Severe acute respiratory syndrome (SARS) coronavirus-induced lung epithelial cytokines exacerbate SARS pathogenesis by modulating intrinsic functions of monocyte-derived macrophages and dendritic cells.
Identifieur interne : 001791 ( PubMed/Checkpoint ); précédent : 001790; suivant : 001792Severe acute respiratory syndrome (SARS) coronavirus-induced lung epithelial cytokines exacerbate SARS pathogenesis by modulating intrinsic functions of monocyte-derived macrophages and dendritic cells.
Auteurs : Tomoki Yoshikawa [États-Unis] ; Terence Hill ; Kui Li ; Clarence J. Peters ; Chien-Te K. TsengSource :
- Journal of virology [ 1098-5514 ] ; 2009.
Descripteurs français
- KwdFr :
- MESH :
- anatomopathologie : Poumon.
- immunologie : Cellules dendritiques, Cellules épithéliales, Macrophages, Poumon, Virus du SRAS.
- métabolisme : Cytokines.
- virologie : Poumon.
- Animaux, Cellules cultivées, Humains.
English descriptors
- KwdEn :
- MESH :
- chemical , biosynthesis : B7-2 Antigen, CD40 Antigens.
- chemical , metabolism : Cytokines.
- immunology : Dendritic Cells, Epithelial Cells, Lung, Macrophages, SARS Virus.
- pathology : Lung.
- virology : Lung.
- Animals, Cells, Cultured, Humans.
Abstract
Severe acute respiratory syndrome (SARS), which is caused by a novel coronavirus (CoV), is a highly communicable disease with the lungs as the major pathological target. Although SARS likely stems from overexuberant host inflammatory responses, the exact mechanism leading to the detrimental outcome in patients remains unknown. Pulmonary macrophages (Mphi), airway epithelium, and dendritic cells (DC) are key cellular elements of the host innate defenses against respiratory infections. While pulmonary Mphi are situated at the luminal epithelial surface, DC reside abundantly underneath the epithelium. Such strategic locations of these cells within the airways make it relevant to investigate their likely impact on SARS pathogenesis subsequent to their interaction with infected lung epithelial cells. To study this, we established highly polarized human lung epithelial Calu-3 cells by using the Transwell culture system. Here we report that supernatants harvested from the apical and basolateral domains of infected Calu-3 cells are potent in modulating the intrinsic functions of Mphi and DC, respectively. They prompted the production of cytokines by both Mphi and DC and selectively induced CD40 and CD86 expression only on DC. However, they compromised the abilities of the DC and Mphi in priming naïve T cells and phagocytosis, respectively. We also identified interleukin-6 (IL-6) and IL-8 as key SARS-CoV-induced epithelial cytokines capable of inhibiting the T-cell-priming ability of DC. Taken together, our results provide insights into the molecular and cellular bases of the host antiviral innate immunity within the lungs that eventually lead to an exacerbated inflammatory cascades and severe tissue damage in SARS patients.
