Effect of Coffee on Lipopolysaccharide-Induced Immortalized Human Oral Keratinocytes

Periodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components; however, current research on the relationship between coffee consumption and periodontitis, as well as its underlying mechanisms, is limited. Based on a...

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Published inFoods Vol. 11; no. 15; p. 2199
Main Authors Song, Jianan, Kim, Byunggook, Kim, Oksu, Yang, Ying, Liu, Danyang, Fu, Wenqi, Ma, Guowu, Kim, Young, Kim, Okjoon
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 24.07.2022
MDPI
Subjects
AMP-activated protein kinase
AMPK pathway
Antibodies
artificial coffee
Caffeine
Care and treatment
Cell viability
Chemical properties
Chlorogenic acid
Coffee
Consumption
Diet
Disease
Food science
Heme
Heme oxygenase (decyclizing)
Inflammatory diseases
Keratinocytes
Kinases
Lipopolysaccharides
Nrf2/HO-1 pathway
Oxygenase
Periodontitis
Phosphorylation
Physiological aspects
Prostaglandin E2
Reactive oxygen species
Risk factors
Synergistic effect
Translocation
Western blotting
South Korea
United States > US
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Abstract Periodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components; however, current research on the relationship between coffee consumption and periodontitis, as well as its underlying mechanisms, is limited. Based on a previous report, caffeine (CA) and chlorogenic acid (CGA) were formulated into artificial coffee (AC) for this experiment. Cell viability, prostaglandin E2 release, Western blotting, cellular reactive oxygen species (ROS) production, and NF-E2-related factor 2 (Nrf2) translocation analyses were performed to explore the effects of AC on lipopolysaccharide (LPS)-induced immortalized human oral keratinocytes (IHOKs) and elucidate their underlying mechanisms. AC pretreatment attenuated LPS-induced inflammatory mediator release, ROS production, and nuclear factor kappa B translocation in IHOKs. CA and CGA promoted AMP-activated protein kinase phosphorylation and down-regulated the nuclear factor-κB pathways to exert anti-inflammatory effects. Additionally, CGA promoted Nrf2 translocation and heme oxygenase-1 expression and showed anti-oxidative effects. Furthermore, AC, CA, and CGA components showed synergistic effects. Thus, we predict that coffee consumption may be beneficial for alleviating periodontitis. Moreover, the main coffee components CA and CGA seem to play a synergistic role in periodontitis.
AbstractList Periodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components; however, current research on the relationship between coffee consumption and periodontitis, as well as its underlying mechanisms, is limited. Based on a previous report, caffeine (CA) and chlorogenic acid (CGA) were formulated into artificial coffee (AC) for this experiment. Cell viability, prostaglandin E[sub.2] release, Western blotting, cellular reactive oxygen species (ROS) production, and NF-E2-related factor 2 (Nrf2) translocation analyses were performed to explore the effects of AC on lipopolysaccharide (LPS)-induced immortalized human oral keratinocytes (IHOKs) and elucidate their underlying mechanisms. AC pretreatment attenuated LPS-induced inflammatory mediator release, ROS production, and nuclear factor kappa B translocation in IHOKs. CA and CGA promoted AMP-activated protein kinase phosphorylation and down-regulated the nuclear factor-κB pathways to exert anti-inflammatory effects. Additionally, CGA promoted Nrf2 translocation and heme oxygenase-1 expression and showed anti-oxidative effects. Furthermore, AC, CA, and CGA components showed synergistic effects. Thus, we predict that coffee consumption may be beneficial for alleviating periodontitis. Moreover, the main coffee components CA and CGA seem to play a synergistic role in periodontitis.
Periodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components; however, current research on the relationship between coffee consumption and periodontitis, as well as its underlying mechanisms, is limited. Based on a previous report, caffeine (CA) and chlorogenic acid (CGA) were formulated into artificial coffee (AC) for this experiment. Cell viability, prostaglandin E2 release, Western blotting, cellular reactive oxygen species (ROS) production, and NF-E2-related factor 2 (Nrf2) translocation analyses were performed to explore the effects of AC on lipopolysaccharide (LPS)-induced immortalized human oral keratinocytes (IHOKs) and elucidate their underlying mechanisms. AC pretreatment attenuated LPS-induced inflammatory mediator release, ROS production, and nuclear factor kappa B translocation in IHOKs. CA and CGA promoted AMP-activated protein kinase phosphorylation and down-regulated the nuclear factor-κB pathways to exert anti-inflammatory effects. Additionally, CGA promoted Nrf2 translocation and heme oxygenase-1 expression and showed anti-oxidative effects. Furthermore, AC, CA, and CGA components showed synergistic effects. Thus, we predict that coffee consumption may be beneficial for alleviating periodontitis. Moreover, the main coffee components CA and CGA seem to play a synergistic role in periodontitis.
AbstractsPeriodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components; however, current research on the relationship between coffee consumption and periodontitis, as well as its underlying mechanisms, is limited. Based on a previous report, caffeine (CA) and chlorogenic acid (CGA) were formulated into artificial coffee (AC) for this experiment. Cell viability, prostaglandin E2 release, Western blotting, cellular reactive oxygen species (ROS) production, and NF-E2-related factor 2 (Nrf2) translocation analyses were performed to explore the effects of AC on lipopolysaccharide (LPS)-induced immortalized human oral keratinocytes (IHOKs) and elucidate their underlying mechanisms. AC pretreatment attenuated LPS-induced inflammatory mediator release, ROS production, and nuclear factor kappa B translocation in IHOKs. CA and CGA promoted AMP-activated protein kinase phosphorylation and down-regulated the nuclear factor-κB pathways to exert anti-inflammatory effects. Additionally, CGA promoted Nrf2 translocation and heme oxygenase-1 expression and showed anti-oxidative effects. Furthermore, AC, CA, and CGA components showed synergistic effects. Thus, we predict that coffee consumption may be beneficial for alleviating periodontitis. Moreover, the main coffee components CA and CGA seem to play a synergistic role in periodontitis.
Periodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components; however, current research on the relationship between coffee consumption and periodontitis, as well as its underlying mechanisms, is limited. Based on a previous report, caffeine (CA) and chlorogenic acid (CGA) were formulated into artificial coffee (AC) for this experiment. Cell viability, prostaglandin E 2 release, Western blotting, cellular reactive oxygen species (ROS) production, and NF-E2-related factor 2 (Nrf2) translocation analyses were performed to explore the effects of AC on lipopolysaccharide (LPS)-induced immortalized human oral keratinocytes (IHOKs) and elucidate their underlying mechanisms. AC pretreatment attenuated LPS-induced inflammatory mediator release, ROS production, and nuclear factor kappa B translocation in IHOKs. CA and CGA promoted AMP-activated protein kinase phosphorylation and down-regulated the nuclear factor-κB pathways to exert anti-inflammatory effects. Additionally, CGA promoted Nrf2 translocation and heme oxygenase-1 expression and showed anti-oxidative effects. Furthermore, AC, CA, and CGA components showed synergistic effects. Thus, we predict that coffee consumption may be beneficial for alleviating periodontitis. Moreover, the main coffee components CA and CGA seem to play a synergistic role in periodontitis.
Audience Academic
Author Kim, Okjoon
Song, Jianan
Fu, Wenqi
Ma, Guowu
Yang, Ying
Kim, Young
Kim, Byunggook
Kim, Oksu
Liu, Danyang
AuthorAffiliation 3 Department of Periodontology, School of Dentistry, Chonnam National University, Gwangju 61186, Korea; periodrk@jnu.ac.kr
4 Department of Oral and Maxillofacial Surgery, School of Stomatology, Dalian Medical University, Dalian 116044, China; mgw640242000@aliyun.com
1 Department of Oral Pathology, School of Dentistry, Chonnam National University, Gwangju 61186, Korea; songjianan87@gmail.com (J.S.); dentistyang@wmu.edu.cn (Y.Y.); liudysunny@gmail.com (D.L.); fwq0369@163.com (W.F.); youngkim2017@jnu.ac.kr (Y.K.)
2 Department of Oral Medicine, School of Dentistry, Chonnam National University, Gwangju 61186, Korea; bkkimom@jnu.ac.kr
AuthorAffiliation_xml – name: 2 Department of Oral Medicine, School of Dentistry, Chonnam National University, Gwangju 61186, Korea; bkkimom@jnu.ac.kr
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– name: 3 Department of Periodontology, School of Dentistry, Chonnam National University, Gwangju 61186, Korea; periodrk@jnu.ac.kr
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Snippet Periodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components; however,...
AbstractsPeriodontitis is a common inflammatory disease that is strongly influenced by dietary habits. Coffee is one of the most common dietary components;...
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SubjectTerms AMP-activated protein kinase
AMPK pathway
Antibodies
artificial coffee
Caffeine
Care and treatment
Cell viability
Chemical properties
Chlorogenic acid
Coffee
Consumption
Diet
Disease
Food science
Heme
Heme oxygenase (decyclizing)
Inflammatory diseases
Keratinocytes
Kinases
Lipopolysaccharides
Nrf2/HO-1 pathway
Oxygenase
Periodontitis
Phosphorylation
Physiological aspects
Prostaglandin E2
Reactive oxygen species
Risk factors
Synergistic effect
Translocation
Western blotting
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Title Effect of Coffee on Lipopolysaccharide-Induced Immortalized Human Oral Keratinocytes
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https://pubmed.ncbi.nlm.nih.gov/PMC9330743
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Volume 11
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