Catalases of Aspergillus fumigatus and Inflammation in Aspergillosis

Abstract

The tissue repair, namely inflammation has been the hallmark of pathology. Knowledge of the basic phenomenon, as well as the consequences, complications, and nuances of this process, constitutes the basis for understanding the pathobiology of opportunistic fungal infections. Meanwhile, an injury agent or a damaged cell and normal inflammatory, homeostatic, and immune responses are the essential ingredients needed for inflammation to occur. Individual response to injury may vary widely with the injurious agent, owing to the unique set of genetic, nutritional, physical, infectious, chemical, hormonal, and immune factors that make up that individual's internal and external milieu. Inflammatory and reparative processes are generally simultaneous, but one phase usually dominates when tissue is examined microscopically at a given time after injury. Accordingly, invasive aspergillosis displays a specific inflammation caused by Aspergillus sp. as an injury agent 1. At the site of infection, alveolar macrophages and polymorphonuclear cells, cellular components of the innate defense Review

Human Leukocytes Kill Aspergillus nidulans by Reactive Oxygen Species-Independent Mechanisms

“…These data were subsequently confirmed by transcriptional responses of Aspergillus conidia to healthy and CGD PMN (27). The role of ROS-independent antifungal mechanisms was underscored by Shibuya et al (25). They found that the mycelium of the double cat1 cat2 mutant of A. fumigatus, which has no catalase activity at all, has only a slightly increased sensitivity to H 2 O 2 and is as sensitive to killing by PMN as the wild-type strain but shows delayed infection in an experimental rat model of invasive aspergillosis.…”

“…Instead, they found that the most strongly upregulated transcripts in vivo encoded chemokines and additional factors that play critical roles in neutrophil and monocyte recruitment. Indirect evidence of NADPH-independent resistance in AM was also found by Shibuya et al, who found that killing of catA conidia by AM and conidial virulence in animals were similar to those with wild-type conidia (25). In contrast, AM from p47 phoxϪ/Ϫ mice were unable to kill A. fumigatus conidia in vivo, as shown by Philippe et al (18).…”

Comparative Transcriptomics of Infectious Spores from the Fungal Pathogen Histoplasma capsulatum Reveals a Core Set of Transcripts That Specify Infectious and Pathogenic States

“…Conidial enriched genes were also implicated in resistance to stress, trehalose metabolism, DNA repair, signal transduction, asexual development, and host interactions. Catalase A is a conidium-specific catalase in A. nidulans and A. fumigatus that is induced by stress conditions and confers increased resistance to hydrogen peroxide stress (26,27). We consistently observed very high levels of expression of catalase A (CATA) in H. capsulatum conidia.…”

Deletion Analysis of the Catalase-Encoding Gene (catB) Promoter fromAspergillus oryzae

“…NS indicates nonspecific competitor. Either 10 pmol (lanes 3,6,9,12,15,20,23,26,29, and 32), 5 pmol (lanes 4, 7, 10, 13, 16, 21, 24, 27, and 30), or 1 pmol (lanes 5,8,11,14,17,22,25,28, and 31) of the competitors were added. SB and FP indicate the shifted band and the free probe, respectively.…”

“…[6][7][8] Further, catB homolog genes such as the Aspergillus fumigatus cat1 gene are involved in Aspergillosis, 9) and hence to elucidate the cis-elements of catB promoter should be useful for understanding this disease. Hence we chose the A. oryzae catB promoter to analyze in this study.…”