Bacterial lipopolysaccharide and antimicrobial LL-37 enhance ICAM-1 expression and NF-κB p65 phosphorylation in senescent endothelial cells

Suzuki, Kaori; Ohkuma, Mari; Nagaoka, Isao

doi:10.3892/ijmm.2019.4294

Cited by 15 publications

(21 citation statements)

References 41 publications

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“…They showed that LPS hyperactivates the expression of SASP molecules (IL-6, IL-1β, CCL2, TNF-α, CCL5, CXCL1, and VCAM-1) and signaling molecules (p38 MAPK and p65 NF-κB) in senescent HUVECs that are generated by ionizing radiation [ 98 ] and long-term culture [ 26 ]. This confirms our speculation that LPS enhances the expression of SASP molecules, including adhesion molecules, cytokines, and chemokines, by enhancing the NF-κB pathway in senescent ECs [ 93 ]. In addition, the SASP-enhancing effect of LPS was suggested in other cell types.…”

Section: Lps Enhances Sasp-associated Proinflammatory Responses Of Se...supporting

confidence: 90%

“…This premise is consistent with the coexistence of LPS and SASP + cells (e.g., high ICAM-1-expressing SA-β-Gal + cells) on the vascular surface of atherosclerotic plaque [ 92 ]. Here, we present our results, demonstrating that LPS indeed increases ICAM-1 expression and NF-κB activation in senescent ECs as an SASP-enhancing agent under culture conditions [ 93 ].…”

Section: Lps Enhances Sasp-associated Proinflammatory Responses Of Se...mentioning

confidence: 99%

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Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis

Suzuki

Susaki

Nagaoka

2022

IJMS

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Atherosclerosis is a chronic inflammatory disease of the vascular walls related to aging. Thus far, the roles of cellular senescence and bacterial infection in the pathogenesis of atherosclerosis have been speculated to be independent of each other. Some types of macrophages, vascular endothelial cells, and vascular smooth muscle cells are in a senescent state at the sites of atherosclerotic lesions. Likewise, bacterial infections and accumulations of lipopolysaccharide (LPS), an outer-membrane component of Gram-negative bacteria, have also been observed in the atherosclerotic lesions of patients. This review introduces the integration of these two potential pathways in atherosclerosis. Previous studies have suggested that LPS directly induces cellular senescence in cultured monocytes/macrophages and vascular cells. In addition, LPS enhances the inflammatory properties (senescence-associated secretory phenotype [SASP]) of senescent endothelial cells. Thus, LPS derived from Gram-negative bacteria could exaggerate the pathogenesis of atherosclerosis by inducing and enhancing cellular senescence and the SASP-associated inflammatory properties of specific vascular cells in atherosclerotic lesions. This proposed mechanism can provide novel approaches to preventing and treating this common age-related disease.

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Section: Lps Enhances Sasp-associated Proinflammatory Responses Of Se...supporting

confidence: 90%

Section: Lps Enhances Sasp-associated Proinflammatory Responses Of Se...mentioning

confidence: 99%

Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis

Suzuki

Susaki

Nagaoka

2022

IJMS

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“…Afterward, we analyzed the morphological changes of gills and skin upon F. columnare infection, which showed similar results to those of IHNV-infected fish. In mammals, previous studies have shown that LPS cannot induce ICAM-1 expression in the intestinal epithelial cells ( 8 ), but enhanced ICAM-1 expression in the abnormal cells, such as senescent endothelial cells and cancer cells ( 43 , 44 ). Importantly, ICAM-1 plays a vital role in airway inflammation and bacterial clearance ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

