GO:0106015 negative regulation of inflammatory response to wounding: Resolution Mechanisms, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0106015 describes any process that stops, prevents, or reduces the frequency, rate or extent of the inflammatory response to wounding.
• This term is a biological_process and is central to understanding how tissues resolve inflammation after injury and avoid chronic inflammation.
• Key molecular players include transcription factors such as FOXO1, Sufu, SLAMF7, Sipa1, METTL3, and BATF, which modulate inflammatory signaling in macrophages, microglia, and fibroblasts [2,4,5,6,8].
• Dysregulation of this process contributes to diseases such as sepsis, myocardial infarction, atopic dermatitis, hepatocellular carcinoma recurrence, and neuroinflammation [2,3,4,5,6,8].
• CRISPR-based models (knockout, point mutation, knock-in, overexpression) enable causal testing of candidate genes in negative regulation of inflammatory response to wounding [1,2,4,5,6,8].
• EDITGENE provides end-to-end services for building such models and for CRISPR library screening and bioinformatics to accelerate discovery in this field.
Description
The Gene Ontology term GO:0106015, negative regulation of inflammatory response to wounding, defines any process that stops, prevents, or reduces the frequency, rate or extent of the inflammatory response to wounding. This term captures the active, coordinated resolution of inflammation after tissue injury, a process essential for restoring homeostasis and preventing chronic inflammatory disease. Researchers study this term to understand how the body limits collateral damage from an initially protective inflammatory response and how failure of these brakes leads to persistent inflammation. The inflammatory response to wounding is a double-edged sword: it is required for pathogen clearance and tissue repair, but when it is not properly resolved, it can drive fibrosis, organ dysfunction, and autoimmunity. Negative regulation of this response involves multiple cell types, including macrophages, fibroblasts, and microglia, and is controlled by intracellular signaling pathways and transcriptional programs [2,4,5,6,8]. For example, SLAMF7 regulates macrophage inflammatory responses during polymicrobial sepsis, and its loss or blockade can alter the balance between inflammation and resolution. Sufu limits sepsis-induced lung inflammation by regulating phase separation of TRAF6, illustrating how intracellular scaffolding and condensate formation can put the brakes on inflammatory signaling. Sipa1 drives a maladaptive fibroblast-myeloid axis after myocardial infarction, and targeting this axis may promote resolution. The m6A methyltransferase METTL3 stabilizes BATF mRNA in microglia, driving neuroinflammation and neurotoxicity, which highlights epitranscriptomic control of this process. FOXO1 regulates Th17 cell-mediated hepatocellular carcinoma recurrence after hepatic ischemia-reperfusion injury, linking negative regulation of inflammation to cancer outcomes. Understanding GO:0106015 therefore has broad implications for sepsis, cardiovascular disease, skin inflammation, neuroinflammation, and cancer [2,3,4,5,6,8]. This article synthesizes the current knowledge of the mechanisms, key genes, disease relevance, and research methods for studying negative regulation of inflammatory response to wounding.
negative regulation of inflammatory response to wounding At A Glance
| GO ID | GO:0106015 |
|---|---|
| GO term | negative regulation of inflammatory response to wounding |
| Ontology | biological_process |
| Synonym | none |
| Definition | Any process that stops, prevents, or reduces the frequency, rate or extent of the inflammatory response to wounding. |
| Major function | Resolution of inflammation after tissue injury; prevention of chronic inflammation and tissue damage. |
| Related processes | Inflammatory response, wound healing, immune cell activation, cytokine production, tissue repair. |
| Cellular context | Macrophages, fibroblasts, microglia, Th17 cells, endothelial cells. |
| Disease relevance | Sepsis, myocardial infarction, atopic dermatitis, hepatocellular carcinoma, neuroinflammation. |
What Is GO:0106015?
