact
    5.91
  • Cited half-life
    8.00
  • Immediacy index
    1.56
  • Eigenfactor
    0.10
  • Article influence
    2.15
  • Other titles
    Journal of infectious diseases (Online), The journal of infectious diseases (Online. University of Chicago Press), JID
  • ISSN
    1537-6613
  • OCLC
    41275996
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The discovery of obligatory intracellular bacteria of the genus Wolbachia in filariae infecting humans led to the use of antibiotics as a potent treatment option. Mansonella perstans is the cause of the second most prevalent filariasis in Gabon, but so far reports on the presence of Wolbachia in this nematode have been inconsistent. We report on the presence of Wolbachia in M. perstans in patients from Gabon, which we identified using PCR with primer sets specific for 16S rDNA and ftsZ. Sequence analysis revealed a single consensus sequence, which could be phylogenetically assigned to Wolbachia of the supergroup F. Wolbachia could only be identified in 5 out of 14 and 7 out of 14 cases, depending on the investigated gene; detection of Wolbachia was associated with higher filaremia. Before generalizing the use of antibiotics for mansonellosis, further clarification of the obligatory nature of the endosymbiosis in this nematode is needed.
    The Journal of Infectious Diseases 06/2014;
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    ABSTRACT: Ingestion of B. anthracis spores causes gastrointestinal (GI) anthrax. Humoral immune responses, in particular, IgA secreting B-1 cells, play a critical role in the clearance of GI pathogens. Here, we investigated whether B. anthracis impacts the function of colonic B-1 cells to establish active infection. GI anthrax infection led to significant inhibition of immunoglobulins (e.g., IgA) and increased program death-1 (PD-1) on B-1 cells. Furthermore, infection also diminished type 2 innate lymphoid cells (ILC2) and their ability to enhance differentiation and immunoglobulin production by secreting IL-5. Such B-1 cell and ILC2 dysfunction is potentially due to cleavage of p38 and Erk1/2 MAPK in these cells. Conversely, mice that survived infection generated neutralizing antibodies via the formation of robust germinal center B cells in Peyer's patches and had restored B-1 and ILC2 function. These data may provide additional insight for designing efficacious vaccines and therapeutics against such a deadly pathogen.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: The development of drugs and vaccines to reduce malaria transmission is an important part of eradication plans. The transmission reducing activity (TRA) of these agents is currently determined in the standard membrane feeding assay (SMFA) based on subjective microscopical read-outs and with limitations in up-scaling and throughput. Utilising a Plasmodium falciparum strain expressing the firefly luciferase protein, we present a luminescence based approach to SMFA evaluation that eliminates the requirement for mosquito dissections in favour of a simple approach where whole mosquitoes are homogenised and examined directly for luciferase activity. Analysis of 6860 Anopheles stephensi mosquitoes across 68 experimental feeds shows that the luminescence assay was as sensitive as microscopy for infection detection. The mean luminescence intensity of individual and pooled mosquitoes accurately quantifies mean oocyst intensity and generates comparable TRA estimates. The luminescence assay presented here could increase SMFA throughput so that 10-30 experimental feeds could be evaluated in a single 96-well plate. This new method of assessing Plasmodium infection and transmission intensity could expedite the screening of novel drug compounds, vaccine candidates and sera from malaria exposed individuals for TRA. Luminescence-based estimates of oocyst intensity in individual mosquitoes should be interpreted with caution.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: Streptococcus (S.) pneumoniae is the most common causative pathogen in community-acquired pneumonia. Mast cells are mainly located at the host-environment interface where they function as sentinels. To study the role of mast cells during pneumonia caused by S.pneumoniae. Lung tissue of patients who had died from pneumococcal pneumonia or a non-pulmonary cause was stained for mast cells and tryptase. Wild type (WT) and mast cell deficient (Kit(W-sh/W-sh)) mice were observed or sacrificed after induction of pneumonia by intranasal inoculation of S.pneumoniae. In separate experiments WT mice were treated with mast cell stabilizing agents doxantrazole or cromoglycate. The constitutive presence of tryptase positive mast cells was reduced in affected lungs from pneumonia patients. Kit(W-sh/W-sh) mice showed a prolonged survival during the first days after LD100 and LD50 infection, while overall mortality did not differ from that in WT mice. Relative to WT mice, Kit(W-sh/W-sh) mice showed reduced bacterial counts with less bacterial dissemination to distant organs and less inflammation. Neither doxantrazole nor cromoglycate influenced antibacterial defense or inflammatory responses after airway infection with S.pneumoniae. Mast cells exhibit an unfavorable role in host defense during pneumococcal pneumonia by a mechanism independent of degranulation.