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CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro
Sepsis is a life-threatening health condition caused by infectious pathogens of the respiratory tract, and accounts for 28-50% of annual deaths in the US alone. Current treatment regimen advocates the use of corticosteroids as adjunct treatment with antibiotics, for their broad inhibitory effect on...
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Published in: | Frontiers in cellular and infection microbiology 2017-06, Vol.7, p.263-263 |
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description | Sepsis is a life-threatening health condition caused by infectious pathogens of the respiratory tract, and accounts for 28-50% of annual deaths in the US alone. Current treatment regimen advocates the use of corticosteroids as adjunct treatment with antibiotics, for their broad inhibitory effect on the activity and production of pro-inflammatory mediators. However, despite their use, corticosteroids have not proven to be able to reverse the death incidence among septic patients. We have previously demonstrated the potential for neuroendocrine factors to directly influence
virulence, which may in turn mediate disease outcome leading to sepsis and septic shock. The current study investigated the role of Corticotropin-releasing hormone (CRH) in mediating key markers of pneumococcal virulence as important phenotypic determinants of sepsis and septic shock risks.
cultures of serotype 1 pneumococcal strain with CRH promoted growth rate, increased capsule thickness and penicillin resistance, as well as induced pneumolysin gene expression. These results thus provide significant insights of CRH-pathogen interactions useful in understanding the underlying mechanisms of neuroendocrine factor's role in the onset of community acquired pneumonias (CAP), sepsis and septic shock. |
doi_str_mv | 10.3389/fcimb.2017.00263 |
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virulence, which may in turn mediate disease outcome leading to sepsis and septic shock. The current study investigated the role of Corticotropin-releasing hormone (CRH) in mediating key markers of pneumococcal virulence as important phenotypic determinants of sepsis and septic shock risks.
cultures of serotype 1 pneumococcal strain with CRH promoted growth rate, increased capsule thickness and penicillin resistance, as well as induced pneumolysin gene expression. These results thus provide significant insights of CRH-pathogen interactions useful in understanding the underlying mechanisms of neuroendocrine factor's role in the onset of community acquired pneumonias (CAP), sepsis and septic shock.</description><identifier>ISSN: 2235-2988</identifier><identifier>EISSN: 2235-2988</identifier><identifier>DOI: 10.3389/fcimb.2017.00263</identifier><identifier>PMID: 28690980</identifier><language>eng</language><publisher>Switzerland: Frontiers Media S.A</publisher><subject>Anti-Bacterial Agents ; Bacterial Capsules - drug effects ; Bacterial Proteins - drug effects ; Bacterial Proteins - genetics ; Biomarkers ; corticotropin releasing hormone ; Corticotropin-Releasing Hormone - pharmacology ; Gene Expression Regulation, Bacterial ; Humans ; Microbiology ; Penicillin Resistance - drug effects ; Phenotype ; Pneumococcal Infections - metabolism ; Pneumococcal Infections - microbiology ; Sepsis - metabolism ; Sepsis - microbiology ; sepsis virulence ; Serogroup ; serotypes ; Shock, Septic - metabolism ; Streptococcus pneumoniae ; Streptococcus pneumoniae - drug effects ; Streptococcus pneumoniae - growth & development ; Streptococcus pneumoniae - pathogenicity ; Streptolysins - genetics ; Virulence - drug effects ; Virulence Factors - metabolism</subject><ispartof>Frontiers in cellular and infection microbiology, 2017-06, Vol.7, p.263-263</ispartof><rights>Copyright © 2017 Ngo Ndjom, Kantor and Jones. 2017 Ngo Ndjom, Kantor and Jones</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3773-9c9cd54ad7e66576238f4bed5919ad47bfa8920d9ab4e536e5e8650cdb89413f3</citedby><cites>FETCH-LOGICAL-c3773-9c9cd54ad7e66576238f4bed5919ad47bfa8920d9ab4e536e5e8650cdb89413f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479890/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5479890/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28690980$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ngo Ndjom, Colette G</creatorcontrib><creatorcontrib>Kantor, Lindsay V</creatorcontrib><creatorcontrib>Jones, Harlan P</creatorcontrib><title>CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro</title><title>Frontiers in cellular and infection microbiology</title><addtitle>Front Cell Infect Microbiol</addtitle><description>Sepsis is a life-threatening health condition caused by infectious pathogens of the respiratory tract, and accounts for 28-50% of annual deaths in the US alone. Current treatment regimen advocates the use of corticosteroids as adjunct treatment with antibiotics, for their broad inhibitory effect on the activity and production of pro-inflammatory mediators. However, despite their use, corticosteroids have not proven to be able to reverse the death incidence among septic patients. We have previously demonstrated the potential for neuroendocrine factors to directly influence
virulence, which may in turn mediate disease outcome leading to sepsis and septic shock. The current study investigated the role of Corticotropin-releasing hormone (CRH) in mediating key markers of pneumococcal virulence as important phenotypic determinants of sepsis and septic shock risks.
