Cytokines in Acute Myocardial Infarction

Latini, Roberto; Bianchi, Marina; Correale, E; Dinarello, Charles A.; Fantuzzi, Giamila; Fresco, Claudio; Maggioni, Aldo P.; Mengozzi, Manuela; Romano, Salvatore; Shapiro, Leland; Sironi, Marina; Tognoni, Gianni; Turato, Roberto; Ghezzi, Pietro

doi:10.1097/00005344-199401000-00026

Cited by 55 publications

(1 citation statement)

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“…Elevated levels of proinflammatory cytokines have also been associated with chronic heart failure, myocardial infarction, cardiomyopathies, cardiac transplant rejection, and atherosclerosis, although it is unclear if elevated cytokines directly contribute to cardiac pathology or if they are a biomarker of overall disease severity. 105 Elevated levels of TNF-α, IL-1, IL-6, IL-15, and IL-17 correlate to decreased functional status in patients with chronic heart failure. 106,107 The role of cytokines in chronic cardiovascular disease are reviewed elsewhere.…”

Section: Cytokines and Cardiovascular Toxicitymentioning

confidence: 99%

Mechanisms of Cardiovascular Toxicities Associated With Immunotherapies

Baik

Oluwole

Johnson

et al. 2021

Circulation Research

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Immune-based therapies have revolutionized cancer treatments. Cardiovascular sequelae from these treatments, however, have emerged as critical complications, representing new challenges in cardio-oncology. Immune therapies include a broad range of novel drugs, from antibodies and other biologics, including immune checkpoint inhibitors and bispecific T-cell engagers, to cell-based therapies, such as chimeric-antigen receptor (CAR) T-cell therapies. The recognition of immunotherapy-associated cardiovascular side effects has also catapulted new research questions revolving around the interactions between the immune and cardiovascular systems, and the signaling cascades affected by T cell activation, cytokine release, and immune system dysregulation. Here, we review the specific mechanisms of immune activation from immunotherapies and the resulting cardiovascular toxicities associated with immune activation and excess cytokine production.

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Section: Cytokines and Cardiovascular Toxicitymentioning

confidence: 99%

Mechanisms of Cardiovascular Toxicities Associated With Immunotherapies

Baik

Oluwole

Johnson

et al. 2021

Circulation Research

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Interleukin‐6 and interleukin‐1 receptor antagonist in acute stroke

Beamer

Coull

Clark

et al. 1995

Annals of Neurology

211

128

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Elevated plasma levels of interleukin-6 (IL-6), a key regulator of the acute phase response that includes increased fibrinogen synthesis, have recently been detected in patients with acute stroke. Nevertheless, the role of the acute phase response in stroke has been controversial, with some studies suggesting that preexisting infection accounts for most of the acute phase response. Increased IL-6 could signal the involvement of antiinflammatory activity, since IL-6 stimulates the production of endogenous antiinflammatory mediators such as interleukin-1 receptor antagonist (IL-1RA). To better understand the interaction of pro- and antiinflammatory acute phase processes in brain infarction, plasma levels of IL-1RA, IL-6, and acute phase proteins including fibrinogen and c-reactive protein (CRP) were measured within 4 +/- 2 days of onset in 50 patients with acute ischemic stroke and in 20 age-matched healthy controls. After excluding patients with evidence of infection, both IL-1RA and IL-6 were significantly elevated in stoke patients compared with controls (p < 0.0001). IL-1RA and IL-6 were both significantly correlated with levels of CRP, p < 0.05 and p < 0.001, respectively, but not with each other. Levels of IL-6 and IL-1RA, together with fibrinogen and CRP were higher in patients with infarcts of greater than 3 cm and lowest in patients with lacunar syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of tumor necrosis factor‐alpha central administration on hippocampal damage in rat induced by amyloid beta‐peptide (25–35)

Stepanichev

Zdobnova

Yakovlev

et al. 2002

J of Neuroscience Research

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Male Wistar rats received unilateral intrahippocampal injections of 3 nmol (3.18 microg) aggregated Abeta(25-35), intracerebroventricular bilateral injections of 0.5 microg human recombinant TNFalpha or both (Abeta(25-35) + TNFalpha-treated animals). Seven days after the surgery brain sections were stained with cresyl violet (Nissl), for fragmented DNA (TUNEL), glial fibrillar acidic protein (GFAP) and isolectin B4-reactive microglia. In addition, caspase-3 activity in brain regions was measured fluorometrically. The morphology of the hippocampus after the injection of Abeta(25-35) or both Abeta(25-35) and TNFalpha (but not TNFalpha alone) showed cell loss in the CA1 pyramidal cell layer. The extension of neuronal degeneration measured in the CA1 field was significantly larger in Abeta(25-35)-treated groups compared to the contralateral hemisphere of both vehicle-treated controls and animals injected with TNFalpha alone. TNFalpha augmented the Abeta(25-35)-induced damage, significantly increasing the extension of degenerating area. Administration of Abeta(25-35) caused reactive gliosis in the ipsilateral hemisphere as demonstrated by upregulation of GFAP expression and the presence of hypertrophic astrocytes in the hippocampus. This effect was much more prominent in the hippocampi of rats treated with Abeta(25-35) + TNFalpha but absent after administration of TNFalpha alone. In both Abeta(25-35)-treated groups, the damaged area of the hippocampal CA1 field and lateral band of dentate gyrus displayed many darkly stained round isolectin B4-positive phagocyte-like microglial cells. Sparse TUNEL-positive nuclei were found in the hippocampi of rats treated with Abeta(25-35) alone or together with TNFalpha, but not in the control brain sections or in brain sections of TNFalpha-injected animals. The activity of caspase-3 increased significantly in the ipsilateral hippocampus after the injection of Abeta(25-35). Surprisingly, administration of TNFalpha into the cerebral ventricles prevented this Abeta(25-35)-induced increase in hippocampal caspase-3 activity. The results are discussed from the perspective of dual (neuroprotective and neurodestructive) roles of TNF in the brain.

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Cytokines in Acute Myocardial Infarction

Cited by 55 publications

References 0 publications

Mechanisms of Cardiovascular Toxicities Associated With Immunotherapies

Mechanisms of Cardiovascular Toxicities Associated With Immunotherapies

Interleukin‐6 and interleukin‐1 receptor antagonist in acute stroke

Effects of tumor necrosis factor‐alpha central administration on hippocampal damage in rat induced by amyloid beta‐peptide (25–35)

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