DOI: 10.1128/JVI.01792-08
PubMed: 19004938
Affiliations:
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Peters</name></author><author><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K" last="Tseng">Chien-Te K. Tseng</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>B7-2 Antigen (biosynthesis)</term><term>CD40 Antigens (biosynthesis)</term><term>Cells, Cultured</term><term>Cytokines (metabolism)</term><term>Dendritic Cells (immunology)</term><term>Epithelial Cells (immunology)</term><term>Humans</term><term>Lung (immunology)</term><term>Lung (pathology)</term><term>Lung (virology)</term><term>Macrophages (immunology)</term><term>SARS Virus (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Cellules dendritiques (immunologie)</term><term>Cellules épithéliales (immunologie)</term><term>Cytokines (métabolisme)</term><term>Humains</term><term>Macrophages (immunologie)</term><term>Poumon (anatomopathologie)</term><term>Poumon (immunologie)</term><term>Poumon (virologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>B7-2 Antigen</term><term>CD40 Antigens</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules dendritiques</term><term>Cellules épithéliales</term><term>Macrophages</term><term>Poumon</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dendritic Cells</term><term>Epithelial Cells</term><term>Lung</term><term>Macrophages</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS), which is caused by a novel coronavirus (CoV), is a highly communicable disease with the lungs as the major pathological target. Although SARS likely stems from overexuberant host inflammatory responses, the exact mechanism leading to the detrimental outcome in patients remains unknown. Pulmonary macrophages (Mphi), airway epithelium, and dendritic cells (DC) are key cellular elements of the host innate defenses against respiratory infections. While pulmonary Mphi are situated at the luminal epithelial surface, DC reside abundantly underneath the epithelium. Such strategic locations of these cells within the airways make it relevant to investigate their likely impact on SARS pathogenesis subsequent to their interaction with infected lung epithelial cells. To study this, we established highly polarized human lung epithelial Calu-3 cells by using the Transwell culture system. Here we report that supernatants harvested from the apical and basolateral domains of infected Calu-3 cells are potent in modulating the intrinsic functions of Mphi and DC, respectively. They prompted the production of cytokines by both Mphi and DC and selectively induced CD40 and CD86 expression only on DC. However, they compromised the abilities of the DC and Mphi in priming naïve T cells and phagocytosis, respectively. We also identified interleukin-6 (IL-6) and IL-8 as key SARS-CoV-induced epithelial cytokines capable of inhibiting the T-cell-priming ability of DC. Taken together, our results provide insights into the molecular and cellular bases of the host antiviral innate immunity within the lungs that eventually lead to an exacerbated inflammatory cascades and severe tissue damage in SARS patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19004938</PMID><DateCompleted><Year>2009</Year><Month>03</Month><Day>30</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>83</Volume><Issue>7</Issue><PubDate><Year>2009</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Severe acute respiratory syndrome (SARS) coronavirus-induced lung epithelial cytokines exacerbate SARS pathogenesis by modulating intrinsic functions of monocyte-derived macrophages and dendritic cells.</ArticleTitle><Pagination><MedlinePgn>3039-48</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.01792-08</ELocationID><Abstract><AbstractText>Severe acute respiratory syndrome (SARS), which is caused by a novel coronavirus (CoV), is a highly communicable disease with the lungs as the major pathological target. Although SARS likely stems from overexuberant host inflammatory responses, the exact mechanism leading to the detrimental outcome in patients remains unknown. Pulmonary macrophages (Mphi), airway epithelium, and dendritic cells (DC) are key cellular elements of the host innate defenses against respiratory infections. While pulmonary Mphi are situated at the luminal epithelial surface, DC reside abundantly underneath the epithelium. Such strategic locations of these cells within the airways make it relevant to investigate their likely impact on SARS pathogenesis subsequent to their