Host responses in an ex-vivo human skin model challenged with Malassezia sympodialis

FUNDING: This project was funded by a Wellcome Trust Strategic Award for Medical Mycology and Fungal Immunology (097377/Z/11/Z). We would like to acknowledge the support of Internal Funding through a Core Facilities Voucher from the University of Aberdeen. ACKNOWLEDGMENTS: The authors gratefully acknowledge the Technology hubs at the University of Aberdeen (Microscopy and Histology, qPCR facility and Proteomics) for their support, sample processing and training. Special thanks to Professor Annika Scheynius from the Karolinska Institute, Stockholm, Sweden for sharing her expertise and constructive discussions and for giving us the inspiration to work on Malassezia.Peer reviewedPublisher PD

Higher In vitro Proliferation Rate of Rhizopus oryzae in Blood of Diabetic Individuals in Chronic Glycaemic Control Compared with Non-diabetic Individuals

We thank all members of the Laboratory of Clinical Microbiology in the Hospital General Dr. Manuel Gea González, Instituto Nacional de Rehabilitacion and Hospital General de México. Also, thanks to the Wellcome Trust Strategic Award, corresponding author’s scholarship sponsor. Financial Support This study did not have pharmaceutical or grant support, and resources were obtained from institutional budgets.Peer reviewedPublisher PD

Malassezia sympodialis Mala s 1 allergen is a potential KELCH protein that cross reacts with human skin

Open Access via the OUP Agreement We thank Giuseppe Ianiri and Joe Heitman for their continuous support and many insightful discussions. Thanks to the Microscopy and Histology Facility at the Institute of Medical Sciences, University of Aberdeen, for sample processing and access to microscopes. Thanks to Dr. David Stead and the Aberdeen Proteomics Facility, University of Aberdeen for the proteomics analysis. Funding This project was funded by a Wellcome Trust Strategic Award for Medical Mycology and Fungal Immunology (097377/Z/11/Z). D.E.C.L., C.M,. and D.M. acknowledge funding from the Wellcome Trust Strategic Award for Medical Mycology and Fungal Immunology 097 377/Z/11/Z. A.S. acknowledges, the Swedish Cancer and Allergy Fund.Peer reviewedPublisher PD

Monoclonal Human Antibodies That Recognise the Exposed N and C Terminal Regions of the Often-Overlooked SARS-CoV-2 ORF3a Transmembrane Protein

Acknowledgments: The authors would like to gratefully acknowledge the efforts of Julia Martinez Fraile, Richard Lofthouse, Lewis Penny, Mohammad Arastoo and Natalia Cattelan for providing training and assistance with various experimental procedures described in this study. The authors also thank the University of Aberdeen Microscopy and Histology Facility for training and access to fluorescence microscopy and Aberdeen Proteomics for access to BiacoreX100 for SPR binding analysis. Funding: Chief Scientist Office, Scottish Government (COV/ABN/20/01). MRC Centre for Medical Mycology at the University of Exeter (MR/P501955/2).Peer reviewedPublisher PD

Methods for SARS-CoV-2 hospital disinfection, in vitro observations.

This work was funded by National Health Service Grampian Charity. DECL received support from UK Biotechnology and Biological Sciences Research Council and the USA National Science Foundation (BB/W002760/1). Acknowledgment We thank John Ellison for provision of the je2Care 222nm UVC Lamp, and Novus ltd for access to the EORG water ozonation unit.Peer reviewedPublisher PD

An ex-vivo human skin model to study superficial fungal infections

Funding This project was funded by a Wellcome Trust Strategic Award for Medical Mycology and Fungal Immunology 097377. We would like to acknowledge the support of the Medical Research Council Centre for Medical Mycology at the University of Aberdeen (MR/N006364/1). Acknowledgments Thanks to Ms. Lucinda Wight in the Microscopy and Histology Facility at the Institute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom for training on the use of microscopes and the SEM processing. Thanks to Dr. David Stead in the Aberdeen Proteomics Facility, University of Aberdeen, Aberdeen, United Kingdom for the processing of protein samples.Peer reviewedPublisher PD

Influenza challenging the diagnosis and management of pulmonary coccidioidomycosis

Funding There was no funding for this manuscript.Peer reviewedPublisher PD

Neutralisation of SARS-CoV-2 by anatomical embalming solutions.

Teaching and learning anatomy by using human cadaveric specimens has been a foundation of medical and biomedical teaching for hundreds of years. Therefore, the majority of institutions that teach topographical anatomy rely on body donation programmes to provide specimens for both undergraduate and postgraduate teaching of gross anatomy. The COVID-19 pandemic has posed an unprecedented challenge to anatomy teaching because of the suspension of donor acceptance at most institutions. This was largely due to concerns about the potential transmissibility of the SARS-CoV-2 virus and the absence of data about the ability of embalming solutions to neutralise the virus. Twenty embalming solutions commonly used in institutions in the United Kingdom and Ireland were tested for their ability to neutralise SARS-CoV-2, using an established cytotoxicity assay. All embalming solutions tested neutralised SARS-CoV-2, with the majority of solutions being effective at high-working dilutions. These results suggest that successful embalming with the tested solutions can neutralise the SARS-CoV-2 virus, thereby facilitating the safe resumption of body donation programmes and cadaveric anatomy teaching

Biofilms formed by isolates from recurrent vulvovaginal candidiasis patients are heterogeneous and insensitive to fluconazole

Vulvovaginal candidiasis (VVC) is a global health problem affecting ∼75% of women at least once in their lifetime. Here we examined the epidemiology of VVC from a patient cohort to identify the causative organisms associated with VVC. Biofilm forming capacity and antifungal sensitivity profiles were also assessed. We report a shifting prevalence of Candida species with heterogeneous biofilm forming capacity, both of which are associated with altered antifungal drug sensitivity

CD11b+, Ly6G+ Cells Produce Type I Interferon and Exhibit Tissue Protective Properties Following Peripheral Virus Infection

The goal of the innate immune system is containment of a pathogen at the site of infection prior to the initiation of an effective adaptive immune response. However, effector mechanisms must be kept in check to combat the pathogen while simultaneously limiting undesirable destruction of tissue resulting from these actions. Here we demonstrate that innate immune effector cells contain a peripheral poxvirus infection, preventing systemic spread of the virus. These innate immune effector cells are comprised primarily of CD11b+Ly6C+Ly6G- monocytes that accumulate initially at the site of infection, and are then supplemented and eventually replaced by CD11b+Ly6C+Ly6G+ cells. The phenotype of the CD11b+Ly6C+Ly6G+ cells resembles neutrophils, but the infiltration of neutrophils typically occurs prior to, rather than following, accumulation of monocytes. Indeed, it appears that the CD11b+Ly6C+Ly6G+ cells that infiltrated the site of VACV infection in the ear are phenotypically distinct from the classical description of both neutrophils and monocyte/macrophages. We found that CD11b+Ly6C+Ly6G+ cells produce Type I interferons and large quantities of reactive oxygen species. We also observed that depletion of Ly6G+ cells results in a dramatic increase in tissue damage at the site of infection. Tissue damage is also increased in the absence of reactive oxygen species, although reactive oxygen species are typically thought to be damaging to tissue rather than protective. These data indicate the existence of a specialized population of CD11b+Ly6C+Ly6G+ cells that infiltrates a site of virus infection late and protects the infected tissue from immune-mediated damage via production of reactive oxygen species. Regulation of the action of this population of cells may provide an intervention to prevent innate immune-mediated tissue destruction