GO:0106015, negative regulation of inflammatory response to wounding, is a biological process defined as any process that stops, prevents, or reduces the frequency, rate or extent of the inflammatory response to wounding. In other words, it encompasses the molecular and cellular events that actively shut down or dampen inflammation after tissue injury, rather than merely the absence of inflammation. This term is distinct from general negative regulation of inflammatory response because it specifically refers to inflammation triggered by wounding, which includes physical, ischemic, or infectious injury.
Why Is negative regulation of inflammatory response to wounding Important in Cell Biology?
GO:0106015 is important because the inflammatory response to wounding must be tightly controlled to prevent collateral tissue damage and chronic disease. When negative regulation fails, persistent inflammation can lead to organ failure in sepsis, adverse cardiac remodeling after myocardial infarction, chronic skin inflammation in atopic dermatitis, and neuroinflammation [2,3,4,5,6]. Understanding the molecular brakes on inflammation provides therapeutic targets to promote resolution rather than merely suppressing inflammation.
• Prevents excessive tissue damage after injury by limiting the duration and intensity of inflammation.
• Promotes resolution and return to homeostasis, which is essential for proper wound healing.
• Dysregulation contributes to sepsis-associated organ dysfunction and mortality [2,4].
• Plays a role in cardiac repair after myocardial infarction; maladaptive fibroblast-myeloid axes worsen outcomes.
• Linked to chronic skin inflammation such as atopic dermatitis, where cytokine responses shift from acute to chronic.
• Involved in neuroinflammation and neurotoxicity via microglial activation.
• Impacts cancer recurrence after ischemia-reperfusion injury, as shown for FOXO1 in hepatocellular carcinoma.
• Provides targets for host-directed therapies that aim to resolve inflammation without full immunosuppression.
• Serves as a framework for CRISPR screens to identify novel negative regulators.
• Enables precision medicine approaches in primary atopic disorders and other inflammatory conditions.
What Happens During negative regulation of inflammatory response to wounding?
Initiation of the inflammatory response to wounding
In simple terms: When tissue is wounded, the body immediately sends immune cells and signals to the injury site.
Wounding triggers a rapid inflammatory response characterized by recruitment of neutrophils and monocytes, release of cytokines and chemokines, and activation of resident macrophages and fibroblasts. This initial phase is essential for pathogen clearance and debris removal, but it must be subsequently resolved to avoid chronic inflammation. Key signaling pathways such as NF-kB and MAPK are activated, and pattern recognition receptors detect damage-associated molecular patterns. In the heart, after myocardial infarction, this response is critical for repair but can become maladaptive if not properly regulated.
Negative regulation by intracellular checkpoints
In simple terms: Inside immune cells, specific proteins act as brakes to stop the inflammatory alarm.
Several intracellular proteins negatively regulate inflammatory signaling. Sufu limits sepsis-induced lung inflammation by regulating phase separation of TRAF6, thereby dampening NF-kB activation. SLAMF7 regulates the inflammatory response in macrophages during polymicrobial sepsis, and its modulation can reduce excessive cytokine production. FOXO1 regulates Th17 cell-mediated hepatocellular carcinoma recurrence after hepatic ischemia-reperfusion injury, acting as a checkpoint that influences the balance between inflammation and tumor immunity. These examples illustrate that negative regulation occurs at the level of signaling complexes, transcription factors, and cell-type-specific programs [2,4,8].
Epitranscriptomic and post-transcriptional control
In simple terms: Chemical marks on RNA can stabilize or destabilize messages that drive inflammation.
The m6A methyltransferase METTL3 stabilizes BATF mRNA in microglia, driving neuroinflammation and neurotoxicity. This indicates that epitranscriptomic modifications can either promote or, when opposed, negatively regulate inflammatory responses. Post-transcriptional control thus represents a layer of negative regulation that can be targeted to resolve inflammation.
Resolution phase and tissue repair
In simple terms: After the danger passes, the body actively switches off inflammation and starts repairing tissue.
