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  • 1. Bereczky, Sándor
    et al.
    Liljander, Anne
    Rooth, Ingegerd
    Faraja, Lea
    Granath, Fredrik
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    Färnert, Anna
    Multiclonal asymptomatic Plasmodium falciparum infections predict a reduced risk of malaria disease in a Tanzanian population2007In: Microbes and infection, ISSN 1286-4579, E-ISSN 1769-714X, Vol. 9, no 1, p. 103-110Article in journal (Refereed)
    Abstract [en]

    Protective immunity to malaria is acquired after repeated exposure to the polymorphic Plasmodium falciparum parasite. Whether the number of concurrent antigenically diverse clones in asymptomatic infections predicts the risk of subsequent clinical malaria needs further understanding. We assessed the diversity of P. falciparum infections by merozoite surface protein 2 genotyping in a longitudinal population based study in Tanzania. The number of clones was highest in children 6–10 years and in individuals with long time to previous anti-malarial treatment. Individual exposure, analysed by circumsporozoite protein antibody levels, was associated with parasite prevalence but not with the number of clones. The risk of subsequent clinical malaria in children free of acute disease or recent treatment was, compared to one clone, reduced in individuals with multiclonal infections or without detectable parasites, with the lowest hazard ratio 0.28 (95% confidence interval 0.10–0.78 Cox regression) for 2–3 clones. The number of clones was not associated with haemoglobin levels. A reduced risk of malaria in asymptomatic individuals with multiclonal persistent P. falciparum infections suggests that controlled maintenance of diverse infections is important for clinical protection in continuously exposed individuals, and needs to be considered in the design and evaluation of new malaria control strategies.

  • 2.
    Berglund, Carolina
    et al.
    Örebro University, School of Health and Medical Sciences.
    Prévost, Gilles
    Laventie, Benoît-Joseph
    Keller, Daniel
    Söderquist, Bo
    Örebro University, School of Health and Medical Sciences.
    The genes for Panton Valentine leukocidin (PVL) are conserved in diverse lines of methicillin-resistant and methicillin-susceptible Staphylococcus aureus2008In: Microbes and infection, ISSN 1286-4579, E-ISSN 1769-714X, Vol. 10, no 8, p. 878-884Article in journal (Other academic)
    Abstract [en]

    Methicillin-resistant Staphylococcus aureus isolated in the community (CA-MRSA) have been reported to carry the loci for Panton Valentine leukocidin (PVL) in high frequency. CA-MRSA in Orebro County, Sweden, constitutes at least 50% of MRSA and the PVL locus is detected in as many as 66% of these CA-MRSA isolates. The aim of this study was to characterize PVL-positive methicillin-resistant and methicillin-susceptible Staphylococcus aureus by molecular methods, to determine the nucleotide sequence of lukS-PV and lukF-PV in S. aureus isolates of different origins, and to investigate the biological consequence of variations occurring in the genes. The PVL-positive MRSA investigated were composed of six different STs (ST8, 36, 80, 152, 154, and 256). Six additional STs (ST5, 22, 25, 30, 88, and 567) were detected when investigating PVL-positive methicillin-susceptible S. aureus with MLST. Despite the different genetic origins of the isolates analyzed, the PVL genes were well conserved and only one mutation was non-synonymous. Evaluation of the consequence of this mutation showed that the mutated toxin and wild-type toxin had comparable biological activity on human polymorphonuclear cells.

  • 3. Jangpatarapongsa, Kulachart
    et al.
    Sirichaisinthop, Jeeraphat
    Sattabongkot, Jetsumon
    Cui, Liwang
    Montgomery, Scott M.
    Örebro University, Department of Clinical Medicine.
    Looareesuwan, Sornchai
    Troye-Blomberg, Marita
    Udomsangpetch, Rachanee
    Memory T cells protect against Plasmodium vivax infection2006In: Microbes and infection, ISSN 1286-4579, E-ISSN 1769-714X, Vol. 8, no 3, p. 680-686Article in journal (Refereed)
    Abstract [en]

    Immunity induced by Plasmodium vivax infection leads to memory T cell recruitment activated during "relapse" or "re-infection". This study aims to characterise memory T cells in patients with acute or convalescent P. vivax infection. Lymphocytes were collected from patients infected by P. vivax, immune controls and naive controls. The proportion of immature memory T cells, expressing CD45RO(+)CD27(+), and mature cells lacking CD27 was assessed. A statistically significant increase in the median percentage of memory T cell subsets expressing CD4(+) was observed in material from patients with an acute infection compared with that from either naive or immune controls. The high percentage of memory T cells in infected patients was maintained until 60 days post treatment. The immune controls living in a malaria endemic area had a somewhat increased proportion of memory T cell subsets expressing CD8(+). An approximately three-fold increase of these cell types was shown in patients with an acute infection and the level persisted until 60 days post treatment. Phenotypic characterisation of the peripheral lymphocytes during acute infection revealed that a large fraction of the lymphocytes carried the gammadelta phenotypes suggesting a role for these cells in the early response against P. vivax. Very low levels of P. vivax specific antibody were found. This might suggest that cell-mediated immunity may play a greater role in the development of naturally acquired protection against P. vivax infection than humoral immunity. Our results provide further insight into the mechanism of cell-mediated immunity to P. vivax infection that could be important for the future development of a successful vaccine and anti-malarial drug designation.

