scholarly journals OP0168 THE ROLE OF VASCULAR INFLAMMATION MARKERS IN DEFICIENCY OF ADENOSINE DEAMINASE 2

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 100.1-101
Author(s):  
U. Kaya Akca ◽  
E. Sag ◽  
Ş. Ünal ◽  
M. Kasap-Cuceoglu ◽  
Y. Bilginer ◽  
...  
Keyword(s):  
Adenosine Deaminase ◽  
Plasma Levels ◽  
Vascular Inflammation ◽  
Healthy Controls ◽  
Inflammation Markers ◽  
Diamond Blackfan Anemia ◽  
Tnf Α ◽  
Significant Difference ◽  
Adenosine Deaminase 2

Background:Deficiency of adenosine deaminase 2 (DADA2) is a monogenic autoinflammatory disease whose pathogenesis has not been clearly elucidated.Objectives:To investigate the role of vascular inflammatory factors in the pathogenesis of DADA2, to compare the vascular inflammation profiles of DADA2 patients with different phenotypes, and to compare DADA2 patients with classic polyarteritis nodosa (PAN).Methods:The study included eighteen DADA2 patients, ten PAN patients, and eight healthy controls. Plasma levels of sST2, sRAGE, Tie-2, sCD40L, Tie-1, sFlt-1, LIGHT, TNF-α, PlGF, IL-6, IL-18, IL-10, MCP-1 were studied by cytometric bead-based multiplex assay panel.Results:Among the DADA2 patients, five had hematological manifestations, 13 had vasculitic findings, and accompanying immunological findings were present in seven patients. Nine patients had neurological findings, five of whom had neuropathy. Hematological findings were Diamond-Blackfan anemia-like phenotype in four patients and bicytopenia (anemia and thrombocytopenia) in one patient. Disease characteristics of DADA2 and PAN patients revealed that neurological involvement and livedo reticularis were more frequent in DADA2 patients (p=0.034 and p=0.009, respectively), while myalgia was more common in PAN patients (p:0.001).Plasma levels of Tie-1 and sFlt-1 were higher in the overall DADA2 patients compared to healthy controls and PAN patients (p<0.001 and p=0.004, respectively). DADA2 patients with PAN-like features had higher sRAGE, Tie-2, and TNF-α levels compared to PAN patients (p=0.013, p=0.003, and p=0.001, respectively).There was no significant difference in the levels of vascular inflammation markers between DADA2 patients with vasculitis and hematological involvement except IL-18. The plasma IL-18 levels were higher in the DADA2 patients with hematological findings compared to vasculitic phenotype (p=0.001). Finally DADA2 patients with neuropathy had higher sRAGE concentrations than patients without neuropathy and healthy controls (p=0.03 and p=0.008, respectively).Conclusion:We suggest that the high plasma IL-18 levels may be associated with an activated IFN pathway, the pathogenesis of hematologic manifestations, and unresponsive to anti-TNF treatment. Higher concentrations of Tie-1, Tie-2, sFlt-1, sRAGE, and TNF-α distinguished DADA2 patients with PAN-like features from PAN patients. We identified sRAGE as a potential biomarker of neuropathy in DADA2 patients.References:[1]Pesciotta EN, Lam H-S, Kossenkov A, et al. In-Depth, Label-Free analysis of the erythrocyte cytoplasmic proteome in Diamond Blackfan Anemia identifies a unique inflammatory signature. PLoS One 2015;10(10):e0140036.[2]Haslbeck KM, Bierhaus A, Erwin S, et al. Receptor for advanced glycation endproduct (RAGE)–mediated nuclear factor-κB activation in vasculitic neuropathy. Muscle Nerve 2004;29(6):853-60.Disclosure of Interests:None declared

The role of vascular inflammation markers in deficiency of adenosine deaminase 2

2021 ◽  
Author(s):  
Ummusen Kaya Akca ◽  
Erdal Sag ◽  
Sule Unal ◽  
Muserref Kasap Cuceoglu ◽  
Yelda Bilginer ◽  
...  
Keyword(s):  
Adenosine Deaminase ◽  
Vascular Inflammation ◽  
Inflammation Markers ◽  
Adenosine Deaminase 2

