HMGB1-TLR4-IL-23-IL-17A axis accelerates renal ischemia-reperfusion injury via the recruitment and migration of neutrophils

Zhang, Jiong; Li, Qing; Zou, Yurong; Wu, Shuizhu; Lu, Xiaoyan; Li, Guisen; Wang, Jia

doi:10.1016/j.intimp.2021.107433

Cited by 30 publications

(19 citation statements)

References 19 publications

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“…These outcomes indicate that the expression of chemoattractant receptors increases in the inflammatory state and aggravates the inflammatory response through various mechanisms. Moreover, the high mobility group protein B1 (HMGB1)‐mediated neutrophil migration has been reported to be critical for defending against infection 31,32 …”

Section: Discussionmentioning

confidence: 99%

A novel computer vision‐based assessment of neutrophil chemotaxis in patients with severe infection

et al. 2021

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Objectives To evaluate the value of chemotactic function of neutrophils in patients with severe infections. Methods A computer vision‐based cellular chemotaxis analysis platform was established for the dynamic assessment of neutrophil chemotaxis. Fifty‐three patients in the intensive care unit were eligible for the study. In parallel, 142 healthy volunteers were recruited to detect and establish the normal values for chemotactic function. Four chemotactic function indicators were determined–chemotaxis distance (CD), chemotaxis cell ratio (CCR), chemotaxis index (CI) and maximum speed of chemotaxis (Vmax). The chemotaxis function scores (CFS) were calculated for further correlation analysis with clinical data. Results The normal ranges of indicators were established as CD ≥ 1755.85 µm, CCR ≥ 3.34%, CI ≥ 39.63, Vmax ≥ 14.63 µm min−1 and CFS ≥ 15. We found that the chemotactic function of neutrophils in patients suffering from infections was significantly impaired. The mean values of CD, CCR, CI, Vmax and CFS were 1452.8 µm (P < 0.0001), 3.1% (P < 0.0001), 34.5 (P < 0.0001), 12.2 µm min−1 (P < 0.0001) and 9 (P < 0.0001), respectively. CD and CFS were significantly negatively correlated with the APACHE II score (rCD = −0.55, rCFS = −0.39), SOFA score (rCD = −0.68, rCFS = −0.56), procalcitonin concentration (rCD = −0.60, rCFS = −0.5) and the expression of P2RX1 (rCD = −0.76, rCFS = −0.56), respectively. Conclusions CD, CCR, CI and Vmax can well reflect the neutrophil chemotactic function in patients with severe infections. CFS systematically indicated neutrophil function and has promising clinical application prospects.

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Section: Discussionmentioning

confidence: 99%

A novel computer vision‐based assessment of neutrophil chemotaxis in patients with severe infection

et al. 2021

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“…Their contribution to IRI pathophysiology results from the adherence to endothelium, release of ROS and proteases, and their ability to synthesize and secrete cytokines/chemokines that recruit other effector cells to the organ, amplifying local inflammation. Recently, Zhang et al [15 ▪▪ ] asked whether the inactivation of neutrophils may be an effective strategy to decrease IRI-related damage. Indeed, mice treated with antibodies directed to HMGB1 alleviated IRI-induced renal dysfunction by suppressing the activation of the HMGB1–TLR4–IL-23–IL-17A signaling axis.…”

Section: Graft-infiltrating Polymorphonuclear Neutrophils and Macroph...mentioning

confidence: 99%

New insights into ischemia-reperfusion injury signaling pathways in organ transplantation

Dery

Kupiec‐Weglinski

2022

Current Opinion in Organ Transplantation

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Purpose of reviewIschemia-reperfusion injury (IRI) leading to allograft rejection in solid organ transplant recipients is a devastating event that compromises graft and patient survival. As our clinical knowledge regarding its definition and presentation has significantly improved over the last years, adequate biomarkers translating to important therapeutic intervention remains a challenge. This review will summarize recent findings in this area.Recent findingsIn the past 18 months, our understanding of organ transplantation IRI has improved. IRI involves a positive amplification feedback loop encompassing damaged cells at the graft site, the activity of redox-sensitive damage-associated molecular patterns, and local sequestration of recipient-derived monocytes, lymphocytes and polymorphonuclear leukocytes, like neutrophils, to sustain the immunological cascade and to enhance the destruction of the foreign tissue. Recent studies have identified critical components leading to IRI, including the oxidation state of high mobility group box 1, a classic danger signal, its role in the Toll-like receptor 4–interleukin (IL)-23–IL-17A signaling axis, and the role of neutrophils and CD321, a marker for transmigration of circulating leukocytes into the inflamed tissue. In addition, recent findings imply that the protective functions mediated by autophagy activation counterbalance the detrimental nucleotide-binding domain-like receptor family, pyrin domain containing 3 inflammasome pathway. Finally, clinical studies reveal the posttransplant variables associated with early allograft dysfunction and IRI.SummaryThe future challenge will be understanding how crosstalk at the molecular and cellular levels integrate prospectively to predict which peri-transplant signals are essential for long-term clinical outcomes.

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“…In one study, infiltration of DCs in damaged tissues resulted in secretion of cytokines such as interleukin (IL)-10 to prevent AKI progression (23). In the IR model, inhibition of neutrophil recruitment can significantly reduce kidney damage, which suggests that neutrophil infiltration is one of the pathogenic mechanisms of renal IR injury (24). In contrast, inhibition of neutrophil infiltration has no effect on cisplatin-induced kidney injury, indicating that neutrophil infiltration is not necessary for cisplatin-induced kidney damage (25).…”

Section: Different Immune Mechanisms Of Drug-induced and Ir-induced Akimentioning

confidence: 99%

“…Infiltration at the injury site, but inhibition of neutrophils can significantly reduce kidney damage (24).…”

Section: Neutrophilsmentioning

confidence: 99%

Immunomodulatory Effects of Mesenchymal Stem Cells on Drug-Induced Acute Kidney Injury

et al. 2021

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Drug-induced nephrotoxicity is an important and increasing cause of acute kidney injury (AKI), which accounts for approximately 20% of hospitalized patients. Previous reviews studies on immunity and AKI focused mainly on ischemia-reperfusion (IR), whereas no systematic review addressing drug-induced AKI and its related immune mechanisms is available. Recent studies have provided a deeper understanding on the mechanisms of drug-induced AKI, among which acute tubular interstitial injury induced by the breakdown of innate immunity was reported to play an important role. Emerging research on mesenchymal stem cell (MSC) therapy has revealed its potential as treatment for drug-induced AKI. MSCs can inhibit kidney damage by regulating the innate immune balance, promoting kidney repair, and preventing kidney fibrosis. However, it is important to note that there are various sources of MSCs, which impacts on the immunomodulatory ability of the cells. This review aims to address the immune pathogenesis of drug-induced AKI versus that of IR-induced AKI, and to explore the immunomodulatory effects and therapeutic potential of MSCs for drug-induced AKI.

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HMGB1-TLR4-IL-23-IL-17A axis accelerates renal ischemia-reperfusion injury via the recruitment and migration of neutrophils

Cited by 30 publications

References 19 publications

A novel computer vision‐based assessment of neutrophil chemotaxis in patients with severe infection

A novel computer vision‐based assessment of neutrophil chemotaxis in patients with severe infection

New insights into ischemia-reperfusion injury signaling pathways in organ transplantation

Immunomodulatory Effects of Mesenchymal Stem Cells on Drug-Induced Acute Kidney Injury

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