IL‐1 receptor antagonist in metabolic diseases: Dr Jekyll or Mr Hyde?

Perrier, Stéphane; Darakhshan, Froogh; Hajduch, Éric

doi:10.1016/j.febslet.2006.10.061

Cited by 136 publications

(107 citation statements)

References 76 publications

(80 reference statements)

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“…Accordingly, the balance between IL1 and IL1RN controls the inflammatory effect of IL1 (37). Indeed, we could demonstrate that PGC-1␣ suppresses the IL1␤-mediated response of acute phase proteins in hepatocytes, and at least in part, this is due to increased expression of IL1RN.…”

Section: Discussionmentioning

confidence: 72%

Energy-sensing Factors Coactivator Peroxisome Proliferator-activated Receptor γ Coactivator 1-α (PGC-1α) and AMP-activated Protein Kinase Control Expression of Inflammatory Mediators in Liver

Buler

Aatsinki

Skoumal

et al. 2012

Journal of Biological Chemistry

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Background: Metabolic disorders are associated with chronic inflammation. Results: Energy-sensing factor PGC-1␣ regulates cytokine expression in hepatocytes. PGC-1␣, AMPK, and metformin induce expression of interleukin 1 receptor antagonist. Conclusion: PGC-1␣ and AMPK mediate effects of fasting, physical exercise, and antidiabetic drug metformin on hepatic inflammatory gene expression. Significance: PGC-1␣ and AMPK are regulatory interlinks between energy homeostasis and inflammation.

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Section: Discussionmentioning

confidence: 72%

Energy-sensing Factors Coactivator Peroxisome Proliferator-activated Receptor γ Coactivator 1-α (PGC-1α) and AMP-activated Protein Kinase Control Expression of Inflammatory Mediators in Liver

Buler

Aatsinki

Skoumal

et al. 2012

Journal of Biological Chemistry

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“…IL-1RA inhibits the pro-inflammatory response of IL-1b, which is released primarily in response to exogenous agents. 33 While IL-1RA expression was similarly increased in infected WT and FPR1-KO mice, no increase was observed in FPR2-deficient mice. The difference between infected WT and infected FPR2-KO and also between infected FPR1-KO and FPR2-KO in the frontal cortex reached statistical significance (P < 0Á05; Fig.…”

Section: Rt-pcrmentioning

confidence: 98%

Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis

et al. 2014

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SummaryBacterial meningitis is, despite progress in research and the development of new treatment strategies, still a cause of severe neuronal sequelae. The brain is protected from penetrating pathogens by both the blood-brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G-protein coupled formyl peptide receptors (FPRs), which are expressed by immune cells of the central nervous system. The expression of FPRs is up-regulated during bacterial meningitis, but the consequence on the progression of inflammation and impact on mortality are far from clear. Therefore, we used mFPR1 and mFPR2-deficient mice to investigate the effects on inflammation, bacterial growth and mortality in a mouse model of pneumococcal meningitis. Our results revealed increased bacterial burden, increased neutrophil infiltration and higher mortality in mFPR1/2-deficient mice in comparison to wild-type mice. The mFPR1-or mFPR2-deficient mice also showed significantly increased glial cell density, whereas the immune responses including the expression of anti-inflammatory cytokines and antimicrobial peptides were decreased in bacterial meningitis. Taken together, the results suggest that FPR1 and FPR2 play an important role in the innate immune responses against Streptococcus pneumoniae within the central nervous system and the lack of the receptors leads to a dysregulation of the inflammatory response compared with wild-type mice.

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“…Moreover, recent data demonstrate a genuine interplay (ie a mutual regulation) between leptin and IL-1 family members in different models including breast cancer [19][20][21]. We have recently reported such an interplay in metabolic diseases and obesity [22] and it may also occur in breast cancer.…”

Section: Introductionmentioning

confidence: 93%

“…In contrast, the inflammatory site is more likely unbalanced in favor of IL-1, especially in severe lesions [27] and insufficient production of endogenous IL-1ra may contribute to the pathogeny of these conditions [see [22] for more details].…”

Section: Il-1 Family: Generalitiesmentioning

confidence: 99%

IL‐1 family in breast cancer: Potential interplay with leptin and other adipocytokines

2008

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Edited by Masayuki MiyasakaKeywords: IL-1 Leptin Adipocytokine Breast cancer Obesity a b s t r a c t Obesity is associated with an increased risk of breast cancer. interleukin-1 (IL-1), a pro-inflammatory cytokine secreted by adipose tissue, is involved in breast cancer development. There is also convincing evidence that other adipocytokines including leptin not only have a role in haematopoiesis, reproduction and immunity but are also growth factors in cancer. Therefore, IL-1 family and leptin family are adipocytokines which could represent a major link between obesity and breast cancer progression. This minireview provides insight into recent findings on the prognostic significance of IL-1 and leptin in mammary tumours, and discusses the potential interplay between IL-1 family members and adipocyte-derived hormones in breast cancer.

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IL‐1 receptor antagonist in metabolic diseases: Dr Jekyll or Mr Hyde?

Cited by 136 publications

References 76 publications

Energy-sensing Factors Coactivator Peroxisome Proliferator-activated Receptor γ Coactivator 1-α (PGC-1α) and AMP-activated Protein Kinase Control Expression of Inflammatory Mediators in Liver

Energy-sensing Factors Coactivator Peroxisome Proliferator-activated Receptor γ Coactivator 1-α (PGC-1α) and AMP-activated Protein Kinase Control Expression of Inflammatory Mediators in Liver

Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis

IL‐1 family in breast cancer: Potential interplay with leptin and other adipocytokines

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