Resolution of inflammation involves macrophage polarization from pro-inflammatory to pro-resolving phenotypes, clearance of apoptotic neutrophils, and release of specialized pro-resolving mediators. In cardiac repair, timely resolution prevents adverse remodeling and heart failure. Sipa1 drives a maladaptive fibroblast-myeloid axis after myocardial infarction, and targeting this axis may promote resolution. Thus, negative regulation of inflammatory response to wounding is an active, coordinated process that overlaps with tissue repair and regeneration [5,7].
Cell-type-specific regulation
In simple terms: Different cells have different brakes on inflammation, depending on the tissue.
Macrophages, fibroblasts, microglia, and Th17 cells each employ distinct negative regulatory mechanisms [2,5,6,8]. For example, SLAMF7 acts in macrophages during sepsis, Sipa1 in fibroblasts and myeloid cells after myocardial infarction, METTL3 in microglia, and FOXO1 in Th17 cells. This cell-type specificity means that therapeutic targeting must consider the cellular context to avoid unintended effects [2,5,6,8].
Key Genes Involved in GO:0106015 negative regulation of inflammatory response to wounding
The following genes and proteins have been experimentally implicated in negative regulation of inflammatory response to wounding or in related inflammatory resolution processes.
| Gene | Major Role | Research Relevance |
|---|---|---|
| SLAMF7 | Regulates macrophage inflammatory response during polymicrobial sepsis | Target for sepsis immunotherapy; KO and overexpression models in macrophages. |
| Sufu | Limits sepsis-induced lung inflammation via TRAF6 phase separation | Potential therapeutic target for acute lung injury; phase separation studies. |
| Sipa1 | Drives maladaptive fibroblast-myeloid axis after myocardial infarction | Target for cardiac repair; fibroblast-specific KO models. |
| METTL3 | m6A methyltransferase stabilizing BATF mRNA in microglia | Epitranscriptomic regulator of neuroinflammation; microglial KO models. |
| BATF | Transcription factor stabilized by METTL3 in microglia | Downstream effector of METTL3; target for neuroinflammation. |
| FOXO1 | Regulates Th17 cell-mediated HCC recurrence after hepatic I/R injury | Link between inflammation and cancer; T-cell-specific KO models. |
| TRAF6 | E3 ubiquitin ligase and signaling adaptor; phase separation regulated by Sufu | Central node in NF-kB activation; target for condensate-modulating drugs. |
| NF-kB | Master transcription factor of inflammatory response | Broad target but requires context-specific modulation. |
| IL-1beta | Pro-inflammatory cytokine | Biomarker and therapeutic target in sepsis and cardiac injury. |
| TNF-alpha | Pro-inflammatory cytokine | Biomarker and therapeutic target in chronic inflammation. |
| IL-6 | Pro-inflammatory cytokine | Biomarker in sepsis and neuroinflammation. |
| TGF-beta | Anti-inflammatory and pro-fibrotic cytokine | Plays dual roles in resolution and fibrosis. |
| IL-10 | Anti-inflammatory cytokine | Key mediator of negative regulation; overexpression models. |
| CCR2 | Chemokine receptor for monocyte recruitment | Target for modulating monocyte infiltration after injury. |
| CX3CR1 | Chemokine receptor on macrophages | Marker for resident macrophages; KO models for resolution. |
| ARG1 | Arginase 1, marker of pro-resolving macrophages | Functional readout of macrophage polarization. |
| MMP9 | Matrix metalloproteinase involved in tissue remodeling | Links inflammation resolution to wound healing. |
| VEGFA | Angiogenic factor in wound healing | Couples resolution to revascularization. |
How Is negative regulation of inflammatory response to wounding Regulated?
