Interleukin-1 and its inhibitors: Implications for disease biology and therapy

Estrov, Zeev; Kurzrock, Razelle; Talpaz, Moshe

doi:10.1007/978-1-4613-1241-3_3

Cited by 8 publications

(5 citation statements)

References 238 publications

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“…IL-1a and Alb levels were most significantly higher, by 51% (p = 0.0007) and 74% (p = 0.0021), respectively. The demonstrated increase in IL-1a seems to result from the inflammatory pathogenesis of the disease, since IL-1a has proinflammatory properties, especially relating to bone destruction and osteoclast activation [14][15][16]. The induced inflammation, in turn, compromises the integrity of the gingival crevicular mucosa, followed by profound leakage of inborn serum Alb.…”

Section: Discussionmentioning

confidence: 93%

Salivary Biomarker Analysis Complementing Regular Clinical Examination

et al. 2013

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Section: Discussionmentioning

confidence: 93%

Salivary Biomarker Analysis Complementing Regular Clinical Examination

et al. 2013

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“…Their biological activities are mostly indistinguishable. 34 IL-1 activates neutrophils, up-regulates adhesion molecules, promotes chemotaxis, and signals other cells to produce pro-inflammatory cytokines, such as TNF-a, further contributing to the inflammatory process. 35 Experimental studies have demonstrated that IL-1 is involved in the mechanism of ischemia-reperfusion injury through its influence on inflammation.…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory Cytokines Gene Expression in Skin Flaps with Arterial and Venous Ischemia in Rats

Zhang¹,

Hu²,

Topp³

et al. 2006

J reconstr Microsurg

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Infiltration of inflammatory cells is the crucial element in ischemia-reperfusion injury of the microsurgical flap. Cytokines are a large functional group of polypeptide regulatory molecules that influence the activity of various cell types through autocrine and paracrine mechanisms. In this study, expression of selected proinflammatory cytokines was examined in skin flaps with arterial and venous ischemia in the rat model. Fifty-four Sprague-Dawley rats were used in the study. The ischemia of each flap was induced by clamping its vascular pedicle for 6 hr. The flap was then replaced and allowed to reperfuse. All flaps were biopsied immediately post-event, and at 3, 6 and 18 hr after reperfusion. Expression of tumor necrosis factor (TNF-alpha), interleukin (IL-1beta), and monocyte chemoattractant protein-1 (MCP-1) mRNA was determined by RT-PCR in each case. The same number of skin flaps without ischemia was used for baseline gene expression. Results showed that the TNF-alpha expression was significantly up-regulated in the flaps with arterial ischemia at 6 hr after reperfusion. In the flaps with venous ischemia, MCP-1 expression was increased with its peak expression at 3 hr after reperfusion. IL-1beta expression was increased threefold in the flaps subjected to venous ischemia and following reperfusion in 3 hr, but the peak expression in the flap with arterial ischemia was observed at 18 hr after reperfusion. This study delineated the changes in expression of these proinflammatory cytokines in flaps with arterial and venous ischemia reperfusion injury, and showed that cytokine expression was different in the arterial and venous injuries.

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“…Interleukin-1β (IL-1β) is a potent proinflammatory cytokine that is crucial for host-defense responses to infection and injury [ 108 ]. Interestingly, C2C12 myotubes release IL-1β after the incubation with free fatty acids [ 109 ].…”

Section: Effect Of Cytokines On Skeletal Musclementioning

confidence: 99%

Reactive Oxygen and Nitrogen Species (RONS) and Cytokines—Myokines Involved in Glucose Uptake and Insulin Resistance in Skeletal Muscle

Palomero

2022

Cells

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Insulin resistance onset in skeletal muscle is characterized by the impairment of insulin signaling, which reduces the internalization of glucose, known as glucose uptake, into the cell. Therefore, there is a deficit of intracellular glucose, which is the main source for energy production in the cell. This may compromise cellular viability and functions, leading to pathological dysfunction. Skeletal muscle fibers continuously generate reactive oxygen and nitrogen species (RONS). An excess of RONS produces oxidative distress, which may evoke cellular damage and dysfunction. However, a moderate level of RONS, which is called oxidative eustress, is critical to maintain, modulate and regulate cellular functions through reversible interactions between RONS and the components of cellular signaling pathways that control those functions, such as the facilitation of glucose uptake. The skeletal muscle releases peptides called myokines that may have endocrine and paracrine effects. Some myokines bind to specific receptors in skeletal muscle fibers and might interact with cellular signaling pathways, such as PI3K/Akt and AMPK, and facilitate glucose uptake. In addition, there are cytokines, which are peptides produced by non-skeletal muscle cells, that bind to receptors at the plasma membrane of skeletal muscle cells and interact with the cellular signaling pathways, facilitating glucose uptake. RONS, myokines and cytokines might be acting on the same signaling pathways that facilitate glucose uptake in skeletal muscle. However, the experimental studies are limited and scarce. The aim of this review is to highlight the current knowledge regarding the role of RONS, myokines and cytokines as potential signals that facilitate glucose uptake in skeletal muscle. In addition, we encourage researchers in the field to lead and undertake investigations to uncover the fundamentals of glucose uptake evoked by RONS, myokines, and cytokines.

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Interleukin-1 and its inhibitors: Implications for disease biology and therapy

Cited by 8 publications

References 238 publications

Salivary Biomarker Analysis Complementing Regular Clinical Examination

Salivary Biomarker Analysis Complementing Regular Clinical Examination

Proinflammatory Cytokines Gene Expression in Skin Flaps with Arterial and Venous Ischemia in Rats

Reactive Oxygen and Nitrogen Species (RONS) and Cytokines—Myokines Involved in Glucose Uptake and Insulin Resistance in Skeletal Muscle

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