Removal of elevated circulating angiopoietin-2 by plasma exchange – A pilot study in critically ill patients with thrombotic microangiopathy and anti-glomerular basement membrane disease

2010 ◽  
Vol 104 (11) ◽  
pp. 1038-1043 ◽  
Author(s):  
Carsten Hafer ◽  
Jan Kielstein ◽  
Marion Haubitz ◽  
Hermann Haller ◽  
Svjetlana Lovric ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Plasma Exchange ◽  
Critically Ill ◽  
Glomerular Basement Membrane ◽  
Critically Ill Patients ◽  
Plasma Levels ◽  
Vascular Inflammation ◽  
Endothelial Damage ◽  
Healthy Controls ◽  
Angiopoietin 2

SummaryIn critically ill patients, the massive release of angiopoietin-2 (Ang-2) from Weibel-Palade bodies interferes with protective angiopoietin-1 (Ang-1)/Tie2 signalling in endothelial cells, thus leading to vascular inflammation and subsequent organ-dysfunction. We hypothesised that plasma exchange (PE) is efficient for lowering excess Ang-2 levels in critically ill patients with thrombocytic microangiopathy (TMA) or anti-glomerular basement membrane (anti-GBM) disease. Plasma Ang-1 and Ang-2 were measured by immuno-luminometric assays in patients with TMA (n=9) or anti-GBM disease (n=4) before and after up to four PE sessions. Twenty apparently healthy volunteers served as controls. Median (IQR) plasma levels of Ang-2 were markedly increased in patients with TMA (7.3 (2.4–21.1) ng/ml) and anti-GBM disease (5.8 (3.4–7.0) ng/ml) compared to healthy controls (1.0 (0.9–1.4) ng/ml, p <0.001). Moreover, Ang-1 plasma levels were decreased in both, TMA (1.02 (0.62–1.62) ng/ml) and anti-GBM disease patients (0.74 (0.59–3.62) ng/ml) compared to healthy controls (2.5 (1.93–3.47) ng/ ml, p <0.005). During a total of 32 treatments, PE effectively lowered elevated mean (SD) Ang-2 plasma levels by 36.7 ± 19.6 % per treatment (p <0.0001), whereas low Ang-1 plasma levels remained unchanged (0.3 ± 58.5 %; p =0.147). Ang-2 levels declined to almost normal values during ≤4 PE treatments (Friedman´s test p <0.0001). PE is an effective method to remove excess circulating Ang-2. It remains to be elucidated if the removal of Ang-2 is crucial to ameliorate endothelial damage in critically ill patients with severely altered endothelial integrity.

scholarly journals The Role of Butyric Acid in Treatment Response in Drug-Naïve First Episode Schizophrenia

2021 ◽  
Vol 12 ◽  
Author(s):  
Xue Li ◽  
Xiaoduo Fan ◽  
Xiuxia Yuan ◽  
Lijuan Pang ◽  
Shaohua Hu ◽  
...  
Keyword(s):  
Treatment Response ◽  
Butyric Acid ◽  
Serum Levels ◽  
First Episode ◽  
Healthy Controls ◽  
Significant Difference ◽  
Drug Naïve ◽  
First Episode Schizophrenia ◽  
Risperidone Treatment

Background: Butyric acid, a major short-chain fatty acid (SCFA), has an important role in the microbiota–gut–brain axis and brain function. This study investigated the role of butyric acid in treatment response in drug-naïve first episode schizophrenia.Methods: The study recruited 56 Chinese Han schizophrenia inpatients with normal body weight and 35 healthy controls. Serum levels of butyric acid were measured using Gas Chromatography-Mass Spectrometer (GC-MS) analysis at baseline (for all participants) and 24 weeks after risperidone treatment (for patients). Clinical symptoms were measured using the Positive and Negative Syndrome Scale (PANSS) for patients at both time points.Results: At baseline, there was no significant difference in serum levels of butyric acid between patients and healthy controls (p = 0.206). However, there was a significant increase in serum levels of butyric acid in schizophrenia patients after 24-week risperidone treatment (p = 0.030). The PANSS total and subscale scores were decreased significantly after 24-week risperidone treatment (p's &lt; 0.001). There were positive associations between baseline serum levels of butyric acid and the reduction ratio of the PANSS total and subscale scores after controlling for age, sex, education, and duration of illness (p's &lt; 0.05). Further, there was a positive association between the increase in serum levels of butyric acid and the reduction of the PANSS positive symptoms subscale scores (r = 0.38, p = 0.019) after controlling for potential confounding factors.Conclusions: Increased serum levels of butyric acid might be associated with a favorable treatment response in drug-naïve, first episode schizophrenia. The clinical implications of our findings were discussed.