  • 4.
    Persson, Alexander
    et al.
    Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Blomgran-Julinder, Robert
    Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Rahman, Sayma
    Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Zheng, Limin
    Department of Biochemistry, College of Life Sciences, Sun Yansen (Zhongshan) University, Guangzhou, People's Republic of China.
    Stendahl, Olle
    Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Mycobacterium tuberculosis-induced apoptotic neutrophils trigger a pro-inflammatory response in macrophages through release of heat shock protein 72, acting in synergy with the bacteria2008In: Microbes and infection, ISSN 1286-4579, E-ISSN 1769-714X, Vol. 10, no 3, p. 233-240Article in journal (Refereed)
    Abstract [en]

    Mycobacterium tuberculosis (Mtb) survive inside macrophages by manipulating microbicidal functions such as phago-lysosome fusion, production of reactive oxygen species and nitric oxide, and by rendering macrophages non-responsive to IFN-gamma. Mtb-infected lung tissue does however not only contain macrophages, but also significant numbers of infiltrating polymorphonuclear neutrophils (PMN). These are able to phagocytose and kill ingested Mtb, but are short-lived cells that constantly need to be removed from tissues to avoid tissue damage. Phagocytosis of aged or UV-induced apoptotic PMN by macrophages induce an anti-inflammatory response in macrophages. However, in the present study, we show that engulfment of Mtb-induced apoptotic PMN by macrophages initiates secretion of TNF-alpha from the macrophages, reflecting a pro-inflammatory response. Moreover, Mtb-induced apoptotic PMN up-regulate heat shock proteins 60 and 72 (Hsp60, Hsp72) intracellularly and also release Hsp72 extracellularly. We found that both recombinant Hsp72 and released Hsp72 enhanced the pro-inflammatory response to both Mtb-induced apoptotic PMN and Mtb. This stimulatory effect of the supernatant was abrogated by depleting the Hsp72 with immunoprecipitation. These findings indicate that released Hsp72 from Mtb-infected PMN can trigger macrophage activation during the early stage of Mtb infections, thereby creating a link between innate and adaptive immunity.

  • 5.
    Winberg, Martin E
    et al.
    Linköping University, Linköping.
    Holm, Asa
    Linköping University, Linköping.
    Särndahl, Eva
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Vinet, Adrien F
    INRS-Institut Armand-Frappier, Laval, QC, Canada .
    Descoteaux, Albert
    INRS-Institut Armand-Frappier, Laval, QC, Canada .
    Magnusson, Karl-Eric
    Linköping University, Linköping.
    Rasmusson, Birgitta
    Linköping University, Linköping.
    Lerm, Maria
    Linköping University, Linköping.
    Leishmania donovani lipophosphoglycan inhibits phagosomal maturation via action on membrane rafts.2009In: Microbes and infection, ISSN 1286-4579, E-ISSN 1769-714X, Vol. 11, no 2, p. 215-22Article in journal (Refereed)
    Abstract [en]

    Lipophosphoglycan (LPG), the major surface glycoconjugate on Leishmania donovani promastigotes, is crucial for the establishment of infection inside macrophages. LPG comprises a polymer of repeating Galbeta1,4Manalpha-PO(4) attached to a lysophosphatidylinositol membrane anchor. LPG is transferred from the parasite to the host macrophage membrane during phagocytosis and induces periphagosomal F-actin accumulation correlating with an inhibition of phagosomal maturation. The biophysical properties of LPG suggest that it may be intercalated into membrane rafts of the host-cell membrane. The aim of this study was to investigate if the effects of LPG on phagosomal maturation are mediated via action on membrane rafts. We show that LPG accumulates in rafts during phagocytosis of L. donovani and that disruption of membrane rafts abolished the effects of LPG on periphagosomal F-actin and phagosomal maturation, indicating that LPG requires intact membrane rafts to manipulate host-cell functions. We conclude that LPG associates with membrane rafts in the host cell and exert its actions on host-cell actin and phagosomal maturation through subversion of raft function.

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