Atherosclerosis

2021

DOI: 10.1016/j.atherosclerosis.2021.04.010

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IL-2Rβγ signalling in lymphocytes promotes systemic inflammation and reduces plasma cholesterol in atherosclerotic mice

Megan Mulholland

¹

,

Gabriel Jakobsson

²

,

³

et al.

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Systemic Immune-inflammation Index1

внутрішні хвороби1

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Cited by 11 publications

(7 citation statements)

References 56 publications

(77 reference statements)

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“…Specifically, neutrophils secrete inflammatory mediators that can lead to endothelial dysfunction and vessel wall degeneration ( 44 ). Platelets may release some chemokines, proinflammatory cytokines, and platelet-derived growth factors that promote endothelial cell depletion ( 45 , 46 ). In addition, neutrophils promote atherosclerosis and thrombosis through interactions with platelets, proteolytic cleavage of coagulation factors, release of prothrombotic molecules, and promotion of monocyte infiltration, ultimately leading to cardiovascular events ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Systemic immune-inflammation index as a potential biomarker of cardiovascular diseases: A systematic review and meta-analysis

¹

,

²

,

³

et al. 2022

Front. Cardiovasc. Med.

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BackgroundSeveral studies have investigated the value of the systemic immune-inflammation index (SII) for predicting cardiovascular disease (CVD), but the results were inconsistent. Therefore, a meta-analysis and systematic review were conducted to assess the correlation between SII and risk of CVD.Materials and methodsTwo investigators systematically searched PubMed, Embase, Web of Science, Cochrane library, and CINAHL databases to identify all studies that examined the association between SII levels and CVD. The risk estimates of CVD for people with high SII compared to those with low SII levels and the weighted mean difference (WMD) between the CVD and control groups were pooled using fixed- or random-effects models based on the heterogeneity test. We used the Newcastle-Ottawa Scale to assess the risk of bias in eligible studies, and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system was applied to rate the certainty of evidence.ResultsA total of 13 studies with 152,996 participants were included for analysis. The overall pooled results showed that higher SII was significantly associated with an increased risk of CVD (HR = 1.39, 95%CI: 1.20–1.61, P < 0.001). This increased risk could be observed in almost all CVD subtypes, including ischemic stroke (HR = 1.31, 95%CI: 1.06–1.63, P = 0.013), hemorrhagic stroke (HR = 1.22, 95%CI: 1.10–1.37, P < 0.001), myocardial infarction (HR = 1.11, 95%CI: 1.01–1.23, P = 0.027), and peripheral arterial disease (HR = 1.51, 95%CI: 1.18–1.93, P = 0.001). There were no significant but still similar trends in venous thrombosis (HR = 4.65, 95%CI: 0.66–32.71, P = 0.122), cerebral small vessel disease (HR = 1.09, 95%CI: 0.95–1.25, P = 0.233), and acute coronary syndrome (HR = 1.08, 95%CI: 0.96–1.22, P = 0.200). Furthermore, the pooled results showed that SII levels at the onset of CVD were significantly higher than that in the general population (WMD = 355.2, 95%CI: 234.8–475.6, P < 0.001), which was consistent across different CVD subtypes. The GRADE assessment suggested that the quality of current evidence from observational studies was low or very low.ConclusionThis study indicated that SII may be a potential biomarker for CVD development and elevated SII is associated with an increased risk of CVD. However, the quality of evidence is generally low. Additional well-designed studies are necessary to determine the optimal cutoff value and to characterize the benefited population.

“…Specifically, neutrophils secrete inflammatory mediators that can lead to endothelial dysfunction and vessel wall degeneration ( 44 ). Platelets may release some chemokines, proinflammatory cytokines, and platelet-derived growth factors that promote endothelial cell depletion ( 45 , 46 ). In addition, neutrophils promote atherosclerosis and thrombosis through interactions with platelets, proteolytic cleavage of coagulation factors, release of prothrombotic molecules, and promotion of monocyte infiltration, ultimately leading to cardiovascular events ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Systemic immune-inflammation index as a potential biomarker of cardiovascular diseases: A systematic review and meta-analysis

¹

,

²

,

³

et al. 2022

Front. Cardiovasc. Med.

