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Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE174676 | GEO | 2024/05/01

REPOSITORIES: GEO

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Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 2]

Project description:Dermal macrophages (Macs) are essential for the timely resolution of staphylococcal skin infections. However the cell intrinsic pathways and microenvironmental cues that mediate this are unclear. Here we analyzed a strictly intradermal ear infection model with Staphylococcus aureus (S. aureus) to explore immunometabolic regulation.

2024-05-01 | GSE174675 | GEO

Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 1]

2024-05-01 | GSE174674 | GEO

Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection

Project description:Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection

| PRJNA731042 | ENA

Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 1]

Project description:Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 1]

| PRJNA731048 | ENA

Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 2]

Project description:Metabolic rewiring tunes dermal macrophages in staphylococcal skin infection [RNA-seq dataset 2]

| PRJNA731049 | ENA

Resident macrophages acquire innate immune memory in staphylococcal skin infection.

Project description:Staphylococcus aureus (S. aureus) is a common colonizer of healthy skin and mucous membranes. At the same time, S. aureus is the most frequent cause of skin and soft tissue infections. Dermal macrophages (Mφ) are critical for the coordinated defense against invading S. aureus, yet they have a limited life span with replacement by bone marrow derived monocytes. It is currently poorly understood whether localized S. aureus skin infections persistently alter the resident Mφ subset composition and resistance to a subsequent infection. In a strictly dermal infection model we found that mice, which were previously infected with S. aureus, showed faster monocyte recruitment, increased bacterial killing and improved healing upon a secondary infection. However, skin infection decreased Mφ half-life, thereby limiting the duration of memory. In summary, resident dermal Mφ are programmed locally, independently of bone marrow-derived monocytes during staphylococcal skin infection leading to transiently increased resistance against a second infection.

| S-EPMC7343389 | biostudies-literature

Metabolic rewiring of macrophages by epidermal-derived lactate promotes sterile inflammation in the murine skin

Project description:Dysregulated macrophage responses and changes in tissue metabolism are hallmarks of chronic inflammation in the skin. However, the metabolic cues that direct and support macrophage functions in the skin are poorly understood. Here, we show that during sterile skin inflammation, the epidermis and macrophages uniquely depend on glycolysis and the TCA cycle, respectively. This compartmentalisation is initiated by ROS-induced HIF-1 stabilization leading to enhanced glycolysis in the epidermis. The end-product of glycolysis, lactate, is then exported by epithelial cells and utilized by the dermal macrophages to induce their M2-like fates through NF-B pathway activation. Additionally, we show that psoriatic skin disorder is also driven by such lactate metabolite-mediated crosstalk between the epidermis and macrophages. Notably, small-molecule inhibitors of lactate transport in this setting attenuate sterile inflammation and psoriasis disease burden, and suppress M2-like fate acquisition in dermal macrophages. Our study identifies an essential role for the metabolite lactate in regulating macrophage responses to inflammation, which may be effectively targeted to treat inflammatory skin disorders such as psoriasis.

| S-SCDT-10_1038-S44318-024-00039-Y | biostudies-other

Metabolic rewiring of macrophages by epidermal-derived lactate promotes sterile inflammation in the murine skin.

Project description:Dysregulated macrophage responses and changes in tissue metabolism are hallmarks of chronic inflammation in the skin. However, the metabolic cues that direct and support macrophage functions in the skin are poorly understood. Here, we show that during sterile skin inflammation, the epidermis and macrophages uniquely depend on glycolysis and the TCA cycle, respectively. This compartmentalisation is initiated by ROS-induced HIF-1α stabilization leading to enhanced glycolysis in the epidermis. The end-product of glycolysis, lactate, is then exported by epithelial cells and utilized by the dermal macrophages to induce their M2-like fates through NF-κB pathway activation. In addition, we show that psoriatic skin disorder is also driven by such lactate metabolite-mediated crosstalk between the epidermis and macrophages. Notably, small-molecule inhibitors of lactate transport in this setting attenuate sterile inflammation and psoriasis disease burden, and suppress M2-like fate acquisition in dermal macrophages. Our study identifies an essential role for the metabolite lactate in regulating macrophage responses to inflammation, which may be effectively targeted to treat inflammatory skin disorders such as psoriasis.

| S-EPMC10987662 | biostudies-literature

Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-18 | GSE184684 | GEO

The infection characteristics and autophagy defect of dermal macrophages in STZ-induced diabetic rats skin wound Staphylococcus aureus infection model.

Project description:IntroductionDiabetic foot ulcer infection (DFI) is an infectious disease of the skin and soft tissue in diabetics notorious for making rapid progress and being hard to cure. Staphylococcus aureus (S. aureus), most frequently detected in DFI, recently was suggested as an intracellular pathogen that can invade and survive within mammalian host cells. Autophagy in macrophages plays a vital immune role in combating intracellular pathogens through bacterial destruction, but there is a lack of empirical research about the infection characteristics and autophagy in diabetic skin infection.MethodsHere, we used streptozotocin-induced Sprague Dawley rats as a diabetic skin wound model to examine the S. aureus clearance ability and wound healing in vitro. Western blot and immunofluorescence staining were used to evaluate the autophagic flux of the macrophages in diabetic rats dermis, even with S. aureus infection.ResultsWe demonstrated that infections in diabetic rats appeared more severe and more invasive with weakened pathogen clearance ability of the host immune system, which coincided with the suppressed autophagic flux in dermal macrophages, featured by a significant increase in endogenous LC3II/I and in p62.ConclusionsOur results first provided convincing evidence that autophagy of macrophages was dysfunctional in diabetes, especially after being infected by S. aureus, which weakens the intracellular killing of S. aureus, potentially worsens the infections, and accelerates the infection spread in the diabetic rat model. Further understanding of the special immune crosstalk between diabetes host and S. aureus infection through autophagic factors will help to explain the complex clinical phenomenon and guarantee the development of effective therapies for diabetic foot infections.

| S-EPMC8589369 | biostudies-literature

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