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: Campylobacter jejuni is a leading cause of bacterial gastroenteritis worldwide. At present the identity of host-pathogen interactions that promote successful bacterial colonisation remain ill defined. Herein, we aimed to investigate C. jejuni-mediated effects on dendritic cell (DC) immunity. We found C. jejuni to be a potent inducer of human and murine DC IL-10 in vitro, a cellular event that was MyD88- and p38 MAPK-signalling dependent. Utilising a series of C. jejuni isogenic mutants we found the major flagellin protein, FlaA, modulated IL-10 expression, an intriguing observation as C. jejuni FlaA is not a TLR5 agonist. Further analysis revealed pseudaminic acid residues on the flagella contributed to DC IL-10 expression. We identified the ability of both viable C. jejuni and purified flagellum to bind to Siglec-10, an immune-modulatory receptor. In vitro infection of Siglec-10 over-expressing cells resulted in increased IL-10 expression in a p38-dependent manner. Detection of Siglec-10 on intestinal CD11c+ CD103+ DCs added further credence to the notion that this novel interaction may contribute to immune outcome during human infection. We propose that unlike the S. Typhimurium flagella-TLR5 driven pro-inflammatory axis, C. jejuni flagella instead promote an anti-inflammatory axis via glycan-Siglec-10 engagement.
    The Journal of Infectious Diseases 05/2014;
  • The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: It is well established that immunization with attenuated malaria sporozoites induces CD8+ T cells that eliminate parasite-infected hepatocytes. Liver memory CD8+ T cells induced by immunization with parasites undergo a unique differentiation program and have enhanced expression of CXCR6. Following immunization with malaria parasites, CXCR6-deficient memory CD8+ T cells recovered from the liver display altered cell-surface expression markers compared to their wild type counterparts but they exhibit normal cytokine secretion and expression of cytotoxic mediators on a per-cell basis. Most importantly, CXCR6-deficient CD8+ T cells migrate to the liver normally after immunization with malaria sporozoites or vaccinia virus, but few weeks later their numbers severely decrease in this organ, losing their capacity to inhibit malaria parasite development in the liver. These studies show for the first time that CXCR6 is critical for the development and maintenance of protective memory CD8+ T cells in the liver.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: The Phase III Zostavax Efficacy and Safety Trial of 1 dose of licensed zoster vaccine (ZV) (Zostavax; Merck) in 50-59 year-olds showed approximately 70% vaccine efficacy (VE) to reduce the incidence of herpes zoster (HZ). An objective of the trial was to assess immune response biomarkers measuring antibodies to varicella zoster virus (VZV) [by glycoprotein enzyme-linked immunosorbent assay] as correlates of protection (CoPs) against HZ. The principal stratification 'vaccine efficacy curve' framework for statistically evaluating immune response biomarkers as CoPs was applied. The VE curve describes how VE against the clinical endpoint (HZ) varies across participant subgroups defined by biomarker readout measuring vaccine-induced immune response. The VE curve was estimated using several subgroup definitions. The fold rise in VZV antibody titers from pre-immunization to 6 weeks was an excellent CoP, with VE increasing sharply with fold rise [VE estimated at 0% for the subgroup with no rise and at 90% for the subgroup with 5.26-fold rise]. In contrast, VZV antibody titers measured 6 weeks after immunization did not predict VE, with similar estimated VE across titer subgroups. The analysis illustrates the value of the VE curve framework for assessing immune response biomarkers as CoPs in vaccine efficacy trials.