interaction with infected lung epithelial cells. To study this, we established highly polarized human lung epithelial Calu-3 cells by using the Transwell culture system. Here we report that supernatants harvested from the apical and basolateral domains of infected Calu-3 cells are potent in modulating the intrinsic functions of Mphi and DC, respectively. They prompted the production of cytokines by both Mphi and DC and selectively induced CD40 and CD86 expression only on DC. However, they compromised the abilities of the DC and Mphi in priming naïve T cells and phagocytosis, respectively. We also identified interleukin-6 (IL-6) and IL-8 as key SARS-CoV-induced epithelial cytokines capable of inhibiting the T-cell-priming ability of DC. 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K</ForeName><Initials>CT</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>U54 AI057156</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01AI25489</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21AI072201</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI072201</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01 AI3009</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01 AI25489</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType 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IdType="pubmed">11343261</ArticleId></ArticleIdList></Reference><Reference><Citation>News Physiol Sci. 2001 Jun;16:126-30</Citation><ArticleIdList><ArticleId IdType="pubmed">11443232</ArticleId></ArticleIdList></Reference><Reference><Citation>Semin Immunol. 2001 Oct;13(5):267-74</Citation><ArticleIdList><ArticleId IdType="pubmed">11502161</ArticleId></ArticleIdList></Reference><Reference><Citation>Semin Immunol. 2001 Oct;13(5):303-10</Citation><ArticleIdList><ArticleId IdType="pubmed">11502165</ArticleId></ArticleIdList></Reference><Reference><Citation>Trends Immunol. 2001 Dec;22(12):691-700</Citation><ArticleIdList><ArticleId IdType="pubmed">11739000</ArticleId></ArticleIdList></Reference><Reference><Citation>Physiol Rev. 2002 Jan;82(1):97-130</Citation><ArticleIdList><ArticleId IdType="pubmed">11773610</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 2002 Jan 7;195(1):43-9</Citation><ArticleIdList><ArticleId IdType="pubmed">11781364</ArticleId></ArticleIdList></Reference><Reference><Citation>Int J Hematol. 2002 Jul;76(1):27-34</Citation><ArticleIdList><ArticleId IdType="pubmed">12138892</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet. 2003 Apr 19;361(9366):1319-25</Citation><ArticleIdList><ArticleId IdType="pubmed">12711465</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1967-76</Citation><ArticleIdList><ArticleId IdType="pubmed">12690091</ArticleId></ArticleIdList></Reference><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1953-66</Citation><ArticleIdList><ArticleId IdType="pubmed">12690092</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 2003 May 30;300(5624):1394-9</Citation><ArticleIdList><ArticleId IdType="pubmed">12730500</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2004 Jun 15;172(12):7841-7</Citation><ArticleIdList><ArticleId IdType="pubmed">15187168</ArticleId></ArticleIdList></Reference><Reference><Citation>FASEB J. 2004 Sep;18(12):1439-41</Citation><ArticleIdList><ArticleId IdType="pubmed">15247147</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol Lung Cell Mol Physiol. 2004 Nov;287(5):L1048-55</Citation><ArticleIdList><ArticleId IdType="pubmed">15273081</ArticleId></ArticleIdList></Reference><Reference><Citation>Am Rev Respir Dis. 1988 Dec;138(6 Pt 2):S17-21</Citation><ArticleIdList><ArticleId IdType="pubmed">3202518</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Immunol. 1990;8:773-93</Citation><ArticleIdList><ArticleId IdType="pubmed">2188679</ArticleId></ArticleIdList></Reference><Reference><Citation>Ciba Found Symp. 1992;167:160-70; discussion 170-3</Citation><ArticleIdList><ArticleId IdType="pubmed">1425011</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol. 1993 Nov;265(5 Pt 1):L472-8</Citation><ArticleIdList><ArticleId IdType="pubmed">8238534</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1993 Dec 15;151(12):6840-52</Citation><ArticleIdList><ArticleId IdType="pubmed">8258694</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1996 Mar 19;93(6):2588-92</Citation><ArticleIdList><ArticleId IdType="pubmed">8637918</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1996 Jun 15;156(12):4774-82</Citation><ArticleIdList><ArticleId IdType="pubmed">8648124</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Med Today. 