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Pneumocystis jirovecii

ABSTRACT: Pneumocystis jirovecii Metagenome

PROVIDER: PRJNA782857 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17729727.fastq.gz	Fastqsanger.gz
	SRR17729728.fastq.gz	Fastqsanger.gz
	SRR17729729.fastq.gz	Fastqsanger.gz
	SRR17729730.fastq.gz	Fastqsanger.gz
	SRR17729731.fastq.gz	Fastqsanger.gz

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β-glucans are Masked but Contribute to Pulmonary Inflammation During Pneumocystis Pneumonia

Project description:β-glucans, which can activate innate immune responses, are a major component in the cell wall of the cyst form of Pneumocystis. In the current study we examined whether β-1,3 glucans are masked by surface proteins in Pneumocystis, and what role β-glucans play in Pneumocystis-associated inflammation. For 3 species, including P. jirovecii, which causes Pneumocystis pneumonia (PCP) in humans, P. carinii, and P. murina, β-1,3 glucans were masked in most organisms, as demonstrated by increased exposure following trypsin treatment. Using Q-PCR and microarray techniques, we demonstrated in a mouse model of PCP that treatment with caspofungin, an inhibitor of β-1,3 glucan synthesis, for 21 days, decreased expression of a broad panel of inflammatory markers, including IFN-γ, TNF-α, IL-1β, IL-6, and multiple chemokines/chemokine ligands. Thus, β-glucans in Pneumocystis cysts are largely masked, which likely decreases innate immune activation; this mechanism presumably was developed for interactions with immunocompetent hosts, in whom organism loads are substantially lower. In immunosuppressed hosts with a high organism burden, organism death and release of glucans appears to be an important contributor to deleterious host inflammatory responses.

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