Extracellular vesicles participate in the pathogenesis of sepsis

Tian, Chang; Wang, Ke; Zhao, Min; Cong, Shan; Di, Xin; Li, Ranwei

doi:10.3389/fcimb.2022.1018692

Cited by 13 publications

(21 citation statements)

References 212 publications

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“…cardiovascular disease; Dickhout & Koenen, 2018) or acutely (e.g. sepsis; Tian et al., 2022) elevated microvesicles in young and old participants and in both sexes.…”

Section: Discussionmentioning

confidence: 99%

Cerebral uptake of microvesicles occurs in normocapnic but not hypocapnic passive hyperthermia in young healthy male adults

Parikh,

Shepley,

Tymko

et al. 2023

The Journal of Physiology

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Passive hyperthermia causes cerebral hypoperfusion primarily from heat‐induced respiratory alkalosis. However, despite the cerebral hypoperfusion, it is possible that the mild alkalosis might help to attenuate cerebral inflammation. In this study, the cerebral exchange of extracellular vesicles (microvesicles), which are known to elicit pro‐inflammatory responses when released in conditions of stress, were examined in hyperthermia with and without respiratory alkalosis. Ten healthy male adults were heated passively, using a warm water‐perfused suit, up to core temperature + 2°C. Blood samples were taken from the radial artery and internal jugular bulb. Microvesicle concentrations were determined in platelet‐poor plasma via cells expressing CD62E (activated endothelial cells), CD31+/CD42b− (apoptotic endothelial cells), CD14 (monocytes) and CD45 (pan‐leucocytes). Cerebral blood flow was measured via duplex ultrasound of the internal carotid and vertebral arteries to determine cerebral exchange kinetics. From baseline to poikilocapnic (alkalotic) hyperthermia, there was no change in microvesicle concentration from any cell origin measured (P‐values all >0.05). However, when blood CO2 tension was normalized to baseline levels in hyperthermia, there was a marked increase in cerebral uptake of microvesicles expressing CD62E (P = 0.028), CD31+/CD42b− (P = 0.003) and CD14 (P = 0.031) compared with baseline, corresponding to large increases in arterial but not jugular venous concentrations. In a subset of seven participants who underwent hypercapnia and hypocapnia in the absence of heating, there was no change in microvesicle concentrations or cerebral exchange, suggesting that hyperthermia potentiated the CO2/pH‐mediated cerebral uptake of microvesicles. These data provide insight into a potential beneficial role of respiratory alkalosis in heat stress. imageKey points The hyperthermia‐induced hyperventilatory response is observed in most humans, despite causing potentially harmful reductions in cerebral blood flow. We tested the hypothesis that the respiratory‐induced alkalosis is associated with lower circulating microvesicle concentrations, specifically in the brain, despite the reductions in blood flow. At core temperature + 2°C with respiratory alkalosis, microvesicles derived from endothelial cells, monocytes and leucocytes were at concentrations similar to baseline in the arterial and cerebral venous circulation, with no changes in cross‐brain microvesicle kinetics. However, when core temperature was increased by 2°C with CO2/pH normalized to resting levels, there was a marked cerebral uptake of microvesicles derived from endothelial cells and monocytes. The CO2/pH‐mediated alteration in cerebral microvesicle uptake occurred only in hyperthermia. These new findings suggest that the heat‐induced hyperventilatory response might serve a beneficial role by preventing potentially inflammatory microvesicle uptake in the brain.

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“…cardiovascular disease; Dickhout & Koenen, 2018) or acutely (e.g. sepsis; Tian et al., 2022) elevated microvesicles in young and old participants and in both sexes.…”

Section: Discussionmentioning

confidence: 99%

Cerebral uptake of microvesicles occurs in normocapnic but not hypocapnic passive hyperthermia in young healthy male adults

Parikh,

Shepley,

Tymko

et al. 2023

The Journal of Physiology

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“…Regarding their role in immunology, EVs act in innate and adaptative immune systems. In the innate, their major role has been described as pro-inflammatory mediators secreted by activated macrophages, neutrophilic granulocytes, NK cells, or mast cells in scenarios such as infection ( 45 – 47 ), sepsis ( 47 – 49 ), or chronic inflammation ( 50 ). In addition, an anti-inflammatory role also has been described through TGF-β secretion or regulation of endogenous lipid mediators ( 51 ).…”

Section: Biological Function and Role In Immunologymentioning

confidence: 99%

Physiopathological role of extracellular vesicles in alloimmunity and kidney transplantation and their use as biomarkers

Cuadrado-Payán,

Ramírez-Bajo,

Bañón-Maneus

et al. 2023

Front. Immunol.

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Antibody-mediated rejection is the leading cause of kidney graft dysfunction. The process of diagnosing it requires the performance of an invasive biopsy and subsequent histological examination. Early and sensitive biomarkers of graft damage and alloimmunity are needed to identify graft injury and eventually limit the need for a kidney biopsy. Moreover, other scenarios such as delayed graft function or interstitial fibrosis and tubular atrophy face the same problem. In recent years, interest has grown around extracellular vesicles, specifically exosomes actively secreted by immune cells, which are intercellular communicators and have shown biological significance. This review presents their potential as biomarkers in kidney transplantation and alloimmunity.

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“…Removal of exosome PD-L1 can inhibit the growth of tumor cells and has a synergistic anti-tumor effect with PD-L1 antibody ( 50 ). EVs are involved in the formation and organ function impairment of sepsis ( 51 ), and β2 integrin and PD-L2 expression are significantly increased in exosomes of sepsis patients ( 52 ). However, whether expression of PD-1 pathway molecules in the exosome has a direct regulatory effect on immune cells associated with sepsis and the specific mechanism remains to be investigated.…”

Section: Problems and Prospectsmentioning

confidence: 99%

Regulatory role of the programmed cell death 1 signaling pathway in sepsis induced immunosuppression

Zhong

Yin

2023

Front. Immunol.

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Sepsis is a multiple organ dysfunction syndrome caused by the host’s immune response to infection, with extremely high incidence and mortality. Immunosuppression is an essential pathophysiological alteration that influences the clinical treatment and prognosis of sepsis. Recent studies have suggested that the programmed cell death 1 signaling pathway is involved in the formation of immunosuppression in sepsis. In this review, we systematically present the mechanisms of immune dysregulation in sepsis and elucidate the expression and regulatory effects of the programmed cell death 1 signaling pathway on immune cells associated with sepsis. We then specify current research developments and prospects for the application of the programmed cell death 1 signaling pathway in immunomodulatory therapy for sepsis. Several open questions and future research are discussed at the end.

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Extracellular vesicles participate in the pathogenesis of sepsis

Cited by 13 publications

References 212 publications

Cerebral uptake of microvesicles occurs in normocapnic but not hypocapnic passive hyperthermia in young healthy male adults

Cerebral uptake of microvesicles occurs in normocapnic but not hypocapnic passive hyperthermia in young healthy male adults

Physiopathological role of extracellular vesicles in alloimmunity and kidney transplantation and their use as biomarkers

Regulatory role of the programmed cell death 1 signaling pathway in sepsis induced immunosuppression

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