Tonic TNF conditioning of macrophages safeguards stimulus-specific inflammatory responses
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ABSTRACT:
PROVIDER: PRJNA861266 | ENA |
REPOSITORIES: ENA
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Project description:TNF is a key inflammatory cytokine that warns recipient cells of a nearby infection or tissue damage. Acute exposure to TNF activates characteristic oscillatory dynamics of the transcription factor NFκB and induces a characteristic gene expression program; these are distinct from the responses of cells directly exposed to pathogen-associated molecular patterns (PAMPs). Here we report that tonic TNF exposure is critical for safeguarding TNF’s specific functions. In the absence of tonic TNF conditioning, acute exposure to TNF causes 1) NFκB signaling dynamics that are less oscillatory and more like PAMP-responsive NFκB dynamics, 2) immune gene expression that is more similar to the Pam3CSK4-response program, 3) broader epigenomic reprogramming that is characteristic of PAMP-responsive changes. We show that tonic TNF signaling effects subtle changes to TNF receptor availability and dynamics such that enhanced pathway activity results in non-oscillatory NFκB. Our results reveal tonic TNF signaling as a key tissue determinant of the specific characteristics of cellular responses to acute paracrine TNF exposure, and their distinction from responses to direct exposure to PAMPs.
2022-07-27 | GSE209565 | GEO
Project description:TNF is a key inflammatory cytokine that warns recipient cells of a nearby infection or tissue damage. Acute exposure to TNF activates characteristic oscillatory dynamics of the transcription factor NFκB and induces a characteristic gene expression program; these are distinct from the responses of cells directly exposed to pathogen-associated molecular patterns (PAMPs). Here we report that tonic TNF exposure is critical for safeguarding TNF's specific functions. In the absence of tonic TNF conditioning, acute exposure to TNF causes 1) NFκB signaling dynamics that are less oscillatory and more like PAMP-responsive NFκB dynamics, 2) immune gene expression that is more similar to the Pam3CSK4-response program, 3) broader epigenomic reprogramming that is characteristic of PAMP-responsive changes. We show that absence of tonic TNF signaling effects subtle changes to TNF receptor availability and dynamics such that enhanced pathway activity results in non-oscillatory NFκB. Our results reveal tonic TNF as a key tissue determinant of the specific cellular responses to acute paracrine TNF exposure, and their distinction from responses to direct exposure to PAMPs.
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Project description:The thalamus may be the critical brain area involved in sensory gating and the relay of respiratory mechanical information to the cerebral cortex for the conscious awareness of breathing. We hypothesized that respiratory mechanical stimuli in the form of tracheal occlusions would modulate the gene expression profile of the thalamus. Specifically, it was reasoned that conditioning to the respiratory loading would induce a state change in the medial thalamus consistent with a change in sensory gating and the activation of molecular pathways associated with learning and memory. In addition, respiratory loading is stressful and thus should elicit changes in gene expressions related to stress, anxiety, and depression. Rats were instrumented with inflatable tracheal cuffs. Following surgical recovery, they underwent ten days (5 days/week) of transient tracheal occlusion conditioning. On day 10, the animals were sacrificed and the brains removed. The medial thalamus was dissected and microarray analysis of gene expression performed. Tracheal obstruction conditioning modulated a total of 661 genes (p < 0.05, log2 fold change ≥ 0.58), 250 genes were down-regulated and 411 up-regulated. There was a significant down-regulation of GAD1, GAD2 and HTR1A, HTR2A genes. CCK, PRKCG, mGluR4, and KCJN9 genes were significantly up-regulated. Some of these genes have been associated with anxiety and depression, while others have been shown to play a role in switching between tonic and burst firing modes in the thalamus and thus may be involved in gating of the respiratory stimuli. Furthermore, gene ontology and pathway analysis showed a significant modulation of learning and memory pathways. These results support the hypothesis that the medial thalamus is involved in the respiratory sensory neural pathway due to the state change of its gene expression profile following repeated tracheal occlusions. Four experimental animals that received tracheal occlusions and four surgical control animals were used. A reference design was used to compare all samples.
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