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Danger signals activate the innate immune system of a filamentous fungus during regeneration

ABSTRACT: The ability to respond to injury is a biological process conserved across kingdoms, which in some cases results in regeneration of an organism’s lost part or structure. Due to their immobility, multicellular fungi are prey to a variety of predators and are therefore constantly exposed to mechanical damage. Nevertheless, our current knowledge of how fungi respond to injury is scarce. Activation of injury responses and regeneration relies on the detection of danger or alarm signals known as Danger- or Damage-Associated Molecular Patterns. We show that Ca2+ influxes and extracellular ATP, two such signals, together with Mitogen-Activated Protein Kinases, play a key role in the control of hyphal regeneration in the filamentous fungus Trichoderma atroviride. We further show that these signaling cascades activate major transcriptional changes early after injury. We identified a set of regeneration genes related to cell signaling, stress responses, regulation of transcription, ribosome biogenesis/translation, replication and DNA repair. We uncovered the activation of an innate immune response, including HET domain genes, until now only known to participate in vegetative incompatibility. We show that fungal and animal regeneration share danger-signals, signaling cascades, and the activation of an immune system, challenging the current notion of the evolution of this process.

ORGANISM(S): Trichoderma atroviride

PROVIDER: GSE115811 | GEO | 2018/08/14

REPOSITORIES: GEO

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Danger signals activate the innate immune system of a filamentous fungus during regeneration

Project description:Danger signals activate the innate immune system of a filamentous fungus during regeneration

| PRJNA476116 | ENA

Drosophila attack inhibits hyphal regeneration and defense mechanisms activation for the fungus Trichoderma atroviride

Project description:Fungi as animals and plants conserves the ability to respond to stressful environmental conditions as biotic an abiotic stress. A correct injury response in Eukaryotes including fungi is carried out thought the activation of signaling pathways Ca2+ related dependent of DAMPs/MAPMPs recognizing for the activation of the innate immune system. During herbivory, plants, in addition to activating pathways related to injury, activates specific responses to combat its predator. Using a transcriptional approach, here, we reported the capacity of the filamentous fungus T. atroviride to activate or not a specific response to injury and predation to different predators also, we provide evidence of how fungivory by Drosophila melanogaster larvae inhibits the reported injury response for T. atroviride, although this predation negatively affects the hyphal regeneration thought the larval salivary compounds. Also, the activation of a putative alternate injury reproduction pathway is proposed.

2021-07-20 | GSE152652 | GEO

Lipid droplet-mediated danger signaling balances Trem2+ macrophage induction and NLRP3 inflammasome activation in NASH

Project description:Macrophages are exquisitely capable of sensing danger-associated molecular patterns (DAMPs) and orchestrating inflammatory response during tissue injury. Nonalcoholic steatohepatitis (NASH) represents an advanced stage of metabolic fatty liver disease that increases the risk for cirrhosis and liver cancer. Pathogenic mechanisms of NASH center on hepatocyte injury and the ensuing immune response within the liver microenvironment. However, the nature of DAMPs released by injured hepatocytes and how they shape the liver immune milieu remain largely unknown. Here we show that lipid droplets (LDs) released by injured fatty hepatocytes provide a potent signal that triggers monocyte infiltration and maturation into Trem2+ macrophages, recently described as NASH-associated macrophages (NAMs) or lipid- associated macrophages. LD treatment exacerbated liver injury in mice with diet-induced NASH. We identified Membrane spanning 4-domains a7 (Ms4a7) as a NAM-specific pathogenic factor that was strongly induced in mouse and human NASH. Ms4a7 inactivation ameliorated key aspects of diet-induced NASH pathologies in mice. At the mechanistic level, Ms4a7 physically interacts with NLR family pyrin domain containing 3 (NLRP3) and is required for endosomal NLRP3 inflammasome activation. These findings illustrate a crucial role of Ms4a7 in driving pro-inflammatory signaling in NASH liver. Surprisingly, LD treatments attenuated Ms4a7 expression and NLRP3 inflammasome activation in cultured macrophages. As such, LDs serve as a DAMP signal that balances the induction of Trem2+ macrophages and NLRP3 inflammasome activation in NASH liver

2024-04-26 | GSE230700 | GEO

IL-10-conditioned dendritic cells elicit innate inflammatory gene products in response to danger signals

Project description:IL-10-Conditioned Dendritic Cells, Decommissioned for Recruitment of Adaptive Immunity, Elicit Innate Inflammatory Gene Products in Response to Danger Signals Dendritic cells (DCs) are the professional APCs of the immune system, enabling T cells to perceive and respond appropriately to potentially dangerous microbes, while also being able to maintain T cell tolerance toward self. In part, such tolerance can be determined by IL-10 released from certain types of regulatory T cells. IL-10 has previously been shown to render DCs unable to activate T cells and it has been assumed that this process represents a general block in maturation. Using serial analysis of gene expression, we show that IL-10 pretreatment of murine bone marrow-derived DCs alone causes significant changes in gene expression. Furthermore, these cells retain the ability to respond to Toll-like receptor agonists, but in a manner skewed toward the selective induction of mediators known to enhance local inflammation and innate immunity, among which we highlight a novel CXCR2 ligand, DC inflammatory protein-1. These data suggest that, while the presence of a protolerogenic and purportedly anti-inflammatory agent such as IL-10 precludes DCs from acquiring their potential as initiators of adaptive immunity, their ability to act as initiators of innate immunity in response to Toll-like receptor signaling is enhanced. Keywords: other

