@article{12119,
  abstract     = {Intravascular neutrophils and platelets collaborate in maintaining host integrity, but their interaction can also trigger thrombotic complications. We report here that cooperation between neutrophil and platelet lineages extends to the earliest stages of platelet formation by megakaryocytes in the bone marrow. Using intravital microscopy, we show that neutrophils “plucked” intravascular megakaryocyte extensions, termed proplatelets, to control platelet production. Following CXCR4-CXCL12-dependent migration towards perisinusoidal megakaryocytes, plucking neutrophils actively pulled on proplatelets and triggered myosin light chain and extracellular-signal-regulated kinase activation through reactive oxygen species. By these mechanisms, neutrophils accelerate proplatelet growth and facilitate continuous release of platelets in steady state. Following myocardial infarction, plucking neutrophils drove excessive release of young, reticulated platelets and boosted the risk of recurrent ischemia. Ablation of neutrophil plucking normalized thrombopoiesis and reduced recurrent thrombosis after myocardial infarction and thrombus burden in venous thrombosis. We establish neutrophil plucking as a target to reduce thromboischemic events.},
  author       = {Petzold, Tobias and Zhang, Zhe and Ballesteros, Iván and Saleh, Inas and Polzin, Amin and Thienel, Manuela and Liu, Lulu and Ul Ain, Qurrat and Ehreiser, Vincent and Weber, Christian and Kilani, Badr and Mertsch, Pontus and Götschke, Jeremias and Cremer, Sophie and Fu, Wenwen and Lorenz, Michael and Ishikawa-Ankerhold, Hellen and Raatz, Elisabeth and El-Nemr, Shaza and Görlach, Agnes and Marhuenda, Esther and Stark, Konstantin and Pircher, Joachim and Stegner, David and Gieger, Christian and Schmidt-Supprian, Marc and Gärtner, Florian R and Almendros, Isaac and Kelm, Malte and Schulz, Christian and Hidalgo, Andrés and Massberg, Steffen},
  issn         = {1074-7613},
  journal      = {Immunity},
  keywords     = {Infectious Diseases, Immunology, Immunology and Allergy},
  number       = {12},
  pages        = {2285--2299.e7},
  publisher    = {Elsevier},
  title        = {{Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease}},
  doi          = {10.1016/j.immuni.2022.10.001},
  volume       = {55},
  year         = {2022},
}

@article{12131,
  abstract     = {Replication-incompetent adenoviral vectors have been extensively used as a platform for vaccine design, with at least four anti-COVID-19 vaccines authorized to date. These vaccines elicit neutralizing antibody responses directed against SARS-CoV-2 Spike protein and confer significant level of protection against SARS-CoV-2 infection. Immunization with adenovirus-vectored vaccines is known to be accompanied by the production of anti-vector antibodies, which may translate into reduced efficacy of booster or repeated rounds of revaccination. Here, we used blood samples from patients who received an adenovirus-based Gam-COVID-Vac vaccine to address the question of whether anti-vector antibodies may influence the magnitude of SARS-CoV-2-specific humoral response after booster vaccination. We observed that rAd26-based prime vaccination with Gam-COVID-Vac induced the development of Ad26-neutralizing antibodies, which persisted in circulation for at least 9 months. Our analysis further indicates that high pre-boost Ad26 neutralizing antibody titers do not appear to affect the humoral immunogenicity of the Gam-COVID-Vac boost. The titers of anti-SARS-CoV-2 RBD IgGs and antibodies, which neutralized both the wild type and the circulating variants of concern of SARS-CoV-2 such as Delta and Omicron, were independent of the pre-boost levels of Ad26-neutralizing antibodies. Thus, our results support the development of repeated immunization schedule with adenovirus-based COVID-19 vaccines.},
  author       = {Byazrova, Maria G. and Astakhova, Ekaterina A. and Minnegalieva, Aygul and Sukhova, Maria M. and Mikhailov, Artem A. and Prilipov, Alexey G. and Gorchakov, Andrey A. and Filatov, Alexander V.},
  issn         = {2059-0105},
  journal      = {npj Vaccines},
  keywords     = {Pharmacology (medical), Infectious Diseases, Pharmacology, Immunology, SARS-COV-2, COVID},
  publisher    = {Springer Nature},
  title        = {{Anti-Ad26 humoral immunity does not compromise SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac booster vaccination}},
  doi          = {10.1038/s41541-022-00566-x},
  volume       = {7},
  year         = {2022},
}

