Aggregation of<i>Cryptococcus neoformans</i>by Surfactant Protein D Is Inhibited by Its Capsular Component Glucuronoxylomannan

Wetering, J. Koenraad van de; Coenjaerts, Frank E. J.; Vaandrager, Arie B.; Golde, L.M.G. Van; Batenburg, Joseph J.

doi:10.1128/iai.72.1.145-153.2004

Cited by 37 publications

(33 citation statements)

References 48 publications

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“…For example, Schelenz et al have shown that SP-A binds to C. neoformans cells but does not enhance phagocytosis by macrophages (53); furthermore, we have demonstrated that SP-A does not play a significant role during C. neoformans infection in vivo (19). Moreover, SP-D has also been shown to bind and aggregate C. neoformans cells in vitro (58). An underlying variable likely affecting these results is the use of various C. neoformans strains in different studies.…”

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confidence: 50%

Surfactant Protein D Facilitates Cryptococcus neoformans Infection

et al. 2012

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ABSTRACTConcurrent with the global escalation of the AIDS pandemic, cryptococcal infections are increasing and are of significant medical importance. Furthermore,Cryptococcus neoformanshas become a primary human pathogen, causing infection in seemingly healthy individuals. Although numerous studies have elucidated the virulence properties ofC. neoformans, less is understood regarding lung host immune factors during early stages of fungal infection. Based on our previous studies documenting that pulmonary surfactant protein D (SP-D) protectsC. neoformanscells against macrophage-mediated defense mechanismsin vitro(S. Geunes-Boyer et al., Infect. Immun. 77:2783–2794, 2009), we postulated that SP-D would facilitate fungal infectionin vivo. To test this hypothesis, we examined the role of SP-D in response toC. neoformansusing SP-D−/−mice. Here, we demonstrate that mice lacking SP-D were partially protected duringC. neoformansinfection; they displayed a longer mean time to death and decreased fungal burden at several time points postinfection than wild-type mice. This effect was reversed by the administration of exogenous SP-D. Furthermore, we show that SP-D bound to the surface of the yeast cells and protected the pathogenic microbes against macrophage-mediated defense mechanisms and hydrogen peroxide (H2O2)-induced oxidative stressin vitroandin vivo. These findings indicate thatC. neoformansis capable of coopting host SP-D to increase host susceptibility to the yeast. This study establishes a new paradigm for the role played by SP-D during host responses toC. neoformansand consequently imparts insight into potential future preventive and/or treatment strategies for cryptococcosis.

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confidence: 50%

Surfactant Protein D Facilitates Cryptococcus neoformans Infection

et al. 2012

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“…Although SP-A binds to C. neoformans, it does not enhance its uptake (58), and the susceptibility of SP-A null mice to C. neoformans infection is similar to that of wild-type animals, suggesting that SP-A does not play a major role in C. neoformans host defense in vivo (26). SP-D, but not SP-A, binds MP1 and GXM in vitro, and GXM has been shown previously to inhibit the SP-Ddependent aggregation of C. neoformans cells (55). In addition, SP-D interacts with ␤-1,6-glucan present in the cell walls of Saccharomyces cerevisiae and Aspergillus fumigatus (2).…”

mentioning

confidence: 78%

Surfactant Protein D Increases Phagocytosis of HypocapsularCryptococcus neoformansby Murine Macrophages and Enhances Fungal Survival

Geunes-Boyer¹,

Oliver²,

Janbon

et al. 2009

Infect Immun

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“…Collectins thus povide early defense against C. neoforms and encapsulation is a protective mechanism adopted by them to prevent the microorganism evading the immune system. (12,50,80) Mannan, a structural component of the cell wall of yeast, Saccharomyces cerevisiae, was one of the first polysaccharides found to interact with collectin molecules. Mannan and b(1-6) linked glucan of S. cerevisiae are the major ligands for SP-D. SP-A has not been found to bind S. cerevisiae.…”

Section: Fungimentioning

confidence: 99%

Collectins: sentinels of innate immunity

Gupta

Surolia

2007

BioEssays

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Collectins, present in plasma and on mucosal surfaces, are humoral molecules of the innate immune system. They were discovered a hundred years ago in 1906 as the first association of an animal lectin with the immune system. They are a family of calcium-dependent lectins that recognize pathogen-associated molecular patterns. They share a similar modular domain architecture consisting of four regions; a cysteine-rich N-terminal domain, a collagen-like region, an alpha-helical neck domain and a C-terminal carbohydrate recognition domain. There have been eight collectins members defined so far, of which, MBL, SP-A and SP-D are the most characterized. Collectins represent the first line of host defense. Upon recognition of the infectious agents, collectins put into action effector mechanisms like direct opsonization, neutralization, agglutination, complement activation and phagocytosis to curb the microbial growth. In addition, they also modulate inflammatory and allergic responses and apoptotic cell clearance. These functions limit infection and subsequently modulate the adaptive immune responses. The role of collectins, their structure, function, characteristics and clinical significance are reviewed in this article.

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Aggregation ofCryptococcus neoformansby Surfactant Protein D Is Inhibited by Its Capsular Component Glucuronoxylomannan

Cited by 37 publications

References 48 publications

Surfactant Protein D Facilitates Cryptococcus neoformans Infection

Surfactant Protein D Facilitates Cryptococcus neoformans Infection

Surfactant Protein D Increases Phagocytosis of HypocapsularCryptococcus neoformansby Murine Macrophages and Enhances Fungal Survival

Collectins: sentinels of innate immunity

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