1996 May;2(5):198-204</Citation><ArticleIdList><ArticleId IdType="pubmed">8796888</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol Methods. 1996 Sep 27;196(2):137-51</Citation><ArticleIdList><ArticleId IdType="pubmed">8841452</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur Respir J. 1997 Sep;10(9):2139-46</Citation><ArticleIdList><ArticleId IdType="pubmed">9311517</ArticleId></ArticleIdList></Reference><Reference><Citation>Exp Lung Res. 1998 Jan-Feb;24(1):85-100</Citation><ArticleIdList><ArticleId IdType="pubmed">9457471</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1998 Mar 19;392(6673):245-52</Citation><ArticleIdList><ArticleId IdType="pubmed">9521319</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann N Y Acad Sci. 1998 May 1;840:194-204</Citation><ArticleIdList><ArticleId IdType="pubmed">9629251</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1998 Oct 1;161(7):3645-51</Citation><ArticleIdList><ArticleId IdType="pubmed">9759888</ArticleId></ArticleIdList></Reference><Reference><Citation>Semin Cell Dev Biol. 1998 Oct;9(5):503-9</Citation><ArticleIdList><ArticleId IdType="pubmed">9835637</ArticleId></ArticleIdList></Reference><Reference><Citation>J Allergy Clin Immunol. 1998 Nov;102(5):714-8</Citation><ArticleIdList><ArticleId IdType="pubmed">9867498</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann N Y Acad Sci. 1998 Nov 17;859:75-84</Citation><ArticleIdList><ArticleId IdType="pubmed">9928371</ArticleId></ArticleIdList></Reference><Reference><Citation>Semin Liver Dis. 1999;19(2):141-55</Citation><ArticleIdList><ArticleId IdType="pubmed">10422197</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Med. 2004 Dec;10(12 Suppl):S88-97</Citation><ArticleIdList><ArticleId IdType="pubmed">15577937</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2005 Apr 29;280(17):16739-47</Citation><ArticleIdList><ArticleId IdType="pubmed">15737993</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 2005 Jun 15;174(12):7977-85</Citation><ArticleIdList><ArticleId IdType="pubmed">15944304</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2005 Aug;79(15):9470-9</Citation><ArticleIdList><ArticleId IdType="pubmed">16014910</ArticleId></ArticleIdList></Reference><Reference><Citation>Blood. 2005 Oct 1;106(7):2366-74</Citation><ArticleIdList><ArticleId IdType="pubmed">15860669</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Chem. 2005 Dec;51(12):2333-40</Citation><ArticleIdList><ArticleId IdType="pubmed">16195357</ArticleId></ArticleIdList></Reference><Reference><Citation>J Pathol. 2006 Jan;208(2):142-51</Citation><ArticleIdList><ArticleId IdType="pubmed">16362992</ArticleId></ArticleIdList></Reference><Reference><Citation>Virol J. 2006;3:17</Citation><ArticleIdList><ArticleId IdType="pubmed">16571117</ArticleId></ArticleIdList></Reference><Reference><Citation>Adv Exp Med Biol. 2006;581:479-84</Citation><ArticleIdList><ArticleId IdType="pubmed">17037581</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2007 Jan;81(2):964-76</Citation><ArticleIdList><ArticleId IdType="pubmed">17093192</ArticleId></ArticleIdList></Reference><Reference><Citation>J Virol. 2007 Feb;81(3):1162-73</Citation><ArticleIdList><ArticleId IdType="pubmed">17108019</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Exp Allergy. 2008 Mar;38(3):466-72</Citation><ArticleIdList><ArticleId IdType="pubmed">18269670</ArticleId></ArticleIdList></Reference><Reference><Citation>Virus Res. 2008 Apr;133(1):101-12</Citation><ArticleIdList><ArticleId IdType="pubmed">17451827</ArticleId></ArticleIdList></Reference><Reference><Citation>Am J Physiol Lung Cell Mol Physiol. 2001 Mar;280(3):L493-502</Citation><ArticleIdList><ArticleId IdType="pubmed">11159033</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Hill, Terence" sort="Hill, Terence" uniqKey="Hill T" first="Terence" last="Hill">Terence Hill</name><name sortKey="Li, Kui" sort="Li, Kui" uniqKey="Li K" first="Kui" last="Li">Kui Li</name><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. Peters</name><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K" last="Tseng">Chien-Te K. Tseng</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Yoshikawa, Tomoki" sort="Yoshikawa, Tomoki" uniqKey="Yoshikawa T" first="Tomoki" last="Yoshikawa">Tomoki Yoshikawa</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:19004938" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a SrasV1
| This area was generated with Dilib version V0.6.33. |  |