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• W2096728005 endingPage "1963" @default.
• W2096728005 startingPage "1953" @default.
• W2096728005 abstract "Aspergillus fumigatus is a ubiquitous saprophytic mold (67) that forms airborne spores (conidia). Humans inhale, on average, hundreds of these infectious propagules daily. In immune competent hosts, these encounters are of no further significance—conidia are killed and cleared by cells of the pulmonary immune system. However, disease occurs when the host response is either too strong or too weak. Thus, understanding how the host interacts with the organism to define this balance is a critical goal, the successful pursuit of which requires recognition of the dynamic nature of both fungal and host molecular participants. In immunocompromised hosts, A. fumigatus represents a major cause of morbidity and mortality. This patient population is expanding due to the increasing use of transplantation for end organ disease, the development of immunosuppressive and myeloablative therapies for autoimmune and neoplastic disease, and the human immunodeficiency virus/AIDS pandemic (38). A. fumigatus is the most common invasive mold infection in these patients, and mortality rates exceed 50% in high-risk groups, such as leukemic patients and hematopoietic stem cell transplant recipients (74). Sensitivity to A. fumigatus antigens is associated with asthma, the prevalence of which is increasing in the developed world, though proving causation has been difficult (49, 54). Regardless, this increased prevalence brings a parallel rise in the number of individuals predisposed to allergic bronchopulmonary aspergillosis, a disease associated with aberrant responses to Aspergillus antigens in the setting of chronic inflammation. The spectrum of invasive, semi-invasive, and allergic disease caused by A. fumigatus is reviewed in several outstanding articles (9, 94). The study of A. fumigatus molecules involved in virulence has been hampered by the lack of an identifiable sexual cycle, limiting classical genetic analysis (21). A recent study, however, indicates that A. fumigatus encodes distinct mating-type loci and the pheromone machinery required for sexual mating (103). Nonetheless, within the past decade, researchers have developed and refined experimental tools to generate mutant strains by homologous recombination (21, 35, 62, 152, 154), utilized RNA interference to repress endogenous transcripts (95), and expressed heterologous genes in A. fumigatus under the control of drug-inducible regulatory elements (145). The completion of the A. fumigatus genome (98) has accelerated gene structure and function studies and made possible comparative genomic analyses with other sequenced Aspergillus species (Aspergillus oryzae and Aspergillus nidulans), as well as other genera of pathogenic (e.g., Candida albicans and Cryptococcus neoformans) and nonpathogenic (e.g., Saccharomyces cerevisiae) fungi. An important insight from the genomes has been that A. fumigatus does not share a common set of genes with other fungal pathogens (98). The types of hosts that are susceptible to invasive aspergillosis and the lack of unique pathways conserved among pathogenic fungi underscore the importance of the host contribution to pathogenesis. Damage from A. fumigatus can result from fungal growth and tissue invasion or from inflammatory cells recruited to sites of infection (130). Included in the latter are responses that are ineffective in clearing the organism, occur in the process of immune reconstitution, or are associated with allergy. For example, in a murine model of chronic granulomatous disease, in which mice have defective phagocyte oxidase systems, administration of killed hyphae results in chronic inflammation due to persistence of fungal elements (92). From the perspective of the mammalian immune system, A. fumigatus represents an organism with continuous respiratory tract exposure that must be cleared from terminal airways with an immune response calibrated to avoid fungal tissue invasion, as well as inflammation-induced tissue damage. Here, we review our growing understanding of the interface between A. fumigatus and host defense mechanisms, with an emphasis on invasive disease in humans and small animal models." @default.
• W2096728005 created "2016-06-24" @default.
• W2096728005 creator A5050576085 @default.
• W2096728005 creator A5056954811 @default.
• W2096728005 date "2007-11-01" @default.
• W2096728005 modified "2023-10-06" @default.
• W2096728005 title "<i>Aspergillus fumigatus</i>: Principles of Pathogenesis and Host Defense" @default.
• W2096728005 cites W1482128986 @default.
• W2096728005 cites W1519886765 @default.
• W2096728005 cites W1524553190 @default.
• W2096728005 cites W1531113262 @default.