scholarly journals TNF-α Activating Osteoclasts in Patients with Psoriatic Arthritis Enhances the Recruitment of Osteoclast Precursors: A Plausible Role of WNT5A-MCP-1 in Osteoclast Engagement in Psoriatic Arthritis

2022 ◽  
Vol 23 (2) ◽  
pp. 921
Author(s):  
Shang-Hung Lin ◽  
Ji-Chen Ho ◽  
Sung-Chou Li ◽  
Yu-Wen Cheng ◽  
Chung-Yuan Hsu ◽  
...  
Keyword(s):  
Psoriatic Arthritis ◽  
Rna Interference ◽  
Joint Destruction ◽  
Neutralizing Antibody ◽  
Healthy Controls ◽  
Osteoclast Precursors ◽  
Tnf Α ◽  
Wnt Ligands

Psoriatic arthritis (PsA) results from joint destruction by osteoclasts. The promising efficacy of TNF-α blockage indicates its important role in osteoclastogenesis of PsA. WNT ligands actively regulate osteoclastogenesis. We investigated how WNT ligands activate osteoclasts amid the TNF-α milieu in PsA. We first profiled the expression of WNT ligands in CD14+ monocyte-derived osteoclasts (MDOC) from five PsA patients and five healthy controls (HC) and then validated the candidate WNT ligands in 32 PsA patients and 16 HC. Through RNA interference against WNT ligands in MDOC, we determined the mechanisms by which TNF-α exerts its effects on osteclastogenesis or chemotaxis. WNT5A was selectively upregulated by TNF-α in MDOC from PsA patients. The number of CD68+WNT5A+ osteoclasts increased in PsA joints. CXCL1, CXCL16, and MCP-1 was selectively increased in supernatants of MDOC from PsA patients. RNA interference against WNT5A abolished the increased MCP-1 from MDOC and THP-1-cell-derived osteoclasts. The increased migration of osteoclast precursors (OCP) induced by supernatant from PsA MDOC was abolished by the MCP-1 neutralizing antibody. WNT5A and MCP-1 expressions were decreased in MDOC from PsA patients treated by biologics against TNF-α but not IL-17. We conclude that TNF-α recruits OCP by increased MCP-1 production but does not directly activate osteoclastogenesis in PsA.

scholarly journals Serum total adenosine deaminase activity in Nepalese patients with Rheumatoid Arthritis

2013 ◽  
Vol 4 (2) ◽  
pp. 30-35
Author(s):  
N Gautam ◽  
J Archana ◽  
R Kumar ◽  
LI Singh ◽  
RM Sapkota ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Adenosine Deaminase ◽  
Healthy Controls ◽  
Medical Sciences ◽  
Potential Marker ◽  
Diagnostic Potential ◽  
Clinical Scenarios ◽  
Adenosine Deaminase Activity ◽  
Significant Difference ◽  
Reliable Marker

Objective: Several studies indicate that serum adenosine deaminase (ADA) activity could be a potential marker for the diagnosis of patients with rheumatoid arthritis (RA). However, there has been no such study that could independently verify this finding in Nepali population. The present study therefore aims to measure the total ADA activity in the sera of Nepalese RA patients and verify its diagnostic potential. Materials and Methods: A total of 69 RA patients who visited Universal College of Medical Sciences Teaching Hospital (UCMSTH), Bhairahawa, Nepal for their medical treatment were enrolled for this study. An equal number of age and sex-matched healthy controls were also included in the study. Blood samples were collected from each study subjects and analyzed for serum total ADA, Creactive protein (CRP) and rheumatoid factor (RF). Results: Serum total ADA activity was found to be significantly (p<0.0001) higher (30.0 }10.1 U/L) in all RA patients compared to healthy controls (13.5 } 3.6 U/L). However, no significant difference (p>0.05) in the ADA activity was found between the smokers and non-smoker RA patients. Out of total 69 RA patients, only 16 (23.1%) were positive for CRP and 11 (15.9%) were positive for RF. Conclusion: Measurement of serum total ADA activity could be a reliable marker for the diagnosis of RA in Nepali population with relevant clinical scenarios when there is absence of CRP and RF in the serum.  DOI: http://dx.doi.org/10.3126/ajms.v4i2.6208 Asian Journal of Medical Sciences 4(2013) 30-35

