IL-17A promotes the formation of deep vein thrombosis in a mouse model

Ding, Peiwu; Zhang, Shaoshao; Yu, Miao; Feng, Yuqian; Long, Qi; Yang, Huimin; Li, Jingdong; Wang, Min

doi:10.1016/j.intimp.2018.02.006

Cited by 42 publications

(32 citation statements)

References 32 publications

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“…With regard to this cytokine, we emphasize that IL-17 is a pro-inflammatory molecule that activates macrophages, fibroblasts, and stromal cells, including the expression of ICAM-1 and cytokine secretion (IL-6, CXCL-8, IL-11, factor granulocyte colony stimulator [G-CSF]), prostaglandin E2, and nitric oxide) (65-67). Ding et al reported that IL-17A promotes the pathogenesis of deep vein thrombosis (DVT), improving platelet activation and aggregation, neutrophil infiltration, and activation of endothelial cells in murine models (68).…”

Section: Discussionmentioning

confidence: 99%

Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

et al. 2020

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Snakebites are considered a major public health problem worldwide. In the Amazon region of Brazil, the snake Bothrops atrox ( B. atrox ) is responsible for 90% of the bites. These bites may cause local and systemic signs from acute inflammatory reaction and hemostatic changes, and present common hemorrhagic disorders. These alterations occur due the action of hemostatically active and immunogenic toxins which are capable of triggering a wide range of hemostatic and inflammatory events. However, the crosstalk between coagulation disorders and inflammatory reaction still has gaps in snakebites. Thus, the goal of this study was to describe the relationship between the consumption of fibrinogen and the profile of inflammatory molecules (chemokines and cytokines) in evenomations by B. atrox snakebites. A prospective study was carried out with individuals who had suffered B. atrox snakebites and presented different levels of fibrinogen consumption (normal fibrinogen [NF] and hypofibrinogenemia [HF]). Seventeen patients with NF and 55 patients with HF were eligible for the study, in addition to 50 healthy controls (CG). The molecules CXCL-8, CCL-5, CXCL-9, CCL-2, CXCL-10, IL-6, TNF, IL-2, IL-10, IFN-γ, IL-4, and IL-17A were quantified in plasma using the CBA technique at three different times (pre-antivenom therapy [T0], 24 h [T1], and 48 h [T2] after antivenom therapy). The profile of the circulating inflammatory response is different between the groups studied, with HF patients having higher concentrations of CCL-5 and lower IFN-γ. In addition, antivenom therapy seems to have a positive effect, leading to a profile of circulating inflammatory response similar in quantification of T1 and T2 on both groups. Furthermore, these results suggest that a number of interactions of CXCL-8, CXCL-9, CCL-2, IL-6, and IFN-γ in HF patients are directly affected by fibrinogen levels, which may be related to the inflammatory response and coagulation mutual relationship induced by B. atrox venom. The present study is the first report on inflammation-coagulation crosstalk involving snakebite patients and supports the better understanding of envenomation's pathophysiology mechanisms and guides in the search for novel biomarkers and prospective therapies.

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Section: Discussionmentioning

confidence: 99%

Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

et al. 2020

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“…The increasing level of IL-17 could also be related to the hypercoagulation status in patients with coronavirus disease 2019 (COVID-19). 5 Specific IL-17 and SARS-CoV-2 Evidence…”

Section: Possible Role Of Interleukin-17 In Severe Acute Respiratory mentioning

confidence: 99%

Severe Acute Respiratory Syndrome–Coronavirus-2 Infection and Patients With Lung Cancer: The Potential Role of Interleukin-17 Target Therapy

Cafarotti¹

2020

Journal of Thoracic Oncology

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“…In contrast, in PV and in ET, the levels of many cytokines or receptors correlated positively with the blood counts of leukocytes, neutrophils and monocytes (IL-1β, IL-1Rα, HGF, MIG), platelets (IL-9, IL-17, SDF-1α) or lymphocytes (IL-9). Of note, recent reports describe IL-9 as a STAT5 activator that enhances megakaryocytopoiesis, and both IL-9 and IL-17 as prothrombotic cytokines [ 58 , 59 , 60 ]. In contrast, the PMF cohort was characterized by negative correlations between numerous cytokines and blood counts of leukocytes, neutrophils and monocytes (TNFα, IL-10, IL-15, VEGF, MIP-1β, IL-8, others) and lymphocytes (IL-17, MIP-1α).…”

Section: Discussionmentioning

confidence: 99%

Anti-Glucosylsphingosine Autoimmunity, JAK2V617F-Dependent Interleukin-1β and JAK2V617F-Independent Cytokines in Myeloproliferative Neoplasms

Allain-Maillet

Bosseboeuf

Mennesson

et al. 2020

Cancers

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Inflammatory cytokines play a major role in myeloproliferative neoplasms (MPNs) as regulators of the MPN clone and as mediators of clinical symptoms and complications. Firstly, we investigated the effect of JAK2V617F on 42 molecules linked to inflammation. For JAK2V617F-mutated patients, the JAK2V617F allele burden (%JAK2V617F) correlated with the levels of IL-1β, IL-1Rα, IP-10 and leptin in polycythemia vera (PV), and with IL-33 in ET; for all other molecules, no correlation was found. Cytokine production was also studied in the human megakaryocytic cell line UT-7. Wild-type UT-7 cells secreted 27/42 cytokines measured. UT-7 clones expressing 50% or 75% JAK2V617F were generated, in which the production of IL-1β, IP-10 and RANTES was increased; other cytokines were not affected. Secondly, we searched for causes of chronic inflammation in MPNs other than driver mutations. Since antigen-driven selection is increasingly implicated in the pathogenesis of blood malignancies, we investigated whether proinflammatory glucosylsphingosine (GlcSph) may play a role in MPNs. We report that 20% (15/75) of MPN patients presented with anti-GlcSph IgGs, distinguished by elevated levels of 11 cytokines. In summary, only IL-1β and IP-10 were linked to JAK2V617F both in patients and in UT-7 cells; other inflammation-linked cytokines in excess in MPNs were not. For subsets of MPN patients, a possible cause of inflammation may be auto-immunity against glucolipids.

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IL-17A promotes the formation of deep vein thrombosis in a mouse model

Cited by 42 publications

References 32 publications

Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

Severe Acute Respiratory Syndrome–Coronavirus-2 Infection and Patients With Lung Cancer: The Potential Role of Interleukin-17 Target Therapy

Anti-Glucosylsphingosine Autoimmunity, JAK2V617F-Dependent Interleukin-1β and JAK2V617F-Independent Cytokines in Myeloproliferative Neoplasms

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