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Helicobacter pylori Induces Increased Expression of Toll-Like Receptors and Decreased Toll-Interacting Protein in Gastric Mucosa that Persists Throughout Gastric Carcinogenesis
Background Toll‐like receptors (TLR) are essential for Helicobacter pylori (HP) recognition. Their role in the progression of gastric lesions leading to cancer is not established. Aim To evaluate for the first time in humans the expression of TLR2, TLR4, and TLR5, as well as the expression of other...
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| Published in: | Helicobacter (Cambridge, Mass.) Mass.), 2013-02, Vol.18 (1), p.22-32 |
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| container_title | Helicobacter (Cambridge, Mass.) |
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| creator | Pimentel-Nunes, Pedro Gonçalves, Nádia Boal-Carvalho, Inês Afonso, Luís Lopes, Paula Roncon-Albuquerque Jr, Roberto Henrique, Rui Moreira-Dias, Luís Leite-Moreira, Adelino F. Dinis-Ribeiro, Mário |
| description | Background
Toll‐like receptors (TLR) are essential for Helicobacter pylori (HP) recognition. Their role in the progression of gastric lesions leading to cancer is not established.
Aim
To evaluate for the first time in humans the expression of TLR2, TLR4, and TLR5, as well as the expression of other related molecules in the entire sequence of gastric lesions.
Methods
Biopsy samples (n = 80, 48% HP+) from normal mucosa, HP gastritis, metaplasia, dysplasia or adenocarcinoma were obtained from 44 patients. mRNA quantification of TLR2, TLR4, TLR5, Toll‐interacting protein (TOLLIP), PPAR‐γ, NF‐κB, TNF‐α, COX‐1, COX‐2, and CDX‐2 was performed by real‐time RT‐PCR. TLR2, TLR4, and TLR5 protein expression was quantified by immunohistochemistry.
Results
When compared to normal mucosa (1.0 arbitrary unit (AU)), HP gastritis presented higher expression of TLR2 (2.23 ± 0.36 AU), TLR4 (1.92 ± 0.40 AU) and TNF‐α (2.14 ± 0.50 AU) and lower TOLLIP and PPARγ expression (0.72 ± 0.12 AU, p |
| doi_str_mv | 10.1111/hel.12008 |
| format | article |
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Toll‐like receptors (TLR) are essential for Helicobacter pylori (HP) recognition. Their role in the progression of gastric lesions leading to cancer is not established.
Aim
To evaluate for the first time in humans the expression of TLR2, TLR4, and TLR5, as well as the expression of other related molecules in the entire sequence of gastric lesions.
Methods
Biopsy samples (n = 80, 48% HP+) from normal mucosa, HP gastritis, metaplasia, dysplasia or adenocarcinoma were obtained from 44 patients. mRNA quantification of TLR2, TLR4, TLR5, Toll‐interacting protein (TOLLIP), PPAR‐γ, NF‐κB, TNF‐α, COX‐1, COX‐2, and CDX‐2 was performed by real‐time RT‐PCR. TLR2, TLR4, and TLR5 protein expression was quantified by immunohistochemistry.
Results
When compared to normal mucosa (1.0 arbitrary unit (AU)), HP gastritis presented higher expression of TLR2 (2.23 ± 0.36 AU), TLR4 (1.92 ± 0.40 AU) and TNF‐α (2.14 ± 0.50 AU) and lower TOLLIP and PPARγ expression (0.72 ± 0.12 AU, p < .05 all genes). Metaplasia and dysplasia/carcinoma presented higher expression of TLR2 (1.66 ± 0.46 and 1.48 ± 0.20 AU, respectively, p < .05), lower expression of TOLLIP (0.66 ± 0.09 and 0.52 ± 0.04 AU, p < .05) and PPARγ (0.73 ± 0.12 and 0.63 ± 0.10 AU, p < .05). The significant trend for decrease in TOLLIP and PPARγ was associated with increasing levels of CDX‐2 from normal mucosa to carcinoma (p < .05), translating that in diffuse and higher TLRs protein expression (p < .05).