scholarly journals Plasma levels of pro-inflammatory molecules and their expressions are associated with severity of heart failure: An investigation in Chinese cohort

2019 ◽  
Vol 17 ◽  
pp. 205873921983657
Author(s):  
Yongxi Xu ◽  
Hongyan Sun ◽  
Zhihao Wang ◽  
Yufeng Wang
Keyword(s):  
Heart Failure ◽  
Plasma Levels ◽  
Adult Population ◽  
Interleukin 1 ◽  
Heart Association ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Significant Difference ◽  
Inflammatory Molecules

Heart failure (HF) is a syndrome with multiple clinical phenotypes affecting around 1%–2% of adult population worldwide, and about 230 million Chinese are affected by cardiovascular diseases. The important role of pro-inflammatory plasma cytokines with HF has been demonstrated in different populations. The aim of this study was to investigate importance of pro-inflammatory cytokines in Chinese HF patients. In all, 134 HF patients were enrolled in this study and further classified in to four clinical distinct groups according to New York Heart Association classification criteria (NYHA-I: n = 34, NYHA-II: n = 35, NYHA-III: n = 22 and NYHA-IV: n = 43). Sixty-eight healthy Chinese were enrolled as controls. Plasma levels of tumour necrosis factor-α (TNF-α), TNF-receptor 1 (TNFRI), TNF-receptor 2 (TNFRII), interleukin 6 (IL-6), soluble IL-6 receptor (sIL-6R), C-reactive protein (CRP), soluble cluster of differentiation 14 (sCD14) and interleukin 1 beta (IL-1β) were quantified by enzyme-linked immunosorbent assay (ELISA). Plasma levels of all parameters investigated in this study remained comparable among healthy controls and NYHA-I group. Plasma levels of TNF-α, TNFRI, TNFRII, IL-6, sIL-6R, CRP, sCD14 and IL-1β were significantly higher in NYHA-III and NYHA-IV clinical categories compared to other HF phenotype (NYHA-I and NYHA-II). Interestingly, TNFR-II levels were significantly higher in NYHA-II compared to NYHA-I. No significant difference of plasma sIL-6R was observed among various clinical categories. In conclusion, plasma levels of pro-inflammatory molecules are elevated in severe HF patients and may be used as possible biomarkers for accessing severity of HF.

Study of the HLA-DPβ1 Locus by the Polymerase Chain Reaction Technique in Patients with Hodgkin's Disease

1993 ◽  
Vol 79 (2) ◽  
pp. 133-136 ◽  
Author(s):  
Guseppe Pellegris ◽  
Claudia Lombardo ◽  
Annelisa Cantoni ◽  
Liliana Devizzi ◽  
Monica Balzarotti
Keyword(s):  
Polymerase Chain Reaction ◽  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Polymerase Chain Reaction Method ◽  
Healthy Controls ◽  
Chain Reaction ◽  
Reaction Method ◽  
Significant Difference ◽  
Polymerase Chain

Background A number of reports have studied associations between Hodgkin's disease and HLA. Some of them established correlation between several antigens and Hodgkin's disease, and others found no correlations. Methods The HLA DP locus was determined by the polymerase chain reaction method in 31 Hodgkin's disease patients and 58 healthy controls. Results No significant difference between patients and controls was noted. Conclusions Further investigations are needed to confirm the hypothesis of a possible role of the HLA complex as one of the factors involved in Hodgkin's disease.

