Pseudomonas aeruginosa outer membrane vesicles ameliorates lung ischemia–reperfusion injury by regulating the balance of regulatory T cells and Th17 cells through Tim-3 and TLR4/NF-κB pathway

Liu, Bo; Ding, Fengxia; Cao, Ding; Liu, Jiang; Wang, Yaping

doi:10.1007/s00011-021-01483-w

Cited by 8 publications

(6 citation statements)

References 34 publications

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“…OMVs from X-ray-irradiated P. aeruginosa alleviate pulmonary edema infected by P. aeruginosa Pseudomonas aeruginosa can release OMVs under natural or stressful conditions such as antibiotic treatment (1,15,16,25). There are reports that OMVs have both pro-inflammatory and antiinflammatory effects, which is related to different P. aeruginosa strains and the conditions under which OMVs are produced (13,14,(26)(27)(28). Our previous study found that X-ray irradiation can induce the release of complete and uniform OMVs from P. aeruginosa, but their activity has never been studied.…”

Section: Resultsmentioning

confidence: 99%

“…For example, OMVs derived from P. aeruginosa cause pneumonia by activating macrophages and epithelial cells (12). In contrast, OMVs from P. aeruginosa ameliorate ischemia-reperfusion-induced lung injury by regulating the balance of regulatory T cells and Th17 cells (13). These different or even opposite functions of OMVs are likely to depend on the components of the specific OMVs, which in turn depend on the bacterial strains that produce OMVs and the conditions that induce the production of OMVs (14)(15)(16)(17).…”

mentioning

confidence: 99%

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Outer membrane vesicles from X‐ray‐irradiated Pseudomonas aeruginosa alleviate lung injury caused by P. aeruginosa infection‐mediated sepsis

Bi,

Qin,

Huang

et al. 2024

APMIS

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Pseudomonas aeruginosa infection causes pneumonia and sepsis. Previous research found that X‐ray radiation can induce P. aeruginosa to release outer membrane vesicles (OMVs) of relatively consistent sizes. This study found that OMVs derived from X‐ray‐irradiated P. aeruginosa can significantly inhibit lung leakage, inflammatory cell infiltrating into lung, and the production of pro‐inflammatory cytokines, IL‐1β and TNFα caused by P. aeruginosa infection under preventive and therapeutic administration conditions. Under the same conditions, OMVs also significantly alleviated pathological characteristics of lung injury, including pulmonary edema, pulmonary hemorrhage, and alveolar wall thickening. OMVs also significantly reduced bacterial burdens in peritoneal cavity, accompanied by a reduction in the number of viable bacteria capable of forming bacterial colonies. Pretreating macrophages and neutrophils with OMVs enhances their bactericidal ability. When bacteria were cocultured with treated cells, the number of viable bacteria capable of forming bacterial colonies was significantly reduced. OMVs themselves have not been shown to cause any lung injury or affect bacterial viability. Therefore, OMVs derived from X‐ray‐irradiated P. aeruginosa may not only be applied in prevention and treatment of diseases associated with P. aeruginosa infection, but also served as an excellent vaccine development platform.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Outer membrane vesicles from X‐ray‐irradiated Pseudomonas aeruginosa alleviate lung injury caused by P. aeruginosa infection‐mediated sepsis

Bi,

Qin,

Huang

et al. 2024

APMIS

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“…Abnormal Tim-3 expression can be detected on the surface of renal parenchymal cells or immune cells in IgA nephropathy [43], lupus nephritis [44], diabetic nephropathy [45], renal tumor [46], and renal transplantation rejection [47]. Tim-3 also participates in the pathogenesis of liver IRI [26,38,40], brain IRI [48,49], and lung IRI [21]. The activation of the Gal-9/Tim-3 signaling pathway has a protective effect on liver IRI via negative regulation [38].…”

Section: Discussionmentioning

confidence: 99%

“…Similar to programmed death-1(PD-1), T immunoglobulin and mucin molecule 3 (Tim-3) is a negative regulatory molecule that is important for T cell tolerance [20]. Tim-3 is expressed on the surface of several immune cells, such as Th1, Th17, Treg cells, and macrophages [21].Among several identi ed ligands of Tim-3, Galectin-9 (Gal-9) is the unique natural ligand of Tim-3 [22]. The Gal-9/Tim-3 signaling pathway plays an important role in modulating immune responses and diseases, such as autoimmune encephalomyelitis, diabetes, in ammatory bowel disease, rheumatoid arthritis, multiple sclerosis, and bronchial asthma [20].…”