Conclusion
Gastric carcinogenesis is associated with decreasing levels of TLRs inhibitors and elevated TLRs levels throughout all the spectrum of lesions. Future studies should investigate if modulation of these receptors activity may influence gastric carcinogenesis and tumor progression.]]></description><identifier>ISSN: 1083-4389</identifier><identifier>EISSN: 1523-5378</identifier><identifier>DOI: 10.1111/hel.12008</identifier><identifier>PMID: 23061653</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adenocarcinoma ; Adult ; Aged ; Aged, 80 and over ; Biopsy ; Carcinogenesis ; Carcinoma ; Cross-Sectional Studies ; Cyclooxygenase-1 ; Cyclooxygenase-2 ; Dysplasia ; Female ; Gastric cancer ; Gastric mucosa ; Gastric Mucosa - immunology ; Gastric Mucosa - microbiology ; Gastric Mucosa - pathology ; Gastritis ; Gene Expression Profiling ; Helicobacter Infections - complications ; Helicobacter Infections - immunology ; Helicobacter Infections - microbiology ; Helicobacter Infections - pathology ; Helicobacter pylori ; Helicobacter pylori - immunology ; Helicobacter pylori - pathogenicity ; Humans ; Immunohistochemistry ; Intracellular Signaling Peptides and Proteins - biosynthesis ; Intracellular Signaling Peptides and Proteins - immunology ; Male ; Metaplasia ; Middle Aged ; mRNA ; NF- Kappa B protein ; Peroxisome proliferator-activated receptors ; Polymerase chain reaction ; PPARγ ; Real-Time Polymerase Chain Reaction ; Stomach Neoplasms - immunology ; Stomach Neoplasms - microbiology ; Stomach Neoplasms - pathology ; TLR2 ; TLR2 protein ; TLR4 ; TLR4 protein ; TLR5 protein ; Toll-interacting protein ; Toll-like receptors ; Toll-Like Receptors - biosynthesis ; Toll-Like Receptors - immunology ; Tumor necrosis factor- alpha ; Tumors</subject><ispartof>Helicobacter (Cambridge, Mass.), 2013-02, Vol.18 (1), p.22-32</ispartof><rights>2012 Blackwell Publishing Ltd</rights><rights>2012 Blackwell Publishing Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3968-356e9817b85a08827fa6e69286ceb51906156efd282aa7daa7aba0cc0cadf9693</citedby><cites>FETCH-LOGICAL-c3968-356e9817b85a08827fa6e69286ceb51906156efd282aa7daa7aba0cc0cadf9693</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23061653$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pimentel-Nunes, Pedro</creatorcontrib><creatorcontrib>Gonçalves, Nádia</creatorcontrib><creatorcontrib>Boal-Carvalho, Inês</creatorcontrib><creatorcontrib>Afonso, Luís</creatorcontrib><creatorcontrib>Lopes, Paula</creatorcontrib><creatorcontrib>Roncon-Albuquerque Jr, Roberto</creatorcontrib><creatorcontrib>Henrique, Rui</creatorcontrib><creatorcontrib>Moreira-Dias, Luís</creatorcontrib><creatorcontrib>Leite-Moreira, Adelino F.</creatorcontrib><creatorcontrib>Dinis-Ribeiro, Mário</creatorcontrib><title>Helicobacter pylori Induces Increased Expression of Toll-Like Receptors and Decreased Toll-Interacting Protein in Gastric Mucosa that Persists Throughout Gastric Carcinogenesis</title><title>Helicobacter (Cambridge, Mass.)</title><addtitle>Helicobacter</addtitle><description><![CDATA[Background
Toll‐like receptors (TLR) are essential for Helicobacter pylori (HP) recognition. Their role in the progression of gastric lesions leading to cancer is not established.
Aim
To evaluate for the first time in humans the expression of TLR2, TLR4, and TLR5, as well as the expression of other related molecules in the entire sequence of gastric lesions.
Methods
Biopsy samples (n = 80, 48% HP+) from normal mucosa, HP gastritis, metaplasia, dysplasia or adenocarcinoma were obtained from 44 patients. mRNA quantification of TLR2, TLR4, TLR5, Toll‐interacting protein (TOLLIP), PPAR‐γ, NF‐κB, TNF‐α, COX‐1, COX‐2, and CDX‐2 was performed by real‐time RT‐PCR. TLR2, TLR4, and TLR5 protein expression was quantified by immunohistochemistry.