Molecular Characterization and Expression Analysis of Intercellular Adhesion Molecule-1 (ICAM-1) Genes in Rainbow Trout (Oncorhynchus mykiss) in Response to Viral, Bacterial and Parasitic Challenge

et al. 2021

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The intercellular adhesion molecule-1 (ICAM-1), known as CD54, is a transmembrane cell surface glycoprotein that interacts with two integrins (i.e., LFA-1 and Mac-l) important for trans-endothelial migration of leukocytes. The level of ICAM-1 expression is upregulated in response to some inflammatory stimulations, including pathogen infection and proinflammatory cytokines. Yet, to date, our knowledge regarding the functional role of ICAM-1 in teleost fish remains largely unknown. In this study, we cloned and characterized the sequence of ICAM-1 in rainbow trout (Oncorhynchus mykiss) for the first time, which exhibited that the molecular features of ICAM-1 in fishes were relatively conserved compared with human ICAM-1. The transcriptional level of ICAM-1 was detected in 12 different tissues, and we found high expression of this gene in the head kidney, spleen, gills, skin, nose, and pharynx. Moreover, upon stimulation with infectious hematopoietic necrosis virus (IHNV), Flavobacterium columnare G4 (F. columnare), and Ichthyophthirius multifiliis (Ich) in rainbow trout, the morphological changes were observed in the skin and gills, and enhanced expression of ICAM-1 mRNA was detected both in the systemic and mucosal tissues. These results indicate that ICAM-1 may be implicated in the mucosal immune responses to viral, bacterial, and parasitic infections in teleost fish, meaning that ICAM-1 emerges as a master regulator of mucosal immune responses against pathogen infections in teleost fish.

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“…It is worth noting that the findings of Lou et al indicated that TRIM22 can regulate autophagy of THP-1 cells by up-regulating the NF-κB/Beclin-1 pathway, and eliminate intracellular Mycobacterium tuberculosis by promoting autophagy (Lou et al, 2018 ). Also, it has been shown that LL-37 can promote the expression of NF-κB (Suzuki et al, 2019 ) and the induction of transcription activity of NF-κB (Lim et al, 2015 ). In the HaCaT cells, we speculated that LL-37 may induce autophagy by TRIM22/NF-κB/Beclin-1 pathway, which remains to be proved in future experiments.…”

Section: Discussionmentioning

confidence: 99%

LL-37-Induced Autophagy Contributed to the Elimination of Live Porphyromonas gingivalis Internalized in Keratinocytes

Yang

Niu

Pan

et al. 2020

Front. Cell. Infect. Microbiol.

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Porphyromonas gingivalis (P. gingivalis), one of the most important pathogens of periodontitis, is closely associated with the aggravation and recurrence of periodontitis and systemic diseases. Antibacterial peptide LL-37, transcribed from the cathelicidin antimicrobial peptide (CAMP) gene, exhibits a broad spectrum of antibacterial activity and regulates the immune system. In this study, we demonstrated that LL-37 reduced the number of live P. gingivalis (ATCC 33277) in HaCaT cells in a dose-dependent manner via an antibiotic-protection assay. LL-37 promoted autophagy of HaCaT cells internalized with P. gingivalis. Inhibition of autophagy with 3-methyladenine (3-MA) weakened the inhibitory effect of LL-37 on the number of intracellular P. gingivalis. A cluster of orthologous groups (COGs) and a gene ontology (GO) functional analysis were used to individually assign 65 (10%) differentially expressed genes (DEGs) to an "Intracellular trafficking, secretion, and vesicular transport" cluster and 306 (47.08%) DEGs to metabolic processes including autophagy. Autophagy-related genes, a tripartite motif-containing 22 (TRIM22), and lysosomal-associated membrane protein 3 (LAMP3) were identified as potentially involved in LL-37-induced autophagy. Finally, bioinformatics software was utilized to construct and predict the protein-protein interaction (PPI) network of CAMP-TRIM22/LAMP3-Autophagy. The findings indicated that LL-37 can reduce the quantity of live P. gingivalis internalized in HaCaT cells by promoting autophagy in these cells. The transcriptome sequencing and analysis also revealed the potential molecular pathway of LL-37-induced autophagy.

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Bacterial lipopolysaccharide and antimicrobial LL-37 enhance ICAM-1 expression and NF-κB p65 phosphorylation in senescent endothelial cells

Cited by 15 publications

References 41 publications

Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis

Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis

Molecular Characterization and Expression Analysis of Intercellular Adhesion Molecule-1 (ICAM-1) Genes in Rainbow Trout (Oncorhynchus mykiss) in Response to Viral, Bacterial and Parasitic Challenge

LL-37-Induced Autophagy Contributed to the Elimination of Live Porphyromonas gingivalis Internalized in Keratinocytes

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