Remote ischemic conditioning causes CD4 T cells shift towards reduced cell-mediated inflammation

Alganabi, Mashriq; Biouss, George; Ganji, Niloofar; Yamoto, Masaya; Lee, Carol; Li, Bo; Pierro, Agostino

doi:10.1007/s00383-022-05093-3

Cited by 7 publications

(3 citation statements)

References 49 publications

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“…Our findings suggest a potentially novel role for RIC in the modulation of T cell mediated innate immunity, as post traumatic shift from Th1 towards an anti-inflammatory Th2 phenotype contributes to susceptibility to nosocomial infections 6 and development of sepsis and poorer outcomes. This suggestion is further supported by recent animal models, where RIC elicited increased T cell anti-inflammatory cytokine production with an attendant shift from Th17 cells towards Treg cells 28 . Importantly, Richter et al revealed a role for MDC in mediating lung inflammation in a murine model of hemorrhagic shock/resuscitation as administration of neutralizing antibodies against MDC significantly reduces pulmonary levels of the chemotactic cytokines KC, MIP-2, and MIP-1α and extravasation of inflammatory cells 29 .…”

Section: Discussionsupporting

confidence: 57%

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Leung

Rizoli

Trypcic

et al. 2023

Sci Rep

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Resuscitation induced ischemia/reperfusion predisposes trauma patients to systemic inflammation and organ dysfunction. We investigated the effect of remote ischemic conditioning (RIC), a treatment shown to prevent ischemia/reperfusion injury in experimental models of hemorrhagic shock/resuscitation, on the systemic immune-inflammatory profile in trauma patients in a randomized trial. We conducted a prospective, single-centre, double-blind, randomized, controlled trial involving trauma patients sustaining blunt or penetrating trauma in hemorrhagic shock admitted to a Level 1 trauma centre. Patients were randomized to receive RIC (four cycles of 5-min pressure cuff inflation at 250 mmHg and deflation on the thigh) or a Sham intervention. The primary outcomes were neutrophil oxidative burst activity, cellular adhesion molecule expression, and plasma levels of myeloperoxidase, cytokines and chemokines in peripheral blood samples, drawn at admission (pre-intervention), 1 h, 3 h, and 24 h post-admission. Secondary outcomes included ventilator, ICU and hospital free days, incidence of nosocomial infections, 24 h and 28 day mortality. 50 eligible patients were randomized; of which 21 in the Sham group and 18 in the RIC group were included in the full analysis. No treatment effect was observed between Sham and RIC groups for neutrophil oxidative burst activity, adhesion molecule expression, and plasma levels of myeloperoxidase and cytokines. RIC prevented significant increases in Th2 chemokines TARC/CCL17 (P < 0.01) and MDC/CCL22 (P < 0.05) at 24 h post-intervention in comparison to the Sham group. Secondary clinical outcomes were not different between groups. No adverse events in relation to the RIC intervention were observed. Administration of RIC was safe and did not adversely affect clinical outcomes. While trauma itself modified several immunoregulatory markers, RIC failed to alter expression of the majority of markers. However, RIC may influence Th2 chemokine expression in the post resuscitation period. Further investigation into the immunomodulatory effects of RIC in traumatic injuries and their impact on clinical outcomes is warranted.ClinicalTrials.gov number: NCT02071290.

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Section: Discussionsupporting

confidence: 57%

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Leung

Rizoli

Trypcic

et al. 2023

Sci Rep

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“…Multiple mechanisms have been put forward to explain the therapeutic effect of RIC and might involve the release of humoral factors such as nitric oxide or biogenic amines such as ornithine, glycine, kynurenine, spermine, carnosine, and serotonin [ 262 ]. These factors modulate the systemic immune response by regulation neutrophils activation [ 263 , 264 ], macrophage polarization [ 265 ], and/or T cell activation [ 266 ]. These mediators are also transported through the bloodstream towards the site of injury, where they attenuate disease progression by regulating multiple pathways at cellular and molecular levels [ 267 ].…”

