S100A8 and S100A9 Secreted by Allergens in Monocytes Inhibit Spontaneous Apoptosis of Normal and Asthmatic Neutrophils via the Lyn/Akt/ERK Pathway

Kim, In Sik; Lee, Ji-Sook

doi:10.15324/kjcls.2017.49.2.128

Cited by 4 publications

(2 citation statements)

References 23 publications

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“…IL-6 and IL-8 are neutrophil survival factors and pleiotropic cytokines, which affect transition of allergic phase, activation of stromal cells, and chemotaxis (Kim and Lee, 2017). Our study supports that S100A8 promotes a pro-inflammatory effect including cytokine release and inhibition of neutrophil apoptosis in allergic diseases.…”

Section: Brief Communicationsupporting

confidence: 79%

Inhibitory Effect of S100A8 on Neutrophil Apoptosis by Cytokine Release of Normal and Allergic Monocytes

Lee

2020

BSL

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S100A8 functions as an essential factor in inflammatory response. Cytokine release of monocytes and regulation of neutrophil apoptosis are important steps in pathogenesis of allergy. This study aims to examine the relation between cytokine release of monocytes due to S100A8 and neutrophil apoptosis. S100A8 enhanced the release of IL-6 and IL-8 in monocytes of normal and allergic subjects. Treatment of supernatants of normal and allergic monocytes with S100A8 blocked neutrophil apoptosis by inhibition of caspase 9 and caspase 3 activation. The secretion signal induced by S100A8 is involved in TLR4, Src family protein, PKCδ, ERK1/2, p38 MAPK, JNK, and NF-κB. These findings may contribute to understanding the complex pathogenesis of allergic diseases by determining inflammatory responses associated with S100A8, monocytes, and neutrophils.

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Section: Brief Communicationsupporting

confidence: 79%

Inhibitory Effect of S100A8 on Neutrophil Apoptosis by Cytokine Release of Normal and Allergic Monocytes

Lee

2020

BSL

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“…S100A8 and S100A9 are included in the S100 family of proteins and constitutively expressed in monocytes and neutrophils (Nam et al, 2016;Kim et al, 2017;Kim and Lee, 2017). Most studies of S100A8 and S100A9 have focused on their roles in inflammatory responses (Goyette and Geczy, 2011;Austermann et al, 2017).…”

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confidence: 99%

The Pro-apoptotic Effects of S100A8 and S100A9 in Human Monocytic Leukemia Cells, THP-1

Kim

Lee

2018

BSL

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S100A8 and S100A9 are involved in pathogenesis of cancer by induction or inhibition of cancer as well as inflammation. In this study, we investigated the association of S100A8 and S100A9 with pathogenesis of leukemia using human monocytic leukemia cells, THP-1. The expression of TLR4, which is a known receptor of S100A8 and S100A9, was examined by using flow cytometry and Western blotting. THP-1 cells have high surface and cytosol expression of TLR4. S100A8 and S100A9 suppressed the cell survival, and this suppression was found to be associated with apoptosis because they increased the number of apoptotic cells in a dose-and a time-dependent manners. However, S100A8 and S100A9 had no effect on the survival and apoptosis of monocytes isolated from the peripheral blood. We next examined the apoptotic effect of lipopolysaccharide (LPS) and monophosphoryl lipid A (MPLA), which are other ligands of TLR4, in THP-1 cells. Lipopolysaccharide had no effect on cell survival, but MPLA is effective on the cell apoptosis. These results suggest that S100A8 and S100A9 may regulate leukemia cell survival via TLR4, which is an essential receptor in the pro-apoptotic mechanism induced by S100A8 and S100A9. These findings may shed light on development of a possible therapeutic drug for leukemia treatment.

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Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells

Choi

Kim

et al. 2020

Korean J Clin Lab Sci.

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Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease that can be described by the occurrence of dementia due to a decline in cognitive function. The disease is characterized by the formation of extracellular and intracellular amyloid plaques. Amyloid beta (Aβ) is a hallmark of AD, and microglia can be activated in the presence of Aβ. Activated microglia secrete pro-inflammatory cytokines. Furthermore, S100A9 is an important innate immunity pro-inflammatory contributor in inflammation and a potential contributor to AD. This study examined the effects of metformin and α-LA on the inflammatory response and NLRP3 inflammasome activation in Aβand S100A9-induced BV-2 microglial cells. Metformin and α-LA attenuated inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, metformin and α-LA inhibited the phosphorylation of JNK, ERK, and p38. They activated the nuclear factor kappa B (NF-κ B) pathway and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Moreover, metformin and α-LA reduced the marker levels of the M1 phenotype, ICAM1, whereas the M2 phenotype, ARG1, was increased. These findings suggest that metformin and α-LA are therapeutic agents against the Aβ-and S100A9-induced neuroinflammatory responses.

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S100A8 and S100A9 Secreted by Allergens in Monocytes Inhibit Spontaneous Apoptosis of Normal and Asthmatic Neutrophils via the Lyn/Akt/ERK Pathway

Cited by 4 publications

References 23 publications

Inhibitory Effect of S100A8 on Neutrophil Apoptosis by Cytokine Release of Normal and Allergic Monocytes

Inhibitory Effect of S100A8 on Neutrophil Apoptosis by Cytokine Release of Normal and Allergic Monocytes

The Pro-apoptotic Effects of S100A8 and S100A9 in Human Monocytic Leukemia Cells, THP-1

Metformin or α-Lipoic Acid Attenuate Inflammatory Response and NLRP3 Inflammasome in BV-2 Microglial Cells

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