@article{HetzerOrthHoellerWuerzneretal.2019,
  author    = {Hetzer, Benjamin and Orth-H{\"o}ller, Dorothea and W{\"u}rzner, Reinhard and Kreidl, Peter and Lackner, Michaela and M{\"u}ller, Thomas and Knabl, Ludwig and Geisler-Moroder, Daniel Rudolf and Mellmann, Alexander and Sesli, {\"O}zcan and Holzknecht, Jeanett and Noce, Damia and Akarathum, Noppadon and Chotinaruemol, Somporn and Prelog, Martina and Oberdorfer, Peninnah},
  title     = {"Enhanced acquisition of antibiotic-resistant intestinal E. coli during the first year of life assessed in a prospective cohort study"},
  series = {Antimicrobial Resistance \& Infection Control},
  volume    = {8},
  journal   = {Antimicrobial Resistance \& Infection Control},
  doi       = {10.1186/s13756-019-0522-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-320284},
  year      = {2019},
  abstract  = {Background Increasing bacterial resistance to antibiotics is a serious problem worldwide. We sought to record the acquisition of antibiotic-resistant Escherichia coli (E. coli) in healthy infants in Northern Thailand and investigated potential determinants. Methods Stool samples from 142 infants after birth, at ages 2wk, 2mo, 4 to 6mo, and 1y, and parent stool samples were screened for E. coli resistance to tetracycline, ampicillin, co-trimoxazole, and cefazoline by culture, and isolates were further investigated for multiresistance by disc diffusion method. Pulsed-field gel electrophoresis was performed to identify persistent and transmitted strains. Genetic comparison of resistant and transmitted strains was done by multilocus sequence typing (MLST) and strains were further investigated for extra- and intra-intestinal virulence factors by multiplex PCR. Results Forty-seven (33\%) neonatal meconium samples contained resistant E. coli. Prevalence increased continuously: After 1y, resistance proportion (tetracycline 80\%, ampicillin 72\%, co-trimoxazole 66\%, cefazoline 35\%) almost matched those in parents. In 8 infants (6\%), identical E. coli strains were found in at least 3 sampling time points (suggesting persistence). Transmission of resistant E. coli from parents to child was observed in only 8 families. MLST showed high diversity. We could not identify any virulence genes or factors associated with persistence, or transmission of resistant E. coli. Full-term, vaginal birth and birth in rural hospital were identified as risk factors for early childhood colonization with resistant E. coli. Conclusion One third of healthy Thai neonates harboured antibiotic-resistant E. coli in meconium. The proportion of resistant E. coli increased during the first year of life almost reaching the value in adults. We hypothesize that enhancement of infection control measures and cautious use of antibiotics may help to control further increase of resistance.},
  language  = {en}
}
@article{SanchezMaldonadoMonizDiezterHorstetal.2020,
  author    = {S{\´a}nchez-Maldonado, Jose Manuel and Mo{\~n}iz-D{\´i}ez, Ana and ter Horst, Rob and Campa, Daniele and Cabrera-Serrano, Antonio Jos{\´e} and Mart{\´i}nez-Bueno, Manuel and Garrido-Collado, Mar{\´i}a del Pilar and Hern{\´a}ndez-Mohedo, Francisca and Fern{\´a}ndez-Puerta, Laura and L{\´o}pez-Nevot, Miguel {\´A}ngel and Cunha, Cristina and Gonz{\´a}lez-Sierra, Pedro Antonio and Springer, Jan and Lackner, Michaela and Alcazar-Fuoli, Laura and Fianchi, Luana and Aguado, Jos{\´e} Mar{\´i}a and Pagano, Livio and L{\´o}pez-Fern{\´a}ndez, Elisa and Clavero, Esther and Potenza, Leonardo and Luppi, Mario and Moratalla, Lucia and Solano, Carlos and Sampedro, Antonio and Cuenca-Estrella, Manuel and Lass-Fl{\"o}rl, Cornelia and Canzian, Federico and Loeffler, Juergen and Li, Yang and Einsele, Hermann and Netea, Mihai G. and V{\´a}zquez, Lourdes and Carvalho, Agostinho and Jurado, Manuel and Sainz, Juan},
  title     = {Polymorphisms within the TNFSF4 and MAPKAPK2 loci influence the risk of developing invasive aspergillosis: a two-stage case control study in the context of the aspBIOmics consortium},
  series = {Journal of Fungi},
  volume    = {7},
  journal   = {Journal of Fungi},
  number    = {1},
  issn      = {2309-608X},
  doi       = {10.3390/jof7010004},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-220107},
  year      = {2020},
