Antifungal innate immunity: recognition and inflammatory networks

Becker, Katharina L.; Ifrim, Daniela C.; Quintin, Jessica; Netea, Mihai G.; Veerdonk, Frank L. van de

doi:10.1007/s00281-014-0467-z

Cited by 81 publications

(77 citation statements)

References 89 publications

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“…ILC3 cells have been shown to secrete IL-17 and IL-22 in the lungs in obesity (45), Streptococcus pneumoniae (46), and fungal infections (47,48). These ILC3 cells may modulate the long-term inflammatory response to S. chartarum, and are likely key mediators of chronic inflammatory responses (49).…”

Section: Cd3mentioning

confidence: 99%

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Lichtenstein¹,

Molina²,

Donaghey³

et al. 2016

Am J Respir Cell Mol Biol

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After a single or multiple intratracheal instillations of Stachybotrys chartarum (S. chartarum or black mold) spores in BALB/c mice, we characterized cytokine production, metabolites, and inflammatory patterns by analyzing mouse bronchoalveolar lavage (BAL), lung tissue, and plasma. We found marked differences in BAL cell counts, especially large increases in lymphocytes and eosinophils in multipledosed mice. Formation of eosinophil-rich granulomas and airway goblet cell metaplasia were prevalent in the lungs of multiple-dosed mice but not in single-or saline-dosed groups. We detected changes in the cytokine expression profiles in both the BAL and plasma. Multiple pulmonary exposures to S. chartarum induced significant metabolic changes in the lungs but not in the plasma. These changes suggest a shift from type 1 inflammation after an acute exposure to type 2 inflammation after multiple exposures to S. chartarum. Eotaxin, vascular endothelial growth factor (VEGF), MIP-1a, MIP-1b, TNF-a, and the IL-8 analogs macrophage inflammatory protein-2 (MIP-2) and keratinocyte chemoattractant (KC), had more dramatic changes in multiplethan in single-dosed mice, and parallel the cytokines that characterize humans with histories of mold exposures versus unexposed control subjects. This repeated exposure model allows us to more realistically characterize responses to mold, such as cytokine, metabolic, and cellular changes.

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Section: Cd3mentioning

confidence: 99%

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Lichtenstein¹,

Molina²,

Donaghey³

et al. 2016

Am J Respir Cell Mol Biol

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“…It was previously shown that galectin-3 on macrophages recognizes β-mannan from C. albicans and, in collaboration with TLR2, is able to induce protective antifungal responses via TNF-α secretion [24]. It has also been suggested that galectin-3 can have a dual role in the regulation of neutrophil function, depending on its cellular location.…”

Section: Additional Mannose-binding Lectinsmentioning

confidence: 99%

“…This interaction can modulate cytokine and ROS production, as well as fungal killing [24]. In addition, dectin-2 can induce cysteinyl leukotriene production, which has been shown to be essential for the initiation of airway inflammation and Th2 immunity against house dust mites.…”

Section: The Dectin-2 Clustermentioning

confidence: 99%

“…In addition to its role in the recognition of mannoproteins from C. albicans , it has also been suggested to interact with polysaccharides from Paracoccidioides extracellular vesicles and to mediate internalization of Aspergillus conidia [24, 39]. SIGNR3, the closest murine homolog of DC-SIGN, has been implicated in sensing fungi present in the microbiota [40].…”

Section: Dc-specific Intercellular Adhesion Molecule-3-grabbing Noninmentioning

confidence: 99%

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Antifungal Innate Immunity: A Perspective from the Last 10 Years

Salazar¹,

Brown²

2018

J Innate Immun

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Fungal pathogens can rarely cause diseases in immunocompetent individuals. However, commensal and normally nonpathogenic environmental fungi can cause life-threatening infections in immunocompromised individuals. Over the last few decades, there has been a huge increase in the incidence of invasive opportunistic fungal infections along with a worrying increase in antifungal drug resistance. As a consequence, research focused on understanding the molecular and cellular basis of antifungal immunity has expanded tremendously in the last few years. This review will provide an overview of the most exciting recent advances in innate antifungal immunity, discoveries that are helping to pave the way for the development of new strategies that are desperately needed to combat these devastating diseases.

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“…In addition, inside a host, defence mechanisms, such as the immune system, complicate the life of fungi, and they have to be able to counteract different host-induced stresses. A lot of reviews have been published concerning the host mechanisms of sensing fungal pathogens (Bourgeois and Kuchler, 2012;Becker et al, 2015;Sanchez-Vallet et al, 2015;Stokes et al, 2015). In contrast, we aim to give an overview on fungal sensing of a host environment.…”

Section: Introductionmentioning

confidence: 99%

Fungal sensing of host environment

Braunsdorf

Mailänder-Sánchez²,

Schaller

2016

Cellular Microbiology

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Summary To survive inside a host, fungi have to adapt to a changing and often hostile environment and therefore need the ability to recognize what is going on around them. To adapt to different host niches, they need to sense external conditions such as temperature, pH and to recognize specific host factors. The ability to respond to physiological changes inside the host, independent of being in a commensal, pathogenic or even symbiotic context, implicates mechanisms for sensing of specific host factors. Because the cell wall is constantly in contact with the surrounding, fungi express receptors on the surface of their cell wall, such as pheromone receptors, which have important roles, besides mediating chemotropism for mating. We are not restricting the discussion to the human host because the receptors and mechanisms used by different fungal species to sense their environment are often similar even for plant pathogens. Furthermore, the natural habitat of opportunistic pathogenic fungi with the potential to cause infection in a human host is in soil and on plants. While the hosts' mechanisms of sensing fungal pathogens have been addressed in the literature, the focus of this review is to fill the gap, giving an overview on fungal sensing of a host‐(ile) environment. Expanding our knowledge on host–fungal interactions is extremely important to prevent and treat diseases of pathogenic fungi, which are important issues in human health and agriculture but also to understand the delicate balance of fungal symbionts in our ecosystem.

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Antifungal innate immunity: recognition and inflammatory networks

Cited by 81 publications

References 89 publications

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Repeated Mouse Lung Exposures toStachybotrys chartarumShift Immune Response from Type 1 to Type 2

Antifungal Innate Immunity: A Perspective from the Last 10 Years

Fungal sensing of host environment

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