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@plosbiology.orgOct 2, 2026, 4:10 PM

Mounting an #immune response is energetically costly, and so host defenses are often influenced by internal metabolic states. This study identifies a gut-brain signaling mechanism in C. elegans, shaping pathogen avoidance and molecular immune responses.
🧪 #AcademicSky #hostPathogen
plos.io/3T9f6bi

Conceptual diagram for how NHR-68 integrates lipid metabolism with behavioral and molecular immunity. NHR-68 acts in the intestine to regulate linoleic acid homeostasis through control of fat-3 expression. Changes in intestinal lipid metabolism influence an AWC-dependent pathogen-avoidance circuit through currently unidentified intestine-to-neuron signaling mechanisms, enhancing survival during P. aeruginosa infection. In parallel, NHR-68 suppresses PMK-1/p38 MAPK and DAF-16/FOXO immune pathways, coordinating behavioral and molecular defenses to optimize host protection. Created in BioRender. Sang, Y. (2026).
@plosbiology.orgOct 1, 2026, 12:10 PM

Mounting an #immune response is energetically costly, and so host defenses are often influenced by internal metabolic states. This study identifies a gut-brain signaling mechanism in C. elegans, shaping pathogen avoidance and molecular immune responses.
🧪 #AcademicSky #hostPathogen
plos.io/3T9f6bi

Conceptual diagram for how NHR-68 integrates lipid metabolism with behavioral and molecular immunity. NHR-68 acts in the intestine to regulate linoleic acid homeostasis through control of fat-3 expression. Changes in intestinal lipid metabolism influence an AWC-dependent pathogen-avoidance circuit through currently unidentified intestine-to-neuron signaling mechanisms, enhancing survival during P. aeruginosa infection. In parallel, NHR-68 suppresses PMK-1/p38 MAPK and DAF-16/FOXO immune pathways, coordinating behavioral and molecular defenses to optimize host protection. Created in BioRender. Sang, Y. (2026).
@karthiks-lab.bsky.socialOct 1, 2026, 10:42 AM

Our new study in #JournalofExtracellularVesicles @isev.org shows that host microvesicles carrying pneumolysin remain membrane-active and damage recipient cells beyond canonical pore formation.
Read on the mechanism:
doi.org/10.1002/jev2...
@isev.org
#ExtracellularVesicles #Pneumolysin #HostPathogen

@plosbiology.orgSep 30, 2026, 8:10 AM

Mounting an #immune response is energetically costly, and so host defenses are often influenced by internal metabolic states. This study identifies a gut-brain signaling mechanism in C. elegans, shaping pathogen avoidance and molecular immune responses.
🧪 #AcademicSky #hostPathogen
plos.io/3T9f6bi

Conceptual diagram for how NHR-68 integrates lipid metabolism with behavioral and molecular immunity. NHR-68 acts in the intestine to regulate linoleic acid homeostasis through control of fat-3 expression. Changes in intestinal lipid metabolism influence an AWC-dependent pathogen-avoidance circuit through currently unidentified intestine-to-neuron signaling mechanisms, enhancing survival during P. aeruginosa infection. In parallel, NHR-68 suppresses PMK-1/p38 MAPK and DAF-16/FOXO immune pathways, coordinating behavioral and molecular defenses to optimize host protection. Created in BioRender. Sang, Y. (2026).
@plosbiology.orgSep 25, 2026, 4:02 PM

How do pathogens alter neuro-epidermal communication to compromise epidermal integrity? This study shows that Pseudomonas aeruginosa infection in C. elegans induces a neuropeptide-like factor, impairing epidermal lysosomes and collagen organization.
🧪 #MicroSky #hostPathogen
buff.ly/l2mgbTN

Schematic model of a neuro-epidermal signaling axis in which Pseudomonas aeruginosa PA14 exploits neuronal NSIF-1 to disrupt epidermal lysosomal function, compromise collagen integrity, and suppress host immunity in C. elegans. NSIF-1 acts as a neuronal secreted factor that mediates PA14-induced pathogenesis, inhibiting epidermal lysosomal activity via the transcription factor ELT-3.
@plosbiology.orgSep 24, 2026, 12:01 PM

How do pathogens alter neuro-epidermal communication to compromise epidermal integrity? This study shows that Pseudomonas aeruginosa infection in C. elegans induces a neuropeptide-like factor, impairing epidermal lysosomes and collagen organization.
🧪 #MicroSky #hostPathogen
buff.ly/l2mgbTN

Schematic model of a neuro-epidermal signaling axis in which Pseudomonas aeruginosa PA14 exploits neuronal NSIF-1 to disrupt epidermal lysosomal function, compromise collagen integrity, and suppress host immunity in C. elegans. NSIF-1 acts as a neuronal secreted factor that mediates PA14-induced pathogenesis, inhibiting epidermal lysosomal activity via the transcription factor ELT-3.
@plosbiology.orgSep 23, 2026, 8:00 AM

How do pathogens alter neuro-epidermal communication to compromise epidermal integrity? This study shows that Pseudomonas aeruginosa infection in C. elegans induces a neuropeptide-like factor, impairing epidermal lysosomes and collagen organization.
🧪 #MicroSky #hostPathogen
buff.ly/l2mgbTN

Schematic model of a neuro-epidermal signaling axis in which Pseudomonas aeruginosa PA14 exploits neuronal NSIF-1 to disrupt epidermal lysosomal function, compromise collagen integrity, and suppress host immunity in C. elegans. NSIF-1 acts as a neuronal secreted factor that mediates PA14-induced pathogenesis, inhibiting epidermal lysosomal activity via the transcription factor ELT-3.
@microbesinfo.bsky.socialSep 13, 2026, 1:30 AM

🦠🔬 Scientists discovered an unusual #bacterium that can penetrate human #cells without relying on the typical invasion mechanisms used by many #bacterial #pathogens.

#Microbes #Bacteria #HostPathogen #Infections #Microsky via @sciencex.bsky.social

phys.org/news/2026-09...