Results
When compared to normal mucosa (1.0 arbitrary unit (AU)), HP gastritis presented higher expression of TLR2 (2.23 ± 0.36 AU), TLR4 (1.92 ± 0.40 AU) and TNF‐α (2.14 ± 0.50 AU) and lower TOLLIP and PPARγ expression (0.72 ± 0.12 AU, p < .05 all genes). Metaplasia and dysplasia/carcinoma presented higher expression of TLR2 (1.66 ± 0.46 and 1.48 ± 0.20 AU, respectively, p < .05), lower expression of TOLLIP (0.66 ± 0.09 and 0.52 ± 0.04 AU, p < .05) and PPARγ (0.73 ± 0.12 and 0.63 ± 0.10 AU, p < .05). The significant trend for decrease in TOLLIP and PPARγ was associated with increasing levels of CDX‐2 from normal mucosa to carcinoma (p < .05), translating that in diffuse and higher TLRs protein expression (p < .05).
Conclusion
Gastric carcinogenesis is associated with decreasing levels of TLRs inhibitors and elevated TLRs levels throughout all the spectrum of lesions. Future studies should investigate if modulation of these receptors activity may influence gastric carcinogenesis and tumor progression.]]></description><subject>Adenocarcinoma</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biopsy</subject><subject>Carcinogenesis</subject><subject>Carcinoma</subject><subject>Cross-Sectional Studies</subject><subject>Cyclooxygenase-1</subject><subject>Cyclooxygenase-2</subject><subject>Dysplasia</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gastric mucosa</subject><subject>Gastric Mucosa - immunology</subject><subject>Gastric Mucosa - microbiology</subject><subject>Gastric Mucosa - pathology</subject><subject>Gastritis</subject><subject>Gene Expression Profiling</subject><subject>Helicobacter Infections - complications</subject><subject>Helicobacter Infections - immunology</subject><subject>Helicobacter Infections - microbiology</subject><subject>Helicobacter Infections - pathology</subject><subject>Helicobacter pylori</subject><subject>Helicobacter pylori - immunology</subject><subject>Helicobacter pylori - pathogenicity</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Intracellular Signaling Peptides and Proteins - biosynthesis</subject><subject>Intracellular Signaling Peptides and Proteins - immunology</subject><subject>Male</subject><subject>Metaplasia</subject><subject>Middle Aged</subject><subject>mRNA</subject><subject>NF- Kappa B protein</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Polymerase chain reaction</subject><subject>PPARγ</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Stomach Neoplasms - immunology</subject><subject>Stomach Neoplasms - microbiology</subject><subject>Stomach Neoplasms - pathology</subject><subject>TLR2</subject><subject>TLR2 protein</subject><subject>TLR4</subject><subject>TLR4 protein</subject><subject>TLR5 protein</subject><subject>Toll-interacting protein</subject><subject>Toll-like receptors</subject><subject>Toll-Like Receptors - biosynthesis</subject><subject>Toll-Like Receptors - immunology</subject><subject>Tumor necrosis factor- alpha</subject><subject>Tumors</subject><issn>1083-4389</issn><issn>1523-5378</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp1kUFv0zAUxy0EYlvhwBdAPsIhmx3PiX1EXUkLBaaqaEfLcV5aszQOtiPWb7WPiFnX3rBsPR9-7ye990foHSWXNJ2rLXSXNCdEvEDnlOcs46wUL9OfCJZdMyHP0EUIvwghnF3L1-gsZ6SgBWfn6HEOnTWu1iaCx8O-c97iRd-MBkKqxoMO0ODZw-AhBOt67Fq8dl2XLe094BUYGKLzAeu-wTdw5J-IRZ-cSWz7Db71LoLtcbqVDtFbg7-NxgWN41ZHfAs-2BADXm-9GzdbN8YTN9Xe2N5toIfEvEGvWt0FePtcJ-jn59l6Os-WP6rF9NMyM0wWImO8ACloWQuuiRB52eoCCpmLwkDNqUzzJ6JtcpFrXTbp6VoTY4jRTSsLySbow8E7ePd7hBDVzgYDXad7cGNQNBecSCHSuifo4wE13oXgoVWDtzvt94oS9S8glQJSTwEl9v2zdqx30JzIYyIJuDoAf2wH-_-b1Hy2PCqzQ0daIDycOrS_V0XJSq7uvldqVdEv1Ureqa_sLzDCrXQ</recordid><startdate>201302</startdate><enddate>201302</enddate><creator>Pimentel-Nunes, Pedro</creator><creator>Gonçalves, Nádia</creator><creator>Boal-Carvalho, Inês</creator><creator>Afonso, Luís</creator><creator>Lopes, Paula</creator><creator>Roncon-Albuquerque Jr, Roberto</creator><creator>Henrique, Rui</creator><creator>Moreira-Dias, Luís</creator><creator>Leite-Moreira, Adelino F.