Tumor Necrosis Factor-α- and Interleukin-1-Induced Cellular Responses: Coupling Proteomic and Genomic Information

Ott, Lee W.; Resing, Katheryn A.; Sizemore, Alecia W.; Heyen, Joshua W.; Cocklin, Ross R.; Pedrick, Nathan M.; Woods, H. Cary; Chen, Jake Y.; Goebl, Mark G.; Witzmann, Frank A.; Harrington, Maureen A.

doi:10.1021/pr200763q

Cited by 9 publications

(11 citation statements)

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“…A noteworthy observation was that CIA did not seem to have an effect on levels of MCP-1 (p = 0.71) or MIF (p = 0.72), cytokines specifically associated with macrophage migration into tissue In response to an insult, TNF-α is released by circulating macrophages, which further stimulate the production and release of more TNF-α as well as IL-1. IL-1 then induces the production of IL-6 (Ott et al, 2007). The significant increase in TNF-α in the current study indicates the presence of active disease and the central role of TNF-α.…”

Section: Discussionsupporting

confidence: 52%

“…In response to an insult, TNF‐α is released by circulating macrophages, which further stimulate the production and release of more TNF‐α as well as IL‐1. IL‐1 then induces the production of IL‐6 (Ott et al, 2007). The significant increase in TNF‐α in the current study indicates the presence of active disease and the central role of TNF‐α.…”

Section: Discussionmentioning

confidence: 99%

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Unresolved intramuscular inflammation, not diminished skeletal muscle regenerative capacity, is at the root of rheumatoid cachexia: insights from a rat CIA model

Ollewagen

Powrie

Myburgh

et al. 2021

Physiological Reports

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Unresolved intramuscular inflammation, not diminished skeletal muscle regenerative capacity, is at the root of rheumatoid cachexia: insights from a rat CIA model

Ollewagen

Powrie

Myburgh

et al. 2021

Physiological Reports

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“…The decreased expression of YKL40 by OA chondrocytes is surprising because increased levels have been reported in patients with RA, patients with neuropsychiatric lupus, and in the synovial fluid of patients with OA (49). Its presence in synovial fluid may derive from activated synovial cells, osteophytic tissue, or increased matrix destruction in the OA joint (39, 51, 52).…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis by two‐dimensional electrophoresis to identify the normal human chondrocyte proteome stimulated by tumor necrosis factor α and interleukin‐1β

Cillero‐Pastor¹,

Ruiz-Romero²,

Caramés³

et al. 2010

Arthritis & Rheumatism

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Objective. To determine the intracellular proteome of normal human chondrocytes stimulated with interleukin-1␤ (IL-1␤) and tumor necrosis factor ␣ (TNF␣) and to ascertain differences in the protein expression patterns of these 2 cytokines.Methods. Normal human knee cartilage chondrocytes were incubated for 48 hours without stimulation or stimulated with IL-1␤ (5 ng/ml) or with TNF␣ (10 ng/ml). For each culture condition, protein extracts from 4 normal subjects were pooled and resolved using 2-dimensional electrophoresis. Protein spots were visualized with Sypro stain, and qualitative and quantitative analyses were performed using PDQuest software. Protein spots were then identified by mass spectrometry, using matrix-assisted laser desorption ionization؊time-of-flight/time-of-flight technology.Results. We identified 37 spots by mass spectrometry (MS) or by MS/MS, corresponding to 35 different proteins. In IL-1␤-stimulated chondrocytes, IL-1␤ was found to modulate 22 proteins, as compared with unstimulated chondrocytes. All of these proteins except connective tissue growth factor (CCND2) were upregulated. Proteins involved in cellular metabolism and energy (23%) that were up-regulated or induced by IL-1␤ included nicotinamide phosphoribosyltransferase, long-chain fatty acid-coenzyme A ligase 4, ␦-aminolevulinic acid dehydratase, triosephosphate isomerase, and an isoform of glyceraldehyde-3-phosphate dehydrogenase. In TNF␣-stimulated chondrocytes, TNF␣ was found to modulate 20 proteins, as compared with unstimulated chondrocytes. All of these except chitinase 3-like 1 (cartilage glycoprotein 39), proteasome activator complex subunit 2, and G3PDH, were up-regulated. Eighteen proteins were differently modulated by IL-1␤ and TNF␣. Of these, 45% were related to metabolism.Conclusion. IL-1␤ and TNF␣ induce different profiles of intracellular protein expression in healthy human chondrocytes. Most of the proteins that are differently regulated are proteins that are implicated in the generation of cellular energy and in glycolysis.

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“…Some of these cytokines decrease the risk of IBS such as anti-inflammatory cytokines as IL-10 [20,21], and some of them are found associated with the development of the IBS [22] such as pro-inflammatory cytokines, which always promote the inflammation response such as IL-1, IL-6, IL-8, IL-12, IL-18, and TNF-α, etc. [23][24][25]. The main pro-inflammatory cytokines associated with IBS are IL-6, IL-8, and TNF-α [26].…”

Section: Pro-inflammatory Cytokines Associated With Ibsmentioning

confidence: 99%

Targeted therapy of irritable bowel syndrome with anti-inflammatory cytokines

Kumar

Singh

Kumar

2021

Clin J Gastroenterol

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Irritable bowel syndrome (IBS) is a multifactorial disease of which infection, as well as inflammation, has recently been considered as an important cause. Inflammation works as a potential pathway for the pathogenesis of IBS. In this review, we have discussed the targeted therapy of IBS. We used the search term “inflammation in IBS” and “proinflammatory” and “antiinflammatory cytokines and IBS” using PubMed, MEDLINE, and Google Scholar. The literature search included only articles written in the English language. We have also reviewed currently available anti-inflammatory treatment and future perspectives. Cytokine imbalance in the systematic circulation and the intestinal mucosa may also characterize IBS presentation. Imbalances of pro-and anti-inflammatory cytokines and polymorphisms in cytokine genes have been reported in IBS. The story of targeted therapy of IBS with anti-inflammatory cytokines is far from complete and it seems that it has only just begun. This review describes the key issues related to pro-inflammatory cytokines associated with IBS, molecular regulation of immune response in IBS, inhibitors of pro-inflammatory cytokines in IBS, and clinical perspectives of pro- and anti-inflammatory cytokines in IBS.

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Tumor Necrosis Factor-α- and Interleukin-1-Induced Cellular Responses: Coupling Proteomic and Genomic Information

Cited by 9 publications

References 0 publications

Unresolved intramuscular inflammation, not diminished skeletal muscle regenerative capacity, is at the root of rheumatoid cachexia: insights from a rat CIA model

Unresolved intramuscular inflammation, not diminished skeletal muscle regenerative capacity, is at the root of rheumatoid cachexia: insights from a rat CIA model

Proteomic analysis by two‐dimensional electrophoresis to identify the normal human chondrocyte proteome stimulated by tumor necrosis factor α and interleukin‐1β

Targeted therapy of irritable bowel syndrome with anti-inflammatory cytokines

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