@article{12173,
  abstract     = {With increasing urbanization and industrialization, the prevalence of inflammatory bowel diseases (IBDs) has steadily been rising over the past two decades. IBD involves flares of gastrointestinal (GI) inflammation accompanied by microbiota perturbations. However, microbial mechanisms that trigger such flares remain elusive. Here, we analyzed the association of the emerging pathogen atypical enteropathogenic E. coli (aEPEC) with IBD disease activity. The presence of diarrheagenic E. coli was assessed in stool samples from 630 IBD patients and 234 age- and sex-matched controls without GI symptoms. Microbiota was analyzed with 16S ribosomal RNA gene amplicon sequencing, and 57 clinical aEPEC isolates were subjected to whole-genome sequencing and in vitro pathogenicity experiments including biofilm formation, epithelial barrier function and the ability to induce pro-inflammatory signaling. The presence of aEPEC correlated with laboratory, clinical and endoscopic disease activity in ulcerative colitis (UC), as well as microbiota dysbiosis. In vitro, aEPEC strains induce epithelial p21-activated kinases, disrupt the epithelial barrier and display potent biofilm formation. The effector proteins espV and espG2 distinguish aEPEC cultured from UC and Crohn’s disease patients, respectively. EspV-positive aEPEC harbor more virulence factors and have a higher pro-inflammatory potential, which is counteracted by 5-ASA. aEPEC may tip a fragile immune–microbiota homeostasis and thereby contribute to flares in UC. aEPEC isolates from UC patients display properties to disrupt the epithelial barrier and to induce pro-inflammatory signaling in vitro.},
  author       = {Baumgartner, Maximilian and Zirnbauer, Rebecca and Schlager, Sabine and Mertens, Daniel and Gasche, Nikolaus and Sladek, Barbara and Herbold, Craig and Bochkareva, Olga and Emelianenko, Vera and Vogelsang, Harald and Lang, Michaela and Klotz, Anton and Moik, Birgit and Makristathis, Athanasios and Berry, David and Dabsch, Stefanie and Khare, Vineeta and Gasche, Christoph},
  issn         = {1949-0984},
  journal      = {Gut Microbes},
  keywords     = {Infectious Diseases, Microbiology (medical), Gastroenterology, Microbiology},
  number       = {1},
  publisher    = {Taylor & Francis},
  title        = {{Atypical enteropathogenic E. coli are associated with disease activity in ulcerative colitis}},
  doi          = {10.1080/19490976.2022.2143218},
  volume       = {14},
  year         = {2022},
}

@article{10812,
  abstract     = {Several promising strategies based on combining or cycling different antibiotics have been proposed to increase efficacy and counteract resistance evolution, but we still lack a deep understanding of the physiological responses and genetic mechanisms that underlie antibiotic interactions and the clinical applicability of these strategies. In antibiotic-exposed bacteria, the combined effects of physiological stress responses and emerging resistance mutations (occurring at different time scales) generate complex and often unpredictable dynamics. In this Review, we present our current understanding of bacterial cell physiology and genetics of responses to antibiotics. We emphasize recently discovered mechanisms of synergistic and antagonistic drug interactions, hysteresis in temporal interactions between antibiotics that arise from microbial physiology and interactions between antibiotics and resistance mutations that can cause collateral sensitivity or cross-resistance. We discuss possible connections between the different phenomena and indicate relevant research directions. A better and more unified understanding of drug and genetic interactions is likely to advance antibiotic therapy.},
  author       = {Römhild, Roderich and Bollenbach, Mark Tobias and Andersson, Dan I.},
  issn         = {1740-1534},
  journal      = {Nature Reviews Microbiology},
  keywords     = {General Immunology and Microbiology, Microbiology, Infectious Diseases},
  pages        = {478--490},
  publisher    = {Springer Nature},
  title        = {{The physiology and genetics of bacterial responses to antibiotic combinations}},
  doi          = {10.1038/s41579-022-00700-5},
  volume       = {20},
  year         = {2022},
}

@article{10103,
  abstract     = {The small cellular molecule inositol hexakisphosphate (IP6) has been known for ~20 years to promote the in vitro assembly of HIV-1 into immature virus-like particles. However, the molecular details underlying this effect have been determined only recently, with the identification of the IP6 binding site in the immature Gag lattice. IP6 also promotes formation of the mature capsid protein (CA) lattice via a second IP6 binding site, and enhances core stability, creating a favorable environment for reverse transcription. IP6 also enhances assembly of other retroviruses, from both the Lentivirus and the Alpharetrovirus genera. These findings suggest that IP6 may have a conserved function throughout the family Retroviridae. Here, we discuss the different steps in the viral life cycle that are influenced by IP6, and describe in detail how IP6 interacts with the immature and mature lattices of different retroviruses.},
  author       = {Obr, Martin and Schur, Florian KM and Dick, Robert A.},
  issn         = {1999-4915},
  journal      = {Viruses},
  keywords     = {virology, infectious diseases},
  number       = {9},
  publisher    = {MDPI},
  title        = {{A structural perspective of the role of IP6 in immature and mature retroviral assembly}},
  doi          = {10.3390/v13091853},
  volume       = {13},
  year         = {2021},
}