</creator><creator>Dinis-Ribeiro, Mário</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>C1K</scope></search><sort><creationdate>201302</creationdate><title>Helicobacter pylori Induces Increased Expression of Toll-Like Receptors and Decreased Toll-Interacting Protein in Gastric Mucosa that Persists Throughout Gastric Carcinogenesis</title><author>Pimentel-Nunes, Pedro ; Gonçalves, Nádia ; Boal-Carvalho, Inês ; Afonso, Luís ; Lopes, Paula ; Roncon-Albuquerque Jr, Roberto ; Henrique, Rui ; Moreira-Dias, Luís ; Leite-Moreira, Adelino F. ; Dinis-Ribeiro, Mário</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3968-356e9817b85a08827fa6e69286ceb51906156efd282aa7daa7aba0cc0cadf9693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenocarcinoma</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biopsy</topic><topic>Carcinogenesis</topic><topic>Carcinoma</topic><topic>Cross-Sectional Studies</topic><topic>Cyclooxygenase-1</topic><topic>Cyclooxygenase-2</topic><topic>Dysplasia</topic><topic>Female</topic><topic>Gastric cancer</topic><topic>Gastric mucosa</topic><topic>Gastric Mucosa - immunology</topic><topic>Gastric Mucosa - microbiology</topic><topic>Gastric Mucosa - pathology</topic><topic>Gastritis</topic><topic>Gene Expression Profiling</topic><topic>Helicobacter Infections - complications</topic><topic>Helicobacter Infections - immunology</topic><topic>Helicobacter Infections - microbiology</topic><topic>Helicobacter Infections - pathology</topic><topic>Helicobacter pylori</topic><topic>Helicobacter pylori - immunology</topic><topic>Helicobacter pylori - pathogenicity</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Intracellular Signaling Peptides and Proteins - biosynthesis</topic><topic>Intracellular Signaling Peptides and Proteins - immunology</topic><topic>Male</topic><topic>Metaplasia</topic><topic>Middle Aged</topic><topic>mRNA</topic><topic>NF- Kappa B protein</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Polymerase chain reaction</topic><topic>PPARγ</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Stomach Neoplasms - immunology</topic><topic>Stomach Neoplasms - microbiology</topic><topic>Stomach Neoplasms - pathology</topic><topic>TLR2</topic><topic>TLR2 protein</topic><topic>TLR4</topic><topic>TLR4 protein</topic><topic>TLR5 protein</topic><topic>Toll-interacting protein</topic><topic>Toll-like receptors</topic><topic>Toll-Like Receptors - biosynthesis</topic><topic>Toll-Like Receptors - immunology</topic><topic>Tumor necrosis factor- alpha</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pimentel-Nunes, Pedro</creatorcontrib><creatorcontrib>Gonçalves, Nádia</creatorcontrib><creatorcontrib>Boal-Carvalho, Inês</creatorcontrib><creatorcontrib>Afonso, Luís</creatorcontrib><creatorcontrib>Lopes, Paula</creatorcontrib><creatorcontrib>Roncon-Albuquerque Jr, Roberto</creatorcontrib><creatorcontrib>Henrique, Rui</creatorcontrib><creatorcontrib>Moreira-Dias, Luís</creatorcontrib><creatorcontrib>Leite-Moreira, Adelino F.</creatorcontrib><creatorcontrib>Dinis-Ribeiro, Mário</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Helicobacter (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pimentel-Nunes, Pedro</au><au>Gonçalves, Nádia</au><au>Boal-Carvalho, Inês</au><au>Afonso, Luís</au><au>Lopes, Paula</au><au>Roncon-Albuquerque Jr, Roberto</au><au>Henrique, Rui</au><au>Moreira-Dias, Luís</au><au>Leite-Moreira, Adelino F.</au><au>Dinis-Ribeiro, Mário</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Helicobacter pylori Induces Increased Expression of Toll-Like Receptors and Decreased Toll-Interacting Protein in Gastric Mucosa that Persists Throughout Gastric Carcinogenesis</atitle><jtitle>Helicobacter (Cambridge, Mass.)</jtitle><addtitle>Helicobacter</addtitle><date>2013-02</date><risdate>2013</risdate><volume>18</volume><issue>1</issue><spage>22</spage><epage>32</epage><pages>22-32</pages><issn>1083-4389</issn><eissn>1523-5378</eissn><abstract><![CDATA[Background
Toll‐like receptors (TLR) are essential for Helicobacter pylori (HP) recognition. Their role in the progression of gastric lesions leading to cancer is not established.