  abstract  = {Here, we assessed whether 36 single nucleotide polymorphisms (SNPs) within the TNFSF4 and MAPKAPK2 loci influence the risk of developing invasive aspergillosis (IA). We conducted a two-stage case control study including 911 high-risk patients diagnosed with hematological malignancies that were ascertained through the aspBIOmics consortium. The meta-analysis of the discovery and replication populations revealed that carriers of the TNFSF4\(_{rs7526628T/T}\) genotype had a significantly increased risk of developing IA (p = 0.00022). We also found that carriers of the TNFSF4\(_{rs7526628T}\) allele showed decreased serum levels of TNFSF14 protein (p = 0.0027), and that their macrophages had a decreased fungicidal activity (p = 0.048). In addition, we observed that each copy of the MAPKAPK2\(_{rs12137965G}\) allele increased the risk of IA by 60\% (p = 0.0017), whereas each copy of the MAPKAPK2\(_{rs17013271T}\) allele was estimated to decrease the risk of developing the disease (p = 0.0029). Mechanistically, we found that carriers of the risk MAPKAPK2\(_{rs12137965G}\) allele showed increased numbers of CD38+IgM-IgD- plasmablasts in blood (p = 0.00086), whereas those harboring two copies of the allele had decreased serum concentrations of thymic stromal lymphopoietin (p = 0.00097). Finally, we also found that carriers of the protective MAPKAPK2\(_{rs17013271T}\) allele had decreased numbers of CD27-IgM-IgD- B cells (p = 0.00087) and significantly lower numbers of CD14+ and CD14+CD16- cells (p = 0.00018 and 0.00023). Altogether, these results suggest a role of the TNFSF4 and MAPKAPK2 genes in determining IA risk.},
  language  = {en}
}
@article{LupianezVillaescusaCarvalhoetal.2016,
  author    = {Lupia{\~n}ez, Carmen B. and Villaescusa, Maria T. and Carvalho, Agostinho and Springer, Jan and Lackner, Michaela and S{\´a}nchez-Maldonado, Jos{\´e} M. and Canet, Luz M. and Cunha, Cristina and Segura-Catena, Joana and Alcazar-Fuoli, Laura and Solano, Carlos and Fianchi, Luana and Pagano, Livio and Potenza, Leonardo and Aguado, Jos{\´e} M. and Luppi, Mario and Cuenca-Estrella, Manuel and Lass-Fl{\"o}rl, Cornelia and Einsele, Hermann and V{\´a}zquez, Lourdes and R{\´i}os-Tamayo, Rafael and Loeffler, J{\"u}rgen and Jurado, Manuel and Sainz, Juan},
  title     = {Common Genetic Polymorphisms within NF kappa B-Related Genes and the Risk of Developing Invasive Aspergillosis},
  series = {Frontiers in Microbiology},
  volume    = {7},
  journal   = {Frontiers in Microbiology},
  number    = {1243},
  doi       = {10.3389/fmicb.2016.01243},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165209},
  year      = {2016},
  abstract  = {Invasive Aspergillosis (IA) is an opportunistic infection caused by Aspergillus, a ubiquitously present airborne pathogenic mold. A growing number of studies suggest a major host genetic component in disease susceptibility. Here, we evaluated whether 14 single-nucleotide polymorphisms within NFκB1, NFκB2, RelA, RelB, Rel, and IRF4 genes influence the risk of IA in a population of 834 high-risk patients (157 IA and 677 non-IA) recruited through a collaborative effort involving the aspBIOmics consortium and four European clinical institutions. No significant overall associations between selected SNPs and the risk of IA were found in this large cohort. Although a hematopoietic stem cell transplantation (HSCT)-stratified analysis revealed that carriers of the IRF4rs12203592T/T genotype had a six-fold increased risk of developing the infection when compared with those carrying the C allele (ORREC = 6.24, 95\%CI 1.25-31.2, P = 0.026), the association of this variant with IA risk did not reach significance at experiment-wide significant threshold. In addition, we found an association of the IRF4AATC and IRF4GGTC haplotypes (not including the IRF4rs12203592T risk allele) with a decreased risk of IA but the magnitude of the association was similar to the one observed in the single-SNP analysis, which indicated that the haplotypic effect on IA risk was likely due to the IRF4rs12203592 SNP. Finally, no evidence of significant interactions among the genetic markers tested and the risk of IA was found. These results suggest that the SNPs on the studied genes do not have a clinically relevant impact on the risk of developing IA.},
  language  = {en}
}