Section: Introductionmentioning

confidence: 99%

Gal-9/Tim-3 signaling pathway activation suppresses the generation of Th17 cells and promotes the induction of Foxp3+regulatory T cells in renal ischemia-reperfusion injury

Tao

WANG

Feng

et al. 2022

Preprint

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CD4+T cells mediate the pathogenesis of renal ischemia-reperfusion injury (IRI). Emerging research suggests that a Th17/regulatory T cell (Treg) imbalance plays a pivotal role in the development of renal IRI. The recently identified negative checkpoint T cell immunoglobulin domain and mucin domain family 3 (Tim-3) inhibits the immune response by binding to its ligand, galectin-9 (Gal-9). However, the role of the Gal-9/Tim-3 signaling pathway in the regulation of CD4+T cell subsets in renal IRI remains unclear. In this study, the effect of the Gal-9/Tim-3 signaling pathway on Th17/Treg subsets in renal IRI was investigated using a mouse model. Renal IRI induced the expression of Gal-9 in renal tubular epithelial cells and increased the percentages of Tim-3+Th17 cells and Tim-3+Foxp3+Treg cells in the IR kidneys. The administration of rAAV9-Gal-9 suppressed kidney inflammation, reduced the mortality of mice with renal IRI, increased Foxp3+Treg cells, and reduced Th17 cells. In contrast, the blockade of Tim-3 in vivo with an anti-Tim-3 mAb aggravated renal inflammation, decreased Foxp3+Treg cells, and promoted Th17 cells. Thus, Gal-9/Tim-3 signaling pathway activation may protect against renal IRI by inhibiting Th17 cell production and inducing Foxp3+Treg cell expansion. Our study suggests that the Gal-9/Tim-3 signaling pathway might become a target of immunotherapy in renal IRI.

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“…In ischemia–reperfusion injury, bEV preconditioning attenuated tissue injury and reduced the total protein concentration. This protective effect was achieved by regulating the balance of regulatory T cells and Th17 cells through the Tim-3 and TLR4/NF-κB pathways ( 67 ).…”

Section: Evs In Specific Systems and Diseasesmentioning

confidence: 99%

Extracellular Vesicles: Recent Insights Into the Interaction Between Host and Pathogenic Bacteria

et al. 2022

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Extracellular vesicles (EVs) are nanosized lipid particles released by virtually every living cell. EVs carry bioactive molecules, shuttle from cells to cells and transduce signals, regulating cell growth and metabolism. Pathogenic bacteria can cause serious infections via a wide range of strategies, and host immune systems also develop extremely complex adaptations to counteract bacterial infections. As notable carriers, EVs take part in the interaction between the host and bacteria in several approaches. For host cells, several strategies have been developed to resist bacteria via EVs, including expelling damaged membranes and bacteria, neutralizing toxins, triggering innate immune responses and provoking adaptive immune responses in nearly the whole body. For bacteria, EVs function as vehicles to deliver toxins and contribute to immune escape. Due to their crucial functions, EVs have great application potential in vaccines, diagnosis and treatments. In the present review, we highlight the most recent advances, application potential and remaining challenges in understanding EVs in the interaction between the host and bacteria.

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Pseudomonas aeruginosa outer membrane vesicles ameliorates lung ischemia–reperfusion injury by regulating the balance of regulatory T cells and Th17 cells through Tim-3 and TLR4/NF-κB pathway

Cited by 8 publications

References 34 publications

Outer membrane vesicles from X‐ray‐irradiated Pseudomonas aeruginosa alleviate lung injury caused by P. aeruginosa infection‐mediated sepsis

Outer membrane vesicles from X‐ray‐irradiated Pseudomonas aeruginosa alleviate lung injury caused by P. aeruginosa infection‐mediated sepsis

Gal-9/Tim-3 signaling pathway activation suppresses the generation of Th17 cells and promotes the induction of Foxp3+regulatory T cells in renal ischemia-reperfusion injury

Extracellular Vesicles: Recent Insights Into the Interaction Between Host and Pathogenic Bacteria

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