Inflammatory monocytes promote granuloma control of Yersinia infection

Sorobetea, Daniel; Matsuda, Rina; Peterson, Stefan T.; Grayczyk, James P.; Rao, Indira; Krespan, Elise; Lanza, Matthew; Assenmacher, Charles-Antoine; Mack, Matthias; Beiting, Daniel P.; Radælli, Enrico; Brodsky, Igor E.

doi:10.1038/s41564-023-01338-6

Cited by 5 publications

(15 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, while Tnfr1 -/mice formed similar numbers of macroscopic intestinal lesions as wild-type (WT) mice (Fig. S1A), histopathologic analyses revealed that intestinal lesions in Tnfr1 -/mice displayed a disorganized appearance and contained a central area of tissue necrosis that was strikingly similar to lesions that we recently described in monocyte-deficient mice 25 , (Fig. 1A).…”

Section: Tnfr1 Is Required For Organized Pyogranuloma Formation and R...supporting

confidence: 69%

“…We recently identified the formation of pyogranulomas (PG) in the murine intestinal mucosa during acute Yersinia pseudotuberculosis (Yp) infection, wherein inflammatory monocytes were required for neutrophil activation, maintenance of PG architecture, and bacterial clearance 25 . Nonetheless, the monocyte-derived signals required for the function and maintenance of these intestinal PG are unknown.…”

Section: Tnfr1 Is Required For Organized Pyogranuloma Formation and R...mentioning

confidence: 99%

“…The enteropathogenic Yersiniae, which also include Y. pseudotuberculosis (Yp) and Y. enterocolitica, colonize the intestinal mucosa and lymphoid tissues of both mice and humans, triggering formation of pyogranulomas (PG) that are composed of extracellular bacterial colonies in close association with neutrophils, bordered in turn by monocytes and macrophages [18][19][20][21][22][23][24][25] . We recently demonstrated that PG containing viable bacteria, inflammatory monocytes, and neutrophils form along the length of the gastrointestinal tract early following oral Yp infection 25 . PG form in response to the activity of Yersinia Outer Proteins (Yops), which are injected into host cells through the Yersinia type III secretion system and block essential antimicrobial functions [25][26][27] .…”

Section: Introductionmentioning

confidence: 99%

“…We recently demonstrated that PG containing viable bacteria, inflammatory monocytes, and neutrophils form along the length of the gastrointestinal tract early following oral Yp infection 25 . PG form in response to the activity of Yersinia Outer Proteins (Yops), which are injected into host cells through the Yersinia type III secretion system and block essential antimicrobial functions [25][26][27] . We further demonstrated that inflammatory monocytes were critical for maintenance of PG architecture and enabling neutrophils to overcome the activity of Yp virulence factors that block host phagocytosis and oxidative burst 25 .…”

Section: Introductionmentioning

confidence: 99%

“…PG form in response to the activity of Yersinia Outer Proteins (Yops), which are injected into host cells through the Yersinia type III secretion system and block essential antimicrobial functions [25][26][27] . We further demonstrated that inflammatory monocytes were critical for maintenance of PG architecture and enabling neutrophils to overcome the activity of Yp virulence factors that block host phagocytosis and oxidative burst 25 . However, the mechanisms by which inflammatory monocytes mediate anti-Yersinia host defense are unclear.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

A TNF-IL-1 circuit controlsYersiniawithin intestinal granulomas

Matsuda

Sorobetea

Zhang

et al. 2023

Preprint

Self Cite

View full text Add to dashboard Cite

Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. Yersinia pseudotuberculosis colonizes the intestinal mucosa and induces recruitment of neutrophils and inflammatory monocytes into organized immune structures termed pyogranulomas that control the bacterial infection. Inflammatory monocytes are essential for control and clearance of Yersinia within intestinal pyogranulomas, but how monocytes mediate Yersinia restriction is poorly understood. Here, we demonstrate that TNF signaling in monocytes is required for bacterial containment following enteric Yersinia infection. We further show that monocyte-intrinsic TNFR1 signaling drives production of monocyte-derived interleukin-1 (IL-1), which signals through IL-1 receptor on non-hematopoietic cells to enable pyogranuloma-mediated control of Yersinia infection. Altogether, our work reveals a monocyte-intrinsic TNF-IL-1 collaborative circuit as a crucial driver of intestinal granuloma function, and defines the cellular target of TNF signaling that restricts intestinal Yersinia infection.

show abstract

Section: Tnfr1 Is Required For Organized Pyogranuloma Formation and R...supporting

confidence: 69%

Section: Tnfr1 Is Required For Organized Pyogranuloma Formation and R...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A TNF-IL-1 circuit controlsYersiniawithin intestinal granulomas

Matsuda

Sorobetea

Zhang

et al. 2023

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

Bioinspired Asymmetric Double-Layer Dressings for Stepwise Treatment of Hemorrhagic Wounds

Yang,

Jia,

Wang

et al. 2024

ACS Materials Lett.

View full text Add to dashboard Cite

Although various dressings have been developed for wound healing, ideal dressings are still lacking to meet the requirements of coordinated hemostasis and angiogenesis for the management of hemorrhagic wounds. Herein, inspired by the gradient structure of natural skin, we propose a novel asymmetric double-layer dressing (BSP-PNS@CMCS) with spatiotemporally controllable functions of hemostasis and angiogenesis for the stepwise treatment of hemorrhagic wounds. The BSP-PNS@CMCS dressings are designed with an inner layer of Bletilla striata polysaccharide (BSP) sponges for initial hemostasis and an outer dense layer of carboxymethyl chitosan (CMCS) hydrogels loaded with panax notoginseng saponines (PNS) for angiogenesis during subsequent tissue reconstruction. Through in vivo experiments, we have demonstrated that the BSP-PNS@CMCS dressings could not only significantly reduce bleeding in rat liver-puncture hemorrhage wounds but also accelerate wound closure by suppressing the inflammatory response, promoting angiogenesis and collagen deposition in infected skin wounds of rats. In vitro and in vivo results indicate that such asymmetric double-layer BSP-PNS@CMCS dressing could be a prospective candidate for the stepwise treatment of hemorrhagic wounds, which also provides an effective strategy for other tissue repair applications.

show abstract

A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas

Matsuda,

Sorobetea,

Zhang

et al. 2024

Journal of Experimental Medicine

View full text Add to dashboard Cite

Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. We previously reported that Yersinia pseudotuberculosis colonizes the intestinal mucosa and induces the recruitment of neutrophils and inflammatory monocytes into organized immune structures termed pyogranulomas (PG) that control Yersinia infection. Inflammatory monocytes are essential for the control and clearance of Yersinia within intestinal PG, but how monocytes mediate Yersinia restriction is poorly understood. Here, we demonstrate that TNF signaling in monocytes is required for bacterial containment following enteric Yersinia infection. We further show that monocyte-intrinsic TNFR1 signaling drives the production of monocyte-derived interleukin-1 (IL-1), which signals through IL-1 receptors on non-hematopoietic cells to enable PG-mediated control of intestinal Yersinia infection. Altogether, our work reveals a monocyte-intrinsic TNF-IL-1 collaborative inflammatory circuit that restricts intestinal Yersinia infection.

show abstract

Inflammatory monocytes promote granuloma control of Yersinia infection

Cited by 5 publications

References 63 publications

A TNF-IL-1 circuit controlsYersiniawithin intestinal granulomas

A TNF-IL-1 circuit controlsYersiniawithin intestinal granulomas

Bioinspired Asymmetric Double-Layer Dressings for Stepwise Treatment of Hemorrhagic Wounds

A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas

Contact Info

Product

Resources

About