Project description:Pochonia chlamydosporia (Goddard) Zare & Gams (Ascomycota, Sordariomycetes, Hypocreales, Pochoniaceae, Pochonia) is a nematophagous fungus with significant potential as a biocontrol agent against animal-parasitic nematode. However, the molecular and cellular mechanisms underlying its infection process remain poorly understood. This study aims to provide a comprehensive investigation of P. chlamydosporia infection dynamics in Parascaris equorum eggs using both microscopic and proteomic approaches. The infection was monitored at three distinct stages (early, middle, and late), with corresponding ultrastructural and molecular changes observed. Microscopic analysis using scanning electron microscopy (SEM), transmission electron microscopy (TEM), and light microscopy (LM) revealed the progressive invasion of P. chlamydosporia into nematode eggs. These observations provided detailed insights into the morphological changes in both fungal structures and nematode eggs, highlighting key infection stages such as fungal attachment, germination, and egg degradation. Furthermore, the observations confirmed the stages of fungal colonization, emphasizing the dynamic host-pathogen interaction at the macroscopic level. To complement these observations, a 4D-DIA-based quantitative proteomics approach was employed to analyze the exoproteomic changes in P. chlamydosporia during infection. A total of 410 differentially expressed proteins (DEPs) were identified across the three infection stages, with 313 proteins upregulated and 403 proteins downregulated. Gene Ontology (GO) enrichment analysis revealed that these DEPs are involved in critical biological processes, including cellular stress response, proteolysis, metabalic process, and hydrolase activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis further identified key infection-associated pathways, such as signal transduction, cell wall biosynthesis, energy metabolism, and host-pathogen interactions. These findings suggest that P. chlamydosporia employs a highly coordinated molecular strategy to adapt to and exploit its host. Quantitative PCR (qPCR) validation of key genes involved in signal transduction and immune evasion mechanisms further supported the molecular basis of P. chlamydosporia's parasitic behavior. These findings contribute to our understanding of fungal-nematode interactions and lay a solid foundation for the development of P. chlamydosporia as a sustainable tool for integrated pest management.

Project description:Macrophages are essential for pathogen clearance and to preserve tissue homeostasis, yet the molecular regulators of this equilibrium remain incompletely defined. Here, we identify SAILR, a primate-specific long noncoding RNA (lncRNA), as a critical modulator of macrophage viability under infection conditions. SAILR is induced during monocyte-to-macrophage differentiation, but rapidly downregulated upon bacterial challenge in an NFκB-dependent manner. In both naïve and immune-activated macrophages, SAILR dampens the expression of adhesion, phagocytosis and invasion factors, including SIGLEC1 and MMP7. During Salmonella Typhimurium infection, depletion of SAILR sensitizes macrophages to apoptosis, resulting in loss of intracellular replication niches and reduced bacterial recovery. Conversely, enforced SAILR expression promotes macrophage survival and increases intracellular pathogen burden. Mechanistically, SAILR interacts with the anti-apoptotic adaptor protein 14-3-3β to support macrophage survival. Notably, downregulation of SAILR is mirrored in circulating immune cells from patients with severe COVID-19 and sepsis. Together, our findings position SAILR as a central regulator linking macrophage survival to host-pathogen interaction and disease pathophysiology. Long noncoding RNAs (lncRNAs) are a class of regulatory molecules whose roles in the immune system remain poorly understood. In this study, we identify a human-specific lncRNA named SAILR that modulates the viability of macrophages - immune cells essential for pathogen clearance. SAILR interacts with the adaptor protein 14-3-3β and is rapidly downregulated upon bacterial infection, which sensitizes macrophages to cell death. This may limit the formation of intracellular niches that support pathogen propagation. Reduced SAILR levels in patients suffering from severe infections (sepsis and COVID-19) further suggest clinical relevance. Together, our findings reveal an RNA-based mechanism linking macrophage survival control to host defense and suggest SAILR as a potential diagnostic marker or therapeutic target in infectious and inflammatory diseases.

			Action	DRS
	241212_DR_124_Sh_10_Slot2-45_1_20276.d.zip	Other
	241212_DR_124_Sh_11_Slot2-46_1_20280.d.zip	Other
	241212_DR_124_Sh_12_Slot2-47_1_20284.d.zip	Other
	241212_DR_124_Sh_1_Slot2-36_1_20270.d.zip	Other
	241212_DR_124_Sh_2_Slot2-37_1_20274.d.zip	Other

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A human-specific long noncoding RNA regulator of antigen-presenting cell viability and antimicrobial defense

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