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: Background. Neurological pathogenesis is associated with mitochondrial dysfunction and differences in neuronal/glial handling of oxygen and glucose. The main side effects attributed to Efavirenz involve the CNS, but the underlying mechanisms are unclear.Methods. Human cell lines and rat primary cultures of neurons and astrocytes were treated with clinically relevant Efavirenz concentration.Results. Efavirenz alters mitochondrial respiration, enhances reactive oxygen species generation, undermines mitochondrial membrane potential and reduces ATP levels in a concentration-dependent fashion in both neurons and glia. However, it triggers AMP-activated protein kinase only in glia, up-regulating glycolysis and increasing intracellular ATP that does not occur in neurons. To reproduce the conditions that often exist in HIV-related neuroinflammatory disorders, the effects of Efavirenz were evaluated in the presence of exogenous nitric oxide, an inflammatory mediator and mitochondrial inhibitor. The combination potentiated the effects on mitochondrial parameters in both neurons and glia, but ATP generation and lactate production were enhanced only in glia.Conclusions. Efavirenz affects the bioenergetics of neurons through a mechanism involving acute mitochondrial inhibition, an action exacerbated in neuroinflammatory conditions. A similar scenario of glia survival and degeneration of neurons with signs of mitochondrial dysfunction and oxidative stress has been associated with neurocognitive disorders.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: Background. Soluble biomarkers of inflammation predict non-AIDS related morbidity and mortality among HIV-infected persons. Exploring associations between plasma biomarkers and cellular phenotypes may identify sources of excess inflammation.Methods. Plasma biomarkers (IL-6, D-dimer, hsCRP, sCD14, sCD163) were measured from cryopreserved samples from the Study to Understand the Natural History of HIV/AIDS in the Era of Effective Therapy (SUN Study). We performed immunophenotyping of peripheral blood mononuclear cells for markers of T-cell and monocyte activation, maturation, and migration. We evaluated associations between cellular phenotypes and soluble biomarkers by Spearman rank correlation and multivariate linear regression.Results. Participants' (n=670) median age was 41 years, 88% were prescribed ART, 72% with plasma HIV RNA <400 copies/mL; median CD4+ T-lymphocyte count was 471 cells/μL. After adjustment, CD14(++)CD16(+) monocytes associated with higher levels of IL-6, hsCRP and sCD163; associations with IL-6 and CRP persisted in persons with suppressed HIV viral replication. While CCR5(+) monocytes positively associated with D-dimer levels, CCR2(+) monocytes were inversely associated with hsCRP.Conclusions. Plasma inflammatory biomarkers that predict morbidity and mortality were strongly associated with monocyte activation and migration, modestly with T-cell maturation, and not with CD8 T-cell activation phenotypes. These findings suggest strategies to control monocyte activation warrant further investigation.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: Plague is transmitted by fleas or contaminated aerosols. To successfully produce disease, the causal agent (Yersinia pestis) must rapidly sense and respond to rapid variations in its environment. Here, we investigated the role of two-component regulatory systems (2CSs) in plague because the latter are known to be key players in bacterial adaptation to environmental change. Along with the previously studied PhoP-PhoQ system, OmpR-EnvZ was the only one of Y. pestis' 23 other 2CSs required for production of bubonic, septicemic and pneumonic plague. In vitro, OmpR-EnvZ was needed to counter serum complement and leukocytes but was not required for the secretion of antiphagocyte exotoxins. In vivo, Y. pestis lacking OmpR-EnvZ did not induce an early immune response in the skin and was fully virulent in neutropenic mice. We conclude that throughout the course of Y. pestis infection, OmpR-EnvZ is required to counter toxic effectors secreted by polymorphonuclear leukocytes in the tissues.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: The mechanisms underlying trophoblasts immune defense against pathogens remain ill defined. We demonstrated that placental cell death was increased upon in vivo exposure to Listeria monocytogenes. The death of infected cells is an important host innate defense mechanism. Meanwhile, double-stranded DNA derived from intracellular bacteria or dsDNA viruses is emerging as a potent PAMP to host cells. We sought to characterize trophoblast cell death in response to cytosolic dsDNA challenge. Our results showed that dsDNA induced caspase-dependent and -independent cell death in human trophoblasts. However, necroptosis, a cell death pathway independent of caspase, couldn't be induced by dsDNA treatment, even in the presence of exogenously expressed RIPK3. L. monocytogenes-derived genomic DNA triggered a similar cell death. Moreover, the cell death in response to dsDNA was IFI16-dependent. These data suggest that cytosolic dsDNA induces non-necroptotic cell death in trophoblasts via IFI16, and this could contribute to placental barrier against infection.
    The Journal of Infectious Diseases 05/2014;
  • The Journal of Infectious Diseases 05/2014;
  • The Journal of Infectious Diseases 05/2014;
  • The Journal of Infectious Diseases 05/2014;
  • The Journal of Infectious Diseases 05/2014;

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