Negative regulation of inflammatory response to wounding is controlled at multiple levels, including intracellular signaling checkpoints, transcription factor activity, and epitranscriptomic modifications [2,4,6,8]. Sufu regulates phase separation of TRAF6 to limit NF-kB activation in sepsis-induced lung inflammation. METTL3 stabilizes BATF mRNA in microglia, and its activity can either promote or, when opposed, negatively regulate neuroinflammation. FOXO1 acts as a transcriptional regulator in Th17 cells, influencing hepatocellular carcinoma recurrence after ischemia-reperfusion injury. SLAMF7 modulates macrophage inflammatory responses in sepsis, and its expression level can determine the magnitude of cytokine release. Sipa1 drives a maladaptive fibroblast-myeloid axis after myocardial infarction, and targeting this axis may restore resolution. These regulatory mechanisms are often cell-type-specific and context-dependent, which has implications for therapeutic targeting [2,4,5,6,8].
negative regulation of inflammatory response to wounding and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| SLAMF7 | Polymicrobial sepsis; macrophage inflammation | Macrophage-specific KO and overexpression in mice; LPS challenge. |
| Sufu | Sepsis-induced lung inflammation | Lung epithelial or macrophage KO; cecal ligation and puncture model. |
| Sipa1 | Myocardial infarction; maladaptive fibroblast-myeloid axis | Fibroblast-specific KO; permanent LAD ligation in mice. |
| METTL3 | Neuroinflammation and neurotoxicity | Microglia-specific KO; LPS-induced neuroinflammation model. |
| FOXO1 | HCC recurrence after hepatic ischemia-reperfusion injury | T-cell-specific KO; hepatic I/R injury model in mice. |
Sepsis and acute organ injury
Sepsis is a life-threatening condition characterized by dysregulated host response to infection, and negative regulation of inflammatory response to wounding is critical to prevent organ damage [2,4]. SLAMF7 regulates macrophage inflammatory responses during polymicrobial sepsis, and its modulation can alter outcomes. Sufu limits sepsis-induced lung inflammation by regulating TRAF6 phase separation, suggesting that enhancing this checkpoint could be therapeutic. These studies highlight the importance of timely resolution in sepsis and acute lung injury [2,4].
Cardiovascular disease and myocardial infarction
After myocardial infarction, the inflammatory response is essential for repair but must be tightly regulated to avoid adverse remodeling [5,7]. Sipa1 drives a maladaptive fibroblast-myeloid axis after myocardial infarction, and targeting this axis may improve cardiac repair. Regulation of the inflammatory response in cardiac repair involves multiple cell types and mediators, and failure of negative regulation can lead to heart failure. Thus, GO:0106015 is directly relevant to cardiovascular outcomes [5,7].
Atopic dermatitis and chronic skin inflammation
Progression of acute-to-chronic atopic dermatitis is associated with quantitative rather than qualitative changes in cytokine responses, indicating that negative regulation of inflammation may be insufficient in chronic disease. Primary atopic disorders can be identified by clinical landmark-guided genomic sequencing, which may reveal mutations in genes that regulate inflammatory resolution. Understanding GO:0106015 in skin inflammation could lead to new therapies that promote resolution [1,3].
Neuroinflammation and neurodegeneration
METTL3 drives neuroinflammation and neurotoxicity through stabilizing BATF mRNA in microglia, demonstrating that epitranscriptomic control is critical for negative regulation of inflammatory response in the brain. Dysregulation of this process contributes to neuroinflammatory and neurodegenerative conditions. Targeting METTL3 or BATF may offer therapeutic avenues to dampen neuroinflammation.
Cancer and ischemia-reperfusion injury
FOXO1 regulates Th17 cell-mediated hepatocellular carcinoma recurrence after hepatic ischemia-reperfusion injury, linking negative regulation of inflammation to cancer recurrence. This suggests that modulating inflammatory resolution pathways could influence tumor outcomes after surgery or ischemia. The interplay between inflammation and cancer is complex, and GO:0106015 provides a framework to study these interactions.
