Interleukin-37: The Effect of Anti-Inflammatory Response in Human Coronary Artery Endothelial Cells

Yan, Xianfeng; Xie, Bin; Wu, Guihai; Hu, Jing; Wang, Di; Cai, Xianbin; Li, Jilin

doi:10.1155/2019/2650590

Cited by 15 publications

(20 citation statements)

References 119 publications

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“…Adenylate cyclase inhibition blocked transendothelial migration [ 24 ]. The downregulated gene interleukin-37 (IL-37, FC = −2.36) inhibits inflammatory response by suppressing the TLR2-NF-κB-ICAM-1 pathway in coronary artery endothelial cells and is possibly involved in the adhesion and transmigration of neutrophils through such endothelial cells [ 25 ]. Additionally, IL-37 promotes endothelial activation and angiogenesis [ 26 ].…”

Section: Resultsmentioning

confidence: 99%

Inter-Tumor Heterogeneity—Melanomas Respond Differently to GM-CSF-Mediated Activation

Moshe

Izraely

Sagi‐Assif

et al. 2020

Cells

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Granulocyte-monocyte colony stimulating factor (GM-CSF) is used as an adjuvant in various clinical and preclinical studies with contradictory results. These were attributed to opposing effects of GM-CSF on the immune or myeloid systems of the treated patients or to lack of optimal dosing regimens. The results of the present study point to inter-tumor heterogeneity as a possible mechanism accounting for the contrasting responses to GM-CSF incorporating therapies. Employing xenograft models of human melanomas in nude mice developed in our lab, we detected differential functional responses of melanomas from different patients to GM-CSF both in vitro as well as in vivo. Whereas cells of one melanoma acquired pro metastatic features following exposure to GM-CSF, cells from another melanoma either did not respond or became less malignant. We propose that inter-melanoma heterogeneity as manifested by differential responses of melanoma cells (and perhaps also of other tumor) to GM-CSF may be developed into a predictive marker providing a tool to segregate melanoma patients who will benefit from GM-CSF therapy from those who will not.

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Section: Resultsmentioning

confidence: 99%

Inter-Tumor Heterogeneity—Melanomas Respond Differently to GM-CSF-Mediated Activation

Moshe

Izraely

Sagi‐Assif

et al. 2020

Cells

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“…Anti-inflammatory factors, by their nature, would be expected to reduce inflammation including inflammageing. This is indeed the case with the potent anti-inflammatory cytokine IL-37 [108,109], which has an unequivocal effect in damping down harmful inflammation. For example, transgenic mice expressing human IL-37 showed little age-related increase in pro-inflammatory cytokines and maintained B cell progenitor function with age [110].…”

Section: Elevation Of Clusters Of Pro-inflammatory Markers With Agementioning

confidence: 89%

Interconnections between Inflammageing and Immunosenescence during Ageing

Teissier

Boulanger

Cox

2022

Cells

106

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Acute inflammation is a physiological response to injury or infection, with a cascade of steps that ultimately lead to the recruitment of immune cells to clear invading pathogens and heal wounds. However, chronic inflammation arising from the continued presence of the initial trigger, or the dysfunction of signalling and/or effector pathways, is harmful to health. While successful ageing in older adults, including centenarians, is associated with low levels of inflammation, elevated inflammation increases the risk of poor health and death. Hence inflammation has been described as one of seven pillars of ageing. Age-associated sterile, chronic, and low-grade inflammation is commonly termed inflammageing—it is not simply a consequence of increasing chronological age, but is also a marker of biological ageing, multimorbidity, and mortality risk. While inflammageing was initially thought to be caused by “continuous antigenic load and stress”, reports from the last two decades describe a much more complex phenomenon also involving cellular senescence and the ageing of the immune system. In this review, we explore some of the main sources and consequences of inflammageing in the context of immunosenescence and highlight potential interventions. In particular, we assess the contribution of cellular senescence to age-associated inflammation, identify patterns of pro- and anti-inflammatory markers characteristic of inflammageing, describe alterations in the ageing immune system that lead to elevated inflammation, and finally assess the ways that diet, exercise, and pharmacological interventions can reduce inflammageing and thus, improve later life health.

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“…Apparently, IL-37 precursor is converted to IL-37 by the action of caspase 1 (Casp1). IL-37 forms a complex with Smad3 (SMAD family member 3), and is translocated into the nucleus to inhibit the signal transduction of proinflammatory cytokines (Yan et al, 2019).…”

Section: Modulation Of the Innate Immunity By Lammentioning

confidence: 99%

Lipoarabinomannan as a Point-of-Care Assay for Diagnosis of Tuberculosis: How Far Are We to Use It?

2021

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Tuberculosis (TB) is still a severe public health problem; the current diagnostic tests have limitations that delay treatment onset. Lipoarabinomannan (LAM) is a glycolipid that is a component of the cell wall of the bacillus Mycobacterium tuberculosis, the etiologic agent of TB. This glycolipid is excreted as a soluble form in urine. The World Health Organization has established that the design of new TB diagnostic methods is one of the priorities within the EndTB Strategy. LAM has been suggested as a biomarker to develop diagnostic tests based on its identification in urine, and it is one of the most prominent candidates to develop point-of-care diagnostic test because urine samples can be easily collected. Moreover, LAM can regulate the immune response in the host and can be found in the serum of TB patients, where it probably affects a wide variety of host cell populations, consequently influencing the quality of both innate and adaptive immune responses during TB infection. Here, we revised the evidence that supports that LAM could be used as a tool for the development of new point-of-care tests for TB diagnosis, and we discussed the mechanisms that could contribute to the low sensitivity of diagnostic testing.

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Interleukin-37: The Effect of Anti-Inflammatory Response in Human Coronary Artery Endothelial Cells

Cited by 15 publications

References 119 publications

Inter-Tumor Heterogeneity—Melanomas Respond Differently to GM-CSF-Mediated Activation

Inter-Tumor Heterogeneity—Melanomas Respond Differently to GM-CSF-Mediated Activation

Interconnections between Inflammageing and Immunosenescence during Ageing

Lipoarabinomannan as a Point-of-Care Assay for Diagnosis of Tuberculosis: How Far Are We to Use It?

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