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BackgroundSeveral studies have investigated the value of the systemic immune-inflammation index (SII) for predicting cardiovascular disease (CVD), but the results were inconsistent. Therefore, a meta-analysis and systematic review were conducted to assess the correlation between SII and risk of CVD.Materials and methodsTwo investigators systematically searched PubMed, Embase, Web of Science, Cochrane library, and CINAHL databases to identify all studies that examined the association between SII levels and CVD. The risk estimates of CVD for people with high SII compared to those with low SII levels and the weighted mean difference (WMD) between the CVD and control groups were pooled using fixed- or random-effects models based on the heterogeneity test. We used the Newcastle-Ottawa Scale to assess the risk of bias in eligible studies, and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system was applied to rate the certainty of evidence.ResultsA total of 13 studies with 152,996 participants were included for analysis. The overall pooled results showed that higher SII was significantly associated with an increased risk of CVD (HR = 1.39, 95%CI: 1.20–1.61, P < 0.001). This increased risk could be observed in almost all CVD subtypes, including ischemic stroke (HR = 1.31, 95%CI: 1.06–1.63, P = 0.013), hemorrhagic stroke (HR = 1.22, 95%CI: 1.10–1.37, P < 0.001), myocardial infarction (HR = 1.11, 95%CI: 1.01–1.23, P = 0.027), and peripheral arterial disease (HR = 1.51, 95%CI: 1.18–1.93, P = 0.001). There were no significant but still similar trends in venous thrombosis (HR = 4.65, 95%CI: 0.66–32.71, P = 0.122), cerebral small vessel disease (HR = 1.09, 95%CI: 0.95–1.25, P = 0.233), and acute coronary syndrome (HR = 1.08, 95%CI: 0.96–1.22, P = 0.200). Furthermore, the pooled results showed that SII levels at the onset of CVD were significantly higher than that in the general population (WMD = 355.2, 95%CI: 234.8–475.6, P < 0.001), which was consistent across different CVD subtypes. The GRADE assessment suggested that the quality of current evidence from observational studies was low or very low.ConclusionThis study indicated that SII may be a potential biomarker for CVD development and elevated SII is associated with an increased risk of CVD. However, the quality of evidence is generally low. Additional well-designed studies are necessary to determine the optimal cutoff value and to characterize the benefited population.

“…The idea behind the hypothesis of this subject is the increase of neutrophil count in endothelial dysfunction and the active role of neutrophils with platelets in the formation of atherosclerosis. [ 104 105 ] Moreover, some lymphocyte subtypes regulate inflammation and negatively affect the formation of atherosclerosis. [ 106 ]…”

Section: Systemic Immune-inflammation Indexmentioning

confidence: 99%

Unraveling the clinical significance and prognostic value of the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, systemic immune-inflammation index, systemic inflammation response index, and delta neutrophil index

Islam,

Satici,

Eroglu

2024

Turkish Journal of Emergency Medicine

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In the field of critical care medicine, substantial research efforts have focused on identifying high-risk patient groups. This research has led to the development of diverse diagnostic tools, ranging from basic biomarkers to complex indexes and predictive algorithms that integrate multiple methods. Given the ever-evolving landscape of medicine, driven by rapid advancements, changing treatment strategies, and emerging diseases, the development and validation of diagnostic tools remains an ongoing and dynamic process. Specific changes in complete blood count components, such as neutrophils, lymphocytes, monocytes, and platelets, are key immune system responses influenced by various factors and crucial in systemic inflammation, injury, and stress. It has been reported that indices such as neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and delta neutrophil index calculated using various ratios of these elements, are important predictors of various outcomes in conditions where the inflammatory process is at the forefront. In this narrative review, we concluded that NLR, PLR, SII, and SIRI show promise in predicting outcomes for different health conditions related to inflammation. While these tests are accessible, reliable, and cost-effective, their standalone predictive performance for a specific condition is limited.

“…Platelets are also capable of secreting pro-inflammatory factors that contribute to the development of MMD through the above pathways. Platelets also secrete chemokines [ 19 , 20 ], and elevated PLTs cause a state of systemic hypercoagulation, leading to intravascular micro thrombosis. Hypercoagulation is another easily overlooked cause of MMD.…”

Section: Discussionmentioning

confidence: 99%

Association between systemic immune-inflammatory markers and the risk of moyamoya disease: a case-control study

Liu,

Liu,

Yu

et al. 2023

Annals of Medicine

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Background: Systemic immune-inflammatory markers such as neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR) and systemic immune-inflammatory index (SII) are associated with the prognosis of many cardiovascular and neoplastic diseases. Moyamoya disease (MMD) is associated with inflammation, but the relationship between systemic immune-inflammatory markers between MMD is unclear. The aim of our study was to analyse the association between systemic immune-inflammatory markers and the risk of MMD and its subtypes. Methods: We consecutively recruited 360 patients with MMD and 89 healthy control subjects in a case-control study to calculate and analyse the association of systemic immune-inflammatory markers with the risk of MMD and its subtypes. Results: The risk of MMD increased with higher levels of NLR (OR 1.237, 95% CI [1.008, 1.520], p = .042). When NLR and SII were assessed as quartile-spaced subgroups, the third quartile grouping of NLR and SII had a higher risk of MMD than the first quartile grouping (NLR: OR 3.206, 95% CI [1.271, 8.088], p = .014; SII: OR 3.074,95% CI [1.232,7.672], p = .016). When NLR was combined with SII, the highest subgroup had a higher risk of MMD than the lowest subgroup (OR2.643, 95% CI [1.340, 5.212], p = .005). The risk of subtypes also increased with higher levels of NLR and SII. The association between the levels of NLR and SII with the staging of the Suzuki stage follows an inverted U-shape. The highest levels of NLR and SII were found in patients with MMD at Suzuki stages 3–4. Conclusion: The risk of MMD increases with elevated systemic immune-inflammatory markers. This study analysed the association of systemic immune-inflammatory markers with the risk of developing MMD and its subtypes, and identified novel inflammatory markers for MMD.

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