From negative regulation of inflammatory response to wounding-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of a candidate gene enhance or impair resolution of inflammation after wounding? | Knockout (KO) in relevant cell type (e.g., macrophage, fibroblast) using CRISPR-Cas9. |
| Does a specific point mutation in a signaling protein alter its anti-inflammatory function? | Point mutation knock-in via CRISPR base editing or HDR. |
| Does tagging an endogenous protein with a fluorescent or affinity tag affect its localization during resolution? | Tagged knock-in (e.g., GFP, HA) using CRISPR-Cas9. |
| Does overexpression of a putative negative regulator suppress inflammation in vivo? | Overexpression via transgenic or viral delivery (e.g., AAV) in mouse models. |
| Which genes are essential for negative regulation of inflammatory response to wounding? | Genome-wide CRISPR knockout or activation library screening in macrophages or fibroblasts. |
| Can a candidate gene's expression be temporally controlled during resolution? | Inducible knock-in or degron knock-in models. |
How to Study the negative regulation of inflammatory response to wounding Process
| Method | What It Measures | Typical Application |
|---|---|---|
| CRISPR knockout screening | Loss-of-function effects on inflammatory resolution | Identify novel negative regulators in macrophages. |
| RNA-seq | Transcriptional changes during resolution | Profile gene expression after wounding stimuli. |
| m6A-seq | RNA methylation sites | Map METTL3-dependent modifications in microglia. |
| Proteomics | Protein abundance and modifications | Quantify NF-kB pathway components. |
| Proximity labeling | Protein-protein interactions and condensates | Study TRAF6 phase separation regulated by Sufu. |
| Live-cell imaging | Protein localization and dynamics | Visualize NF-kB nuclear translocation. |
| Cytokine assays | Secreted inflammatory mediators | Measure IL-6, TNF-alpha, IL-10 in macrophage cultures. |
| In vivo models | Organ-level inflammation and resolution | Myocardial infarction, sepsis, hepatic I/R [5,7,8]. |
CRISPR screening for negative regulators
Genome-wide CRISPR knockout or activation screens in macrophages or fibroblasts can identify genes whose loss or overexpression alters inflammatory cytokine production after wounding stimuli. Such screens have been used to discover regulators of primary atopic disorders and can be adapted to resolution biology. Hits can be validated in secondary assays and in vivo models.
Transcriptomic and epitranscriptomic profiling
RNA-seq and m6A-seq can reveal changes in gene expression and RNA modifications during resolution of inflammation. METTL3-dependent m6A modifications stabilize BATF mRNA in microglia, and similar approaches can identify other epitranscriptomic regulators. Single-cell RNA-seq can resolve cell-type-specific programs in heterogeneous tissues.
Proteomic and phosphoproteomic analysis
Mass spectrometry-based proteomics can quantify signaling changes during negative regulation, including phosphorylation of NF-kB and MAPK pathways [4,7]. Phase separation of TRAF6 regulated by Sufu can be studied using proximity labeling and condensate purification. These methods provide mechanistic insights into how checkpoints operate [4,7].
Imaging and functional assays
Live-cell imaging of fluorescently tagged proteins (e.g., TRAF6, NF-kB) can visualize condensate formation and nuclear translocation during resolution. Macrophage efferocytosis and cytokine secretion assays quantify functional resolution. In vivo imaging in mouse models of myocardial infarction or sepsis can assess resolution dynamics [5,7].
How CRISPR Can Be Used to Study GO:0106015 negative regulation of inflammatory response to wounding
Knockout
CRISPR-Cas9 knockout of candidate genes in macrophages, fibroblasts, or microglia can test whether they are required for negative regulation of inflammatory response to wounding [2,4,5,6,8]. For example, SLAMF7 knockout macrophages show altered cytokine responses in sepsis models. Sufu knockout exacerbates lung inflammation, confirming its negative regulatory role. Cell-type-specific KO in mice (e.g., fibroblast-specific Sipa1) can reveal in vivo functions.
Point Mutation
Point mutations can dissect specific residues required for anti-inflammatory function, such as phosphorylation sites or ubiquitination sites in TRAF6 or FOXO1 [4,8]. CRISPR base editing or HDR can introduce these mutations at endogenous loci to study their effects on resolution [4,8]. Such models are valuable for understanding mechanistic details without confounding effects of protein loss [4,8].