• W2096728005 cites W1562117121 @default.
• W2096728005 cites W1592394199 @default.
• W2096728005 cites W1600813584 @default.
• W2096728005 cites W1649649531 @default.
• W2096728005 cites W1735007449 @default.
• W2096728005 cites W1789911598 @default.
• W2096728005 cites W180072684 @default.
• W2096728005 cites W1830139161 @default.
• W2096728005 cites W1942899011 @default.
• W2096728005 cites W1960821628 @default.
• W2096728005 cites W1963672691 @default.
• W2096728005 cites W1974227348 @default.
• W2096728005 cites W1974295668 @default.
• W2096728005 cites W1976925504 @default.
• W2096728005 cites W1978482918 @default.
• W2096728005 cites W1978974268 @default.
• W2096728005 cites W1979171308 @default.
• W2096728005 cites W1980422468 @default.
• W2096728005 cites W1980921693 @default.
• W2096728005 cites W1981172039 @default.
• W2096728005 cites W1984057139 @default.
• W2096728005 cites W1984079027 @default.
• W2096728005 cites W1984710508 @default.
• W2096728005 cites W1985371834 @default.
• W2096728005 cites W1985530448 @default.
• W2096728005 cites W1987544400 @default.
• W2096728005 cites W1988822418 @default.
• W2096728005 cites W1988940275 @default.
• W2096728005 cites W1989231398 @default.
• W2096728005 cites W1992379070 @default.
• W2096728005 cites W1993254232 @default.
• W2096728005 cites W1993730028 @default.
• W2096728005 cites W1995441274 @default.
• W2096728005 cites W1995629350 @default.
• W2096728005 cites W2000626205 @default.
• W2096728005 cites W2003581234 @default.
• W2096728005 cites W2005998335 @default.
• W2096728005 cites W2008191665 @default.
• W2096728005 cites W2008805469 @default.
• W2096728005 cites W2010630254 @default.
• W2096728005 cites W2013277175 @default.
• W2096728005 cites W2013439407 @default.
• W2096728005 cites W2013858599 @default.
• W2096728005 cites W2015568263 @default.
• W2096728005 cites W2016289237 @default.
• W2096728005 cites W2016984863 @default.
• W2096728005 cites W2017017949 @default.
• W2096728005 cites W2029685645 @default.
• W2096728005 cites W2032348735 @default.
• W2096728005 cites W2033179792 @default.
• W2096728005 cites W2033493201 @default.
• W2096728005 cites W2033848698 @default.
• W2096728005 cites W2037539696 @default.
• W2096728005 cites W2038112945 @default.
• W2096728005 cites W2041414113 @default.
• W2096728005 cites W2042662964 @default.
• W2096728005 cites W2043474036 @default.
• W2096728005 cites W2053403241 @default.
• W2096728005 cites W2054537975 @default.
• W2096728005 cites W2054605333 @default.
• W2096728005 cites W2058782633 @default.
• W2096728005 cites W2059507666 @default.
• W2096728005 cites W2061789597 @default.
• W2096728005 cites W2066967399 @default.
• W2096728005 cites W2067206496 @default.
• W2096728005 cites W2078897040 @default.
• W2096728005 cites W2079928619 @default.
• W2096728005 cites W2081384682 @default.
• W2096728005 cites W2095763666 @default.
• W2096728005 cites W2096130020 @default.
• W2096728005 cites W2096209592 @default.
• W2096728005 cites W2096790583 @default.
• W2096728005 cites W2096989812 @default.
• W2096728005 cites W2097192281 @default.
• W2096728005 cites W2097216675 @default.
• W2096728005 cites W2097753409 @default.
• W2096728005 cites W2097867626 @default.
• W2096728005 cites W2098820394 @default.
• W2096728005 cites W2099170652 @default.
• W2096728005 cites W2099769947 @default.
• W2096728005 cites W2100920812 @default.
• W2096728005 cites W2101286028 @default.
• W2096728005 cites W2104633998 @default.
• W2096728005 cites W2105379241 @default.
• W2096728005 cites W2106551616 @default.
• W2096728005 cites W2107711120 @default.
• W2096728005 cites W2108313755 @default.

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