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-Host Interactions Mediating Airway Wall Remodelling in Asthma.
J Fungi (Basel)
February 2022
School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester and Manchester Academic Health Science Centre, Manchester M13 9PT, UK.
Asthma is a chronic heterogeneous respiratory condition that is mainly associated with sensitivity to airborne agents such as pollen, dust mite products and fungi. Key pathological features include increased airway inflammation and airway wall remodelling. In particular, goblet cell hyperplasia, combined with excess mucus secretion, impairs clearance of the inhaled foreign material.
View Article and Find Full Text PDFExperimental Models for Fungal Keratitis: An Overview of Principles and Protocols.
Cells
July 2020
Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Fungal keratitis is a potentially blinding infection of the cornea that afflicts diverse patient populations worldwide. The development of better treatment options requires a more thorough understanding of both microbial and host determinants of pathology, and a spectrum of experimental models have been developed toward this end. In vivo (animal) models most accurately capture complex pathological outcomes, but protocols may be challenging to implement and vary widely across research groups.
View Article and Find Full Text PDFThe NK receptor NKp30 mediates direct fungal recognition and killing and is diminished in NK cells from HIV-infected patients.
Cell Host Microbe
October 2013
Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, AB T2N 4N1, Canada; The Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, University of Calgary, Calgary, AB T2N 4N1, Canada.
Natural killer (NK) cells are a subset of immune effectors that directly bind and kill fungi via a perforin-dependent mechanism. The receptor mediating this activity and its potential role in disease remain unknown. Using an unbiased approach, we determined that NKp30 is responsible for recognition and killing of the fungal pathogens Cryptococcus and Candida.
View Article and Find Full Text PDFInduction of brain microvascular endothelial cell urokinase expression by Cryptococcus neoformans facilitates blood-brain barrier invasion.
PLoS One
June 2013
Research Institute for Children, Louisiana State University Health Sciences Center, New Orleans, Louisiana, United States of America.
Article Synopsis
- The blood-borne fungal pathogen Cryptococcus neoformans can enhance its invasiveness by interacting with host plasma components like plasminogen.
- Previous research revealed that plasminogen coats the surface of C. neoformans, converting to active plasmin through host activators, which boosts fungal invasion of brain endothelial cells.
- In this study, viable C. neoformans were shown to increase urokinase expression in brain microvascular endothelial cells, facilitating plasminogen activation and enhancing the pathogen's invasiveness, indicating that it exploits the host urokinase-plasmin system to become more virulent.
Characterisation of innate fungal recognition in the lung.
PLoS One
August 2012
Division of Immunology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory, South Africa.
The innate recognition of fungi by leukocytes is mediated by pattern recognition receptors (PRR), such as Dectin-1, and is thought to occur at the cell surface triggering intracellular signalling cascades which lead to the induction of protective host responses. In the lung, this recognition is aided by surfactant which also serves to maintain the balance between inflammation and pulmonary function, although the underlying mechanisms are unknown. Here we have explored pulmonary innate recognition of a variety of fungal particles, including zymosan, Candida albicans and Aspergillus fumigatus, and demonstrate that opsonisation with surfactant components can limit inflammation by reducing host-cell fungal interactions.
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