2004-04-15 | GSE1316 | GEO

A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (RNA-seq)

Project description:Following injury, differentiated epithelial cells can serve as a stem cell-independent source for tissue regeneration by undergoing reprogramming into other cell types. The intrinsic molecular basis underlying plasticity of differentiated cells remains largely unaddressed. Here we show that Arid1a, a key component of the SWI/SNF chromatin remodeling complex, controls liver regeneration and gene expression associated with emergence of injury-induced progenitor-like cells (LPLCs). Hepatocyte-specific Arid1a ablation reduces LPLC gene expression in several models of periportal liver injury and impairs liver regeneration, leading to organ dysfunction. Arid1a establishes a permissive chromatin state at LPLC-enriched genes during homeostasis, suggesting it endows hepatocytes with competence to respond to injury-induced signals. Consistently, Arid1a facilitates binding of YAP, a critical regeneration signaling pathway, to LPLC-enriched genes, and Arid1a deletion prevents their YAP-associated induction following injury. Together, these findings provide a framework for studying the contributions of injury-induced LPLCs to periportal liver regeneration.

2019-07-07 | GSE111501 | GEO

A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ChIP-seq)

2019-07-07 | GSE111500 | GEO

A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ATAC-seq)

2019-07-07 | GSE111499 | GEO

Type 2 innate signals regulate functionality of fibro/adipogenic progenitors to facilitate muscle regeneration

Project description:In vertebrates, activation of innate immunity is an early response to injury, implicating it in the regenerative process. However, the mechanisms by which innate signals might regulate stem cell functionality are unknown. Here we demonstrate that type 2 innate immunity is required for regeneration of skeletal muscle after injury. Muscle damage results in rapid recruitment of eosinophils, which secrete IL-4 to activate the regenerative actions of muscle resident fibro/adipocyte progenitors (FAPs). In FAPs, IL-4/IL-13 signaling serves as a key switch to control their fate and functions. Activation of IL-4/IL-13 signaling promotes proliferation of FAPs to support myogenesis, while inhibiting their differentiation into adipocytes. Surprisingly, type 2 cytokine signaling is also required in FAPs, but not myeloid cells, for rapid clearance of necrotic debris, a process that is necessary for timely and complete regeneration of tissues. Fibroadipocyte progenitors were isolated from wild-type and IL-4Ra knockout (IL-4Ra -/-) mice and were treated with vehicle or IL4 stimulation in culture prior to microarray analysis. 4 biological replicates of each condition were performed.

2013-04-11 | E-GEOD-44933 | biostudies-arrayexpress

Acute Gene Induction by Tienilic Acid in the Male Sprague Dawley Rat: Possible Role for Danger

Project description:Tienilic acid (TA) was withdrawn from the US market due to numerous cases of liver necrosis. Two major hypotheses currently used to understand the mechanisms of idiosyncratic reactions such as TA-induced hepatotoxicity are the hapten and danger hypotheses. Both human cytochrome (CYP) P450 2C9 and the rat ortholog CYP 2C11 metabolize TA, and it was reported that a reactive metabolite of TA binds almost exclusively to these enzymes, thus acting as a mechanism-based inhibitor. TA-induced liver toxicity is associated with antibodies against CYP 2C9, thus TA appears to act as a hapten. However, if the binding were limited to CYP 2C, it is unlikely that this would lead to significant cell stress. Thus, if TA does not cause cell stress it would suggest that a drug does not have to generate a “danger signal” in order to cause an idiosyncratic drug reaction and acting as a hapten is sufficient. In order to test whether TA can cause cell stress, male Sprague Dawley rats were orally dosed with TA, and hepatic gene expression was profiled at 6 and 24 h after drug administration. Results showed that TA induced robust changes in genes involved in oxidative stress (e.g. aldo-keto reductase, glutathione-S-transferase, thioredoxin reductase, epoxide hydrolase), inflammation and cytotoxicity (e.g. IL-1b, interferon regulatory factor 1, macrophage stimulating protein 1, caspase-12), as well as those promoting liver regeneration (e.g. p27Kip1, DUSP6, serine dehydratase, spectrin bII, inhibin bA). These data support the hypothesis that danger signals in the form of cell-stress proteins and the generation of oxidative stress may be involved in initiating the immune response observed in TA-induced toxicity. Other recent data also indicate that the reactive metabolite of TA binds to other proteins in addition to CYP 2C Keywords: time course, stress response

2007-06-23 | GSE8252 | GEO

Comparative global transcriptomic profiling of mild and severe neurotrauma in an in vitro neuronal model

Project description:Traumatic brain injury is one of the common cause of adult permanent disability. As its physio-pathological mechanism has yet to be elucidated, by adopting microarray technique we hope to decipher the novel signaling cascades involved, and if different severity of injury would induce any form of neuronal regeneration.

2013-12-31 | GSE23653 | GEO

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