Physiological persona differences based on stress and inflammation between meditators and healthy controls

2019 ◽  
Vol 17 (2) ◽  
Author(s):  
Dipti Magan ◽  
Raj Kumar Yadav
Keyword(s):  
Blood Pressure ◽  
Body Mass Index ◽  
Plasma Levels ◽  
Inflammatory Markers ◽  
Tumor Necrosis ◽  
Healthy Controls ◽  
Short Term ◽  
Tnf Α ◽  
Necrosis Factor

AbstractBackgroundNowadays, yoga is endorsed and advised routinely to stay fit and healthy, as well as control many chronic diseases including diabetes type 2, hypertension, coronary artery diseases, etc. Now, our assumption is that those who do regular yoga have different persona than who do not do yoga regularly. We planned to test our hypothesis scientifically, and therefore baseline physiological characteristics with stress and inflammation levels in long-term and short-term meditators and healthy novice controls were analyzed.MethodsIn this retrospective analysis, 97 male participants were included for their Baseline analysis. Fifteen apparently healthy subjects practicing preksha meditation (since >5 years, at least 5 days a week) were included as long-term meditators (LTMs); 58 subjects who attended one of our short-term yoga-based lifestyle intervention programs for 2 weeks were included as short-term meditators (STMs); 24 male novice subjects, who did not participate in any yogic intervention, were included as healthy controls. Here, we analyzed the Baseline plasma levels of stress and inflammatory markers, cortisol, β-endorphin, interleukin (IL)-6 and tumor necrosis factor (TNF)-α in long-term meditators vs. short-term meditators vs. healthy controls.Outcome measuresThe study parameters body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), plasma levels of stress and immune markers, cortisol, β-endorphin (β-Ed), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), were assessed in all the three groups at baseline.ResultsSignificant (p<0.05) differences were observed at baseline for plasma levels of stress and inflammatory markers as well as body mass index and systolic blood pressure among LTM vs. STM vs. healthy controls.ConclusionsOur observations suggest that the subjects who do regular yoga-meditation practice have better stress & inflammation status than comparable age matched healthy controls.

scholarly journals Knockdown of miR-660 protects nucleus pulposus cells from TNF-a-induced apoptosis by targeting serum amyloid A1

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Hao Jie Zhang ◽  
Xue Hai Ma ◽  
Song Lin Xie ◽  
Shu lian Qin ◽  
Cong Zhi Liu ◽  
...  
Keyword(s):  
Nucleus Pulposus ◽  
General Characteristic ◽  
Luciferase Reporter ◽  
Healthy Controls ◽  
Nucleus Pulposus Cells ◽  
Apoptosis Rate ◽  
Tnf Α ◽  
Significant Difference ◽  
Induced Apoptosis

Abstract Background Intervertebral disc degeneration (IVDD) is a well-known cause of lower back pain, which is induced by multiple factors including increased apoptosis and decreased survival of nucleus pulposus cells. In this study, we evaluate the effect and potential mechanism of miR-660 on the nucleus pulposus cells apoptosis induced by TNF-α. Methods First, we collected tissue of nucleus pulposus from IVDD and healthy controls. General characteristic of the IVDD and healthy control was also collected. And, we also collected nucleus pulposus cells that stimulated by TNF-α or control. miRNA microarray was performed to identify the differentially expressed miRNAs. Apoptosis rate and miR-660 relative expression was measured after stimulated with different concentration of TNF-α to identify the optimal concentration of TNF-α. Second, we successfully constructed antigomiR-660 to block the miR-660 expression in nucleus pulposus cells and then stimulated with TNF-α (100 ng/ml, 12 h). The apoptosis rates and relative protein expression were then measured again. The target association between miR-660 and SAA1 was confirmed by dual-luciferase reporter. Results There was no significant difference between the age (IVDD: 39 ± 10 years, healthy controls: 36 ± 7 years), BMI and sex between IVDD and healthy controls. Microarray analysis found that miR-660 was significantly up-regulated in IVDD and TNF-α treated groups, which was further identified by PCR. We found that the rate of apoptosis and miR-660 expression increased with TNF-α concentration increased. Finally, TNF-a with 100 ng/ml was used for further experiment. Compared with TNF-α group, TNF-α + antigomiR-660 could significantly down-regulated the apoptosis rate and relative protein (c-Caspase3 and c-Caspase7). Dual-luciferase reporter revealed that miR-660 could directly binding to the SAA1 at 80–87 sites. Compared with TNF-α alone group, TNF-α + antigomiR-660 significantly up-regulated the SAA1 expression (P < 0.05). Conclusion These results indicated that knockdown of miR-660 protected the nucleus pulposus from apoptosis that induced TNF-α via up-regulation of SAA1. Further studies should focus on the role of miR-660 in protecting IVDD in vivo.