Section: Future Prospectivementioning

confidence: 99%

Understanding Acquired Brain Injury: A Review

et al. 2022

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Any type of brain injury that transpires post-birth is referred to as Acquired Brain Injury (ABI). In general, ABI does not result from congenital disorders, degenerative diseases, or by brain trauma at birth. Although the human brain is protected from the external world by layers of tissues and bone, floating in nutrient-rich cerebrospinal fluid (CSF); it remains susceptible to harm and impairment. Brain damage resulting from ABI leads to changes in the normal neuronal tissue activity and/or structure in one or multiple areas of the brain, which can often affect normal brain functions. Impairment sustained from an ABI can last anywhere from days to a lifetime depending on the severity of the injury; however, many patients face trouble integrating themselves back into the community due to possible psychological and physiological outcomes. In this review, we discuss ABI pathologies, their types, and cellular mechanisms and summarize the therapeutic approaches for a better understanding of the subject and to create awareness among the public.

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“…Remote ischemic preconditioning (RIPC) has been shown to have anti-inflammatory effects in rat models of acute inflammation, such as carrageenan-induced paw oedema, ifosfamide-induced haemorrhagic cystitis and indomethacin-induced gastric injury [14]. It was determined that RIPC caused anti-inflammatory effects by shifting the balance between CD4 + T lymphocytes Treg/T17 towards Treg in the necrotising enterocolitis mouse model [15]. It has been reported that remote ischemic postconditioning (RIPsC) plays a protective role by activating Treg in an ischemic stroke model, and that the protective effect of RIPsC is abolished in mice in which these cells are depleted [16].…”

Section: Introductionmentioning

confidence: 99%

Anti-Inflammatory and Antipruritic Effects of Remote Ischaemic Postconditioning in a Mouse Model of Experimental Allergic Contact Dermatitis

Gunduz,

Sapmaz-Metin,

Topuz

et al. 2023

Medicina

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Background and Objectives: Allergic contact dermatitis is a common type IV hypersensitivity reaction characterised by redness, itching, oedema and thickening of the skin. It occurs in about 7% of the population and its incidence is increasing. It has been observed that the preconditioning of tissues by exposing them to transient ischemia increases resistance to subsequent permanent ischemia, and this phenomenon is called ischemic preconditioning. It has been shown that conditioning in one organ can also protect other organs. The protective effect of remote ischemic preconditioning is thought to be based on the induction of anti-inflammatory responses. The aim of this project was to investigate the anti-inflammatory and antipruritic effects of remote ischemic postconditioning in a mouse model of experimental allergic contact dermatitis. Methods: Experimental allergic contact dermatitis was induced with 1-fluoro-2,4-dinitrobenzene. Remote ischemic postconditioning was performed at 3 and 25 h after the challenge. Ear thickness and number of scratches 24 and 48 h after challenge, as well as cytokine levels and the infiltration of mast cells, neutrophils, CD4+ and CD8+ T lymphocytes in serum and ear tissue at 48 h were measured to determine the effect of RIPsC. Results: Remote ischemic postconditioning decreased ear thickness, one of the symptoms of allergic contact dermatitis (p < 0.0001). It had no significant effect on the number of scratches. It reduced serum IL-17 levels (p < 0.01). It alleviated local inflammation by suppressing CD8+ T lymphocyte and neutrophil infiltration. Conclusions: It was concluded that remote ischemic postconditioning may alleviate the symptoms of allergic contact dermatitis by suppressing CD8+ T lymphocyte and neutrophil infiltration and reducing IL-17 secretion.

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Remote ischemic conditioning causes CD4 T cells shift towards reduced cell-mediated inflammation

Cited by 7 publications

References 49 publications

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Effect of remote ischemic conditioning on the immune-inflammatory profile in patients with traumatic hemorrhagic shock in a randomized controlled trial

Understanding Acquired Brain Injury: A Review

Anti-Inflammatory and Antipruritic Effects of Remote Ischaemic Postconditioning in a Mouse Model of Experimental Allergic Contact Dermatitis

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