Aim
To evaluate for the first time in humans the expression of TLR2, TLR4, and TLR5, as well as the expression of other related molecules in the entire sequence of gastric lesions.
Methods
Biopsy samples (n = 80, 48% HP+) from normal mucosa, HP gastritis, metaplasia, dysplasia or adenocarcinoma were obtained from 44 patients. mRNA quantification of TLR2, TLR4, TLR5, Toll‐interacting protein (TOLLIP), PPAR‐γ, NF‐κB, TNF‐α, COX‐1, COX‐2, and CDX‐2 was performed by real‐time RT‐PCR. TLR2, TLR4, and TLR5 protein expression was quantified by immunohistochemistry.
Results
When compared to normal mucosa (1.0 arbitrary unit (AU)), HP gastritis presented higher expression of TLR2 (2.23 ± 0.36 AU), TLR4 (1.92 ± 0.40 AU) and TNF‐α (2.14 ± 0.50 AU) and lower TOLLIP and PPARγ expression (0.72 ± 0.12 AU, p < .05 all genes). Metaplasia and dysplasia/carcinoma presented higher expression of TLR2 (1.66 ± 0.46 and 1.48 ± 0.20 AU, respectively, p < .05), lower expression of TOLLIP (0.66 ± 0.09 and 0.52 ± 0.04 AU, p < .05) and PPARγ (0.73 ± 0.12 and 0.63 ± 0.10 AU, p < .05). The significant trend for decrease in TOLLIP and PPARγ was associated with increasing levels of CDX‐2 from normal mucosa to carcinoma (p < .05), translating that in diffuse and higher TLRs protein expression (p < .05).
Conclusion
Gastric carcinogenesis is associated with decreasing levels of TLRs inhibitors and elevated TLRs levels throughout all the spectrum of lesions. Future studies should investigate if modulation of these receptors activity may influence gastric carcinogenesis and tumor progression.]]></abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>23061653</pmid><doi>10.1111/hel.12008</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1083-4389 |
| ispartof | Helicobacter (Cambridge, Mass.), 2013-02, Vol.18 (1), p.22-32 |
| issn | 1083-4389 1523-5378 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1285098852 |
| source | Wiley |
| subjects | Adenocarcinoma Adult Aged Aged, 80 and over Biopsy Carcinogenesis Carcinoma Cross-Sectional Studies Cyclooxygenase-1 Cyclooxygenase-2 Dysplasia Female Gastric cancer Gastric mucosa Gastric Mucosa - immunology Gastric Mucosa - microbiology Gastric Mucosa - pathology Gastritis Gene Expression Profiling Helicobacter Infections - complications Helicobacter Infections - immunology Helicobacter Infections - microbiology Helicobacter Infections - pathology Helicobacter pylori Helicobacter pylori - immunology Helicobacter pylori - pathogenicity Humans Immunohistochemistry Intracellular Signaling Peptides and Proteins - biosynthesis Intracellular Signaling Peptides and Proteins - immunology Male Metaplasia Middle Aged mRNA NF- Kappa B protein Peroxisome proliferator-activated receptors Polymerase chain reaction PPARγ Real-Time Polymerase Chain Reaction Stomach Neoplasms - immunology Stomach Neoplasms - microbiology Stomach Neoplasms - pathology TLR2 TLR2 protein TLR4 TLR4 protein TLR5 protein Toll-interacting protein Toll-like receptors Toll-Like Receptors - biosynthesis Toll-Like Receptors - immunology Tumor necrosis factor- alpha Tumors |
| title | Helicobacter pylori Induces Increased Expression of Toll-Like Receptors and Decreased Toll-Interacting Protein in Gastric Mucosa that Persists Throughout Gastric Carcinogenesis |
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