CIGB-258, a peptide derived from human heat-shock protein 60, decreases hyperinflammation in COVID-19 patients
Hyperinflammation distinguishes COVID-19 patients who develop a slight disease or none, from those progressing to severe and critical conditions. CIGB-258 is a therapeutic option for the latter group of patients. This drug is an altered peptide ligand (APL) derived from the cellular stress protein 6...
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| Veröffentlicht in: | Cell stress & chaperones 2021-05, Vol.26 (3), p.515-525 |
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| creator | Hernandez-Cedeño, M. Venegas-Rodriguez, R. Peña-Ruiz, R. Bequet-Romero, M. Santana-Sanchez, R. Penton-Arias, E. Martinez-Donato, G. Guillén-Nieto, G. del Carmen Dominguez-Horta, María |
| description | Hyperinflammation distinguishes COVID-19 patients who develop a slight disease or none, from those progressing to severe and critical conditions. CIGB-258 is a therapeutic option for the latter group of patients. This drug is an altered peptide ligand (APL) derived from the cellular stress protein 60 (HSP60). In preclinical models, this peptide developed anti-inflammatory effects and increased regulatory T cell (Treg) activity. Results from a phase I clinical trial with rheumatoid arthritis (RA) patients indicated that CIGB-258 was safe and reduced inflammation. The aim of this study was to examine specific biomarkers associated with hyperinflammation, some cytokines linked to the cytokine storm granzyme B and perforin in a cohort of COVID-19 patients treated with this peptide. All critically ill patients were under invasive mechanical ventilation and received the intravenous administration of 1 or 2 mg of CIGB-258 every 12 h. Seriously ill patients were treated with oxygen therapy receiving 1 mg of CIGB-258 every 12 h and all patients recovered from their severe condition. Biomarker levels associated with hyperinflammation, such as interleukin (IL)-6, IL-10, tumor necrosis factor (TNF-a), granzyme B, and perforin, significantly decreased during treatment. Furthermore, we studied the ability of CIGB-258 to induce Tregs in COVID-19 patients and found that Tregs were induced in all patients studied. Altogether, these results support the therapeutic potential of CIGB-258 for diseases associated with hyperinflammation. |
| doi_str_mv | 10.1007/s12192-021-01197-2 |
| format | Article |
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CIGB-258 is a therapeutic option for the latter group of patients. This drug is an altered peptide ligand (APL) derived from the cellular stress protein 60 (HSP60). In preclinical models, this peptide developed anti-inflammatory effects and increased regulatory T cell (Treg) activity. Results from a phase I clinical trial with rheumatoid arthritis (RA) patients indicated that CIGB-258 was safe and reduced inflammation. The aim of this study was to examine specific biomarkers associated with hyperinflammation, some cytokines linked to the cytokine storm granzyme B and perforin in a cohort of COVID-19 patients treated with this peptide. All critically ill patients were under invasive mechanical ventilation and received the intravenous administration of 1 or 2 mg of CIGB-258 every 12 h. Seriously ill patients were treated with oxygen therapy receiving 1 mg of CIGB-258 every 12 h and all patients recovered from their severe condition. Biomarker levels associated with hyperinflammation, such as interleukin (IL)-6, IL-10, tumor necrosis factor (TNF-a), granzyme B, and perforin, significantly decreased during treatment. Furthermore, we studied the ability of CIGB-258 to induce Tregs in COVID-19 patients and found that Tregs were induced in all patients studied. Altogether, these results support the therapeutic potential of CIGB-258 for diseases associated with hyperinflammation.