cultures of serotype 1 pneumococcal strain with CRH promoted growth rate, increased capsule thickness and penicillin resistance, as well as induced pneumolysin gene expression. These results thus provide significant insights of CRH-pathogen interactions useful in understanding the underlying mechanisms of neuroendocrine factor's role in the onset of community acquired pneumonias (CAP), sepsis and septic shock.</description><subject>Anti-Bacterial Agents</subject><subject>Bacterial Capsules - drug effects</subject><subject>Bacterial Proteins - drug effects</subject><subject>Bacterial Proteins - genetics</subject><subject>Biomarkers</subject><subject>corticotropin releasing hormone</subject><subject>Corticotropin-Releasing Hormone - pharmacology</subject><subject>Gene Expression Regulation, Bacterial</subject><subject>Humans</subject><subject>Microbiology</subject><subject>Penicillin Resistance - drug effects</subject><subject>Phenotype</subject><subject>Pneumococcal Infections - metabolism</subject><subject>Pneumococcal Infections - microbiology</subject><subject>Sepsis - metabolism</subject><subject>Sepsis - microbiology</subject><subject>sepsis virulence</subject><subject>Serogroup</subject><subject>serotypes</subject><subject>Shock, Septic - metabolism</subject><subject>Streptococcus pneumoniae</subject><subject>Streptococcus pneumoniae - drug effects</subject><subject>Streptococcus pneumoniae - growth & development</subject><subject>Streptococcus pneumoniae - pathogenicity</subject><subject>Streptolysins - genetics</subject><subject>Virulence - drug effects</subject><subject>Virulence Factors - metabolism</subject><issn>2235-2988</issn><issn>2235-2988</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVks1r3DAQxU1paUKae09Fx168lSVZH5fCsiTNQiChaXsVsjTKKngtV5JDF_rH17ubhmQuGkbzfk-gV1UfG7ygVKov3oZttyC4EQuMCadvqlNCaFsTJeXbF_1JdZ7zA55LYCIVfV-dEMkVVhKfVn9X36_Q0nuwJaOyAXS7gSGW3RgsuvgzJsg5xAFFj-5gzCHXy5yjDaaAQ79CmnoYLKBLY0tMGXU7dFcSjCXaaO2U0TjAtI1DMDDr054LqEHrAT2GkuKH6p03fYbzp_Os-nl58WN1VV_ffFuvlte1pULQWlllXcuME8B5Kzih0rMOXKsaZRwTnTdSEeyU6Ri0lEMLkrfYuk4q1lBPz6r1keuiedBjCluTdjqaoA-DmO61SSXYHjSWXsw2YJWwzGEumYOmI41qSEMptTPr65E1Tt0WnIWhJNO_gr6-GcJG38dH3TKhpMIz4PMTIMXfE-SityFb6HszQJyynq0E54wxNa_i46pNMecE_tmmwXqfAX3IgN5nQB8yMEs-vXzes-D_j9N_Ry2v-A</recordid><startdate>20170622</startdate><enddate>20170622</enddate><creator>Ngo Ndjom, Colette G</creator><creator>Kantor, Lindsay V</creator><creator>Jones, Harlan P</creator><general>Frontiers Media S.A</general><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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20170622</creationdate><title>CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro</title><author>Ngo Ndjom, Colette G ; Kantor, Lindsay V ; Jones, Harlan P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3773-9c9cd54ad7e66576238f4bed5919ad47bfa8920d9ab4e536e5e8650cdb89413f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Anti-Bacterial Agents</topic><topic>Bacterial Capsules - drug effects</topic><topic>Bacterial Proteins - drug effects</topic><topic>Bacterial Proteins - genetics</topic><topic>Biomarkers</topic><topic>corticotropin releasing hormone</topic><topic>Corticotropin-Releasing Hormone - pharmacology</topic><topic>Gene Expression Regulation, Bacterial</topic><topic>Humans</topic><topic>Microbiology</topic><topic>Penicillin Resistance - drug effects</topic><topic>Phenotype</topic><topic>Pneumococcal Infections - metabolism</topic><topic>Pneumococcal Infections - microbiology</topic><topic>Sepsis - metabolism</topic><topic>Sepsis - microbiology</topic><topic>sepsis virulence</topic><topic>Serogroup</topic><topic>serotypes</topic><topic>Shock, Septic - metabolism</topic><topic>Streptococcus pneumoniae</topic><topic>Streptococcus pneumoniae - drug effects</topic><topic>Streptococcus pneumoniae - growth & development</topic><topic>Streptococcus pneumoniae - pathogenicity</topic><topic>Streptolysins - genetics</topic><topic>Virulence - drug effects</topic><topic>Virulence Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ngo Ndjom, Colette G</creatorcontrib><creatorcontrib>Kantor, Lindsay V</creatorcontrib><creatorcontrib>Jones, Harlan P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in cellular and infection microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ngo Ndjom, Colette G</au><au>Kantor, Lindsay V</au><au>Jones, Harlan P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro</atitle><jtitle>Frontiers in cellular and infection microbiology</jtitle><addtitle>Front Cell Infect Microbiol</addtitle><date>2017-06-22</date><risdate>2017</risdate><volume>7</volume><spage>263</spage><epage>263</epage><pages>263-263</pages><issn>2235-2988</issn><eissn>2235-2988</eissn><abstract>Sepsis is a life-threatening health condition caused by infectious pathogens of the respiratory tract, and accounts for 28-50% of annual deaths in the US alone. Current treatment regimen advocates the use of corticosteroids as adjunct treatment with antibiotics, for their broad inhibitory effect on the activity and production of pro-inflammatory mediators. However, despite their use, corticosteroids have not proven to be able to reverse the death incidence among septic patients. We have previously demonstrated the potential for neuroendocrine factors to directly influence
virulence, which may in turn mediate disease outcome leading to sepsis and septic shock. The current study investigated the role of Corticotropin-releasing hormone (CRH) in mediating key markers of pneumococcal virulence as important phenotypic determinants of sepsis and septic shock risks.
cultures of serotype 1 pneumococcal strain with CRH promoted growth rate, increased capsule thickness and penicillin resistance, as well as induced pneumolysin gene expression. These results thus provide significant insights of CRH-pathogen interactions useful in understanding the underlying mechanisms of neuroendocrine factor's role in the onset of community acquired pneumonias (CAP), sepsis and septic shock.</abstract><cop>Switzerland</cop><pub>Frontiers Media S.A</pub><pmid>28690980</pmid><doi>10.3389/fcimb.2017.00263</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Anti-Bacterial Agents Bacterial Capsules - drug effects Bacterial Proteins - drug effects Bacterial Proteins - genetics Biomarkers corticotropin releasing hormone Corticotropin-Releasing Hormone - pharmacology Gene Expression Regulation, Bacterial Humans Microbiology Penicillin Resistance - drug effects Phenotype Pneumococcal Infections - metabolism Pneumococcal Infections - microbiology Sepsis - metabolism Sepsis - microbiology sepsis virulence Serogroup serotypes Shock, Septic - metabolism Streptococcus pneumoniae Streptococcus pneumoniae - drug effects Streptococcus pneumoniae - growth & development Streptococcus pneumoniae - pathogenicity Streptolysins - genetics Virulence - drug effects Virulence Factors - metabolism |
title | CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro |
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