Knock-in
Knock-in of tags (e.g., GFP, HA) or reporter genes allows visualization and purification of endogenous proteins during resolution [4,6]. For example, tagging TRAF6 can reveal its phase separation dynamics. Knock-in of m6A reader domains or mutant METTL3 can probe epitranscriptomic regulation. These models enable precise tracking of protein behavior in live cells and tissues [4,6].
Overexpression
Overexpression of putative negative regulators (e.g., IL-10, Sufu) via transgenic or viral vectors can test whether increasing their levels suppresses inflammation and improves outcomes [4,7]. Overexpression models are useful for gain-of-function studies and for validating therapeutic potential [4,7]. In vivo overexpression in mouse models of myocardial infarction or sepsis can assess benefit [4,5,7].
How EDITGENE Supports negative regulation of inflammatory response to wounding Research
Researchers studying negative regulation of inflammatory response to wounding-related genes often need to determine whether a candidate gene is causally involved in resolution or merely a bystander. EDITGENE provides the tools and services to build precise CRISPR models and to screen for novel regulators, enabling rigorous causal testing in relevant cell types and animal models.
Contact EDITGENE today to design your custom CRISPR model for negative regulation of inflammatory response to wounding research.
Frequently Asked Questions About negative regulation of inflammatory response to wounding
What is GO:0106015?
GO:0106015 is the Gene Ontology term for negative regulation of inflammatory response to wounding, defined as any process that stops, prevents, or reduces the frequency, rate or extent of the inflammatory response to wounding.
What genes are involved in negative regulation of inflammatory response to wounding?
Genes experimentally implicated include SLAMF7, Sufu, Sipa1, METTL3, BATF, and FOXO1, among others [2,4,5,6,8].
How does negative regulation of inflammation after wounding work?
It involves intracellular checkpoints (e.g., Sufu-TRAF6), epitranscriptomic control (e.g., METTL3-BATF), and cell-type-specific programs that resolve inflammation and promote tissue repair [4,6,7].
Why is negative regulation of inflammatory response to wounding important in sepsis?
In sepsis, failure to resolve inflammation leads to organ damage; SLAMF7 and Sufu have been shown to modulate macrophage and lung inflammation in sepsis models [2,4].
What is the role of METTL3 in neuroinflammation?
METTL3 stabilizes BATF mRNA in microglia, driving neuroinflammation and neurotoxicity, indicating that epitranscriptomic modifications regulate this process.
How can CRISPR be used to study GO:0106015?
CRISPR knockout, point mutation, knock-in, and overexpression models allow causal testing of candidate genes in macrophages, fibroblasts, and microglia [2,4,5,6,8].
What diseases are linked to defective negative regulation of inflammatory response to wounding?
Sepsis, myocardial infarction, atopic dermatitis, hepatocellular carcinoma recurrence, and neuroinflammation are associated with dysregulation of this process [2,3,4,5,6,8].
What is the role of FOXO1 in inflammation and cancer?
FOXO1 regulates Th17 cell-mediated hepatocellular carcinoma recurrence after hepatic ischemia-reperfusion injury, linking inflammatory resolution to cancer outcomes.
How does Sipa1 affect cardiac repair after myocardial infarction?
Sipa1 drives a maladaptive fibroblast-myeloid axis after myocardial infarction, and targeting this axis may improve repair.
What research methods are used to study negative regulation of inflammatory response to wounding?
Methods include CRISPR screens, RNA-seq, m6A-seq, proteomics, live-cell imaging, and in vivo models of sepsis, myocardial infarction, and hepatic I/R [1,4,5,6,7,8].
Conclusion
GO:0106015, negative regulation of inflammatory response to wounding, is a critical biological process that ensures inflammation is resolved after injury. Key genes such as SLAMF7, Sufu, Sipa1, METTL3, BATF, and FOXO1 have been shown to modulate this process in sepsis, cardiac injury, neuroinflammation, and cancer [2,4,5,6,8]. Understanding these mechanisms offers therapeutic opportunities to promote resolution without compromising host defense. EDITGENE supports this research with comprehensive CRISPR modeling and screening services.
References
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