</description><identifier>ISSN: 1355-8145</identifier><identifier>EISSN: 1466-1268</identifier><identifier>DOI: 10.1007/s12192-021-01197-2</identifier><identifier>PMID: 33629254</identifier><language>eng</language><publisher>Dordrecht: Springer Science + Business Media</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Anti-Inflammatory Agents - chemistry ; Anti-Inflammatory Agents - therapeutic use ; Arthritis ; Biochemistry ; Biomarkers ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Biology ; Cellular stress response ; Chaperonin 60 - chemistry ; Chaperonin 60 - therapeutic use ; Clinical trials ; Coronaviruses ; COVID-19 ; COVID-19 - blood ; COVID-19 - complications ; COVID-19 Drug Treatment ; Cytokine Release Syndrome - blood ; Cytokine Release Syndrome - complications ; Cytokine Release Syndrome - drug therapy ; Cytokine storm ; Cytokines ; Female ; Granzyme B ; Heat shock proteins ; Hsp60 protein ; Humans ; Immunology ; Inflammation ; Inflammation - blood ; Inflammation - complications ; Inflammation - drug therapy ; Interleukin 10 ; Interleukin-10 - blood ; Interleukin-6 - blood ; Intravenous administration ; Lymphocytes ; Lymphocytes T ; Male ; Mechanical ventilation ; Middle Aged ; Neurosciences ; ORIGINAL PAPER ; Patients ; Peptides ; Perforin ; Rheumatoid arthritis ; SARS-CoV-2 - drug effects ; T-Lymphocytes, Regulatory - drug effects ; Tumor Necrosis Factor-alpha - blood ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Young Adult</subject><ispartof>Cell stress & chaperones, 2021-05, Vol.26 (3), p.515-525</ispartof><rights>Cell Stress Society International 2021</rights><rights>Cell Stress Society International 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-384a96673b0c0068b73f9e77b2c963d68887308d28531b5ceef7ad1721f209a93</citedby><cites>FETCH-LOGICAL-c496t-384a96673b0c0068b73f9e77b2c963d68887308d28531b5ceef7ad1721f209a93</cites><orcidid>0000-0002-0616-7376</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/48724327$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/48724327$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,41464,42533,51294,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33629254$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hernandez-Cedeño, M.</creatorcontrib><creatorcontrib>Venegas-Rodriguez, R.</creatorcontrib><creatorcontrib>Peña-Ruiz, R.</creatorcontrib><creatorcontrib>Bequet-Romero, M.</creatorcontrib><creatorcontrib>Santana-Sanchez, R.</creatorcontrib><creatorcontrib>Penton-Arias, E.</creatorcontrib><creatorcontrib>Martinez-Donato, G.</creatorcontrib><creatorcontrib>Guillén-Nieto, G.</creatorcontrib><creatorcontrib>del Carmen Dominguez-Horta, María</creatorcontrib><title>CIGB-258, a peptide derived from human heat-shock protein 60, decreases hyperinflammation in COVID-19 patients</title><title>Cell stress & chaperones</title><addtitle>Cell Stress and Chaperones</addtitle><addtitle>Cell Stress Chaperones</addtitle><description>Hyperinflammation distinguishes COVID-19 patients who develop a slight disease or none, from those progressing to severe and critical conditions. CIGB-258 is a therapeutic option for the latter group of patients. This drug is an altered peptide ligand (APL) derived from the cellular stress protein 60 (HSP60). In preclinical models, this peptide developed anti-inflammatory effects and increased regulatory T cell (Treg) activity. Results from a phase I clinical trial with rheumatoid arthritis (RA) patients indicated that CIGB-258 was safe and reduced inflammation. The aim of this study was to examine specific biomarkers associated with hyperinflammation, some cytokines linked to the cytokine storm granzyme B and perforin in a cohort of COVID-19 patients treated with this peptide. All critically ill patients were under invasive mechanical ventilation and received the intravenous administration of 1 or 2 mg of CIGB-258 every 12 h. Seriously ill patients were treated with oxygen therapy receiving 1 mg of CIGB-258 every 12 h and all patients recovered from their severe condition. Biomarker levels associated with hyperinflammation, such as interleukin (IL)-6, IL-10, tumor necrosis factor (TNF-a), granzyme B, and perforin, significantly decreased during treatment. Furthermore, we studied the ability of CIGB-258 to induce Tregs in COVID-19 patients and found that Tregs were induced in all patients studied. Altogether, these results support the therapeutic potential of CIGB-258 for diseases associated with hyperinflammation.