scholarly journals Neutrophil DREAM Promotes Neutrophil Recruitment in Vascular Inflammation Via Nuclear Factor Kappa B-Dependent and Independent Mechanisms

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 435-435
Author(s):  
Tripti Kumari ◽  
Jing Li ◽  
Andrew Barazia, ◽  
Vishwanath Jha ◽  
Amber Hansch ◽  
...  
Keyword(s):  
Vascular Inflammation ◽  
Term Treatment ◽  
Neutrophil Recruitment ◽  
Neutrophil Adhesion ◽  
Short Term ◽  
Short Term Treatment ◽  
Tnf Α ◽  
Inflammatory Molecules ◽  
Β2 Integrins

Abstract The interaction between neutrophils and endothelial cells (ECs) is critical for the pathogenesis of vascular inflammation. Neutrophil recruitment to inflamed tissues is initiated by rolling on activated ECs through the interactions between P-/E-selectins and their ligands. Subsequently, activated integrins (mainly αLβ2 and αMβ2) and chemokine receptors bind to their ligands on ECs and mediate slow-rolling, adhesion, crawling, and transmigration of neutrophils. Although many neutrophil adhesion receptors have been identified, the regulation of their ligand-binding function remains not fully understood. Using real-time intravital microscopy with mice lacking downstream regulatory element antagonist modulator (DREAM) and their bone marrow chimeric mice, we demonstrated that hematopoietic cell DREAM contributes to neutrophil recruitment to sites of vascular inflammation induced by TNF-α- but not a G protein-coupled receptor ligand, MIP-2 or fMLP. Our studies using adoptive neutrophil transfers and flow chamber assays revealed that neutrophil DREAM positively regulates the neutrophil recruitment processes under TNF-α-induced inflammatory conditions. Using RNA-seq and biochemical and cell biological studies, we found that neutrophil DREAM upregulates numerous pro-inflammatory molecules and down-regulates anti-inflammatory molecules after TNF-α treatment. In particular, neutrophil DREAM repressed expression of A20, a negative regulator of NF-κB signaling, and enhanced phosphorylation of IκB kinase (IKK) in response to TNF-α, suggesting the role of neutrophil DREAM in NF-κB activity. Furthermore, we observed that DREAM deletion and IKK inhibition significantly diminishes the ligand-binding activity of β2 integrins in neutrophils after short-term treatment with TNF-α and that deletion of neutrophil DREAM does not affect the expression of other neutrophil adhesion receptors, such as PSGL-1, L-selectin, CD44, CXCR2, and CXCR4. As assessed by flow cytometry using conformation-specific reporter antibodies, knockdown of DREAM in neutrophil-like HL-60 cells decreased TNF-α-induced activation of β2 integrins. Neutrophil DREAM promoted degranulation through IKK-mediated SNAP-23 phosphorylation after short-term treatment with TNF-α, implying the role of neutrophil DREAM-IKK signaling in NF-κB-independent signaling. Using intravital microscopy with Berkeley mice (a mouse model of sickle cell disease) deficient in hematopoietic or nonhematopoietic DREAM, we demonstrated that hematopoietic cell DREAM is crucial for inducing intravascular cell-cell aggregation and vaso-occlusive events in microvessels following the TNF-α challenge. Furthermore, infusion of DREAM KO neutrophils, compared with WT neutrophils, significantly reduced neutrophil recruitment and vaso-occlusive events in TNF-α-challenged SCD mice. These results demonstrate that neutrophil DREAM positively regulates β2 integrin function and promotes neutrophil recruitment during sterile inflammation via NF-κB-dependent and independent mechanisms. Our study provides evidence that targeting DREAM might be a novel therapeutic strategy to reduce excessive neutrophil recruitment in inflammatory diseases. Disclosures No relevant conflicts of interest to declare.

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