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Anti-Inflammatory Agents - chemistry</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Arthritis</subject><subject>Biochemistry</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell Biology</subject><subject>Cellular stress response</subject><subject>Chaperonin 60 - chemistry</subject><subject>Chaperonin 60 - therapeutic use</subject><subject>Clinical trials</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>COVID-19 - blood</subject><subject>COVID-19 - complications</subject><subject>COVID-19 Drug Treatment</subject><subject>Cytokine Release Syndrome - blood</subject><subject>Cytokine Release Syndrome - complications</subject><subject>Cytokine Release Syndrome - drug therapy</subject><subject>Cytokine storm</subject><subject>Cytokines</subject><subject>Female</subject><subject>Granzyme B</subject><subject>Heat shock proteins</subject><subject>Hsp60 protein</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - complications</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin 10</subject><subject>Interleukin-10 - blood</subject><subject>Interleukin-6 - blood</subject><subject>Intravenous administration</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Mechanical ventilation</subject><subject>Middle Aged</subject><subject>Neurosciences</subject><subject>ORIGINAL PAPER</subject><subject>Patients</subject><subject>Peptides</subject><subject>Perforin</subject><subject>Rheumatoid arthritis</subject><subject>SARS-CoV-2 - drug effects</subject><subject>T-Lymphocytes, Regulatory - drug effects</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Young Adult</subject><issn>1355-8145</issn><issn>1466-1268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhS0EomXgDyCBLLFhUYN97fixQYIBykiVugG2lpM4TYaJndpJpf57DCnDY8HKlu93zvHVQegpo68Ypep1ZsAMEAqMUMaMInAPnTIhJWEg9f1y51VFNBPVCXqU854WkVLsITrhXIKBSpyisN2dvyNQ6TPs8OSneWg9bn0abnyLuxRH3C-jC7j3bia5j803PKU4-yFgSc8K2STvss-4v52KKnQHN45uHmLABdleft29J8zgqTz5MOfH6EHnDtk_uTs36MvHD5-3n8jF5flu-_aCNMLImXAtnJFS8Zo2lEpdK94Zr1QNjZG8lVprxaluQVec1VXjfadcyxSwDqhxhm_Qm9V3WurRt03JTu5gpzSMLt3a6Ab79yQMvb2KN1YZKqBkbNDLO4MUrxefZzsOufGHgws-LtmCMFwIA5IX9MU_6D4uKZT1LFRMCZCGq0LBSjUp5px8d_wMo_ZHnXat05Y67c86LRTR8z_XOEp-9VcAvgK5jMKVT7-z_2v7bFXt8xzT0VVoBYKD4t8B3HOynQ</recordid><startdate>20210501</startdate><enddate>20210501</enddate><creator>Hernandez-Cedeño, M.</creator><creator>Venegas-Rodriguez, R.</creator><creator>Peña-Ruiz, R.</creator><creator>Bequet-Romero, M.</creator><creator>Santana-Sanchez, R.</creator><creator>Penton-Arias, E.</creator><creator>Martinez-Donato, G.</creator><creator>Guillén-Nieto, G.</creator><creator>del Carmen Dominguez-Horta, María</creator><general>Springer Science + Business Media</general><general>Springer Netherlands</general><general>Springer Nature B.V</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>7QL</scope><scope>7QP</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0616-7376</orcidid></search><sort><creationdate>20210501</creationdate><title>CIGB-258, a peptide derived from human heat-shock protein 60, decreases hyperinflammation in COVID-19 patients</title><author>Hernandez-Cedeño, M. ; Venegas-Rodriguez, R. ; Peña-Ruiz, R. ; Bequet-Romero, M. ; Santana-Sanchez, R. ; Penton-Arias, E. ; Martinez-Donato, G. ; Guillén-Nieto, G. ; del Carmen Dominguez-Horta, María</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-384a96673b0c0068b73f9e77b2c963d68887308d28531b5ceef7ad1721f209a93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Anti-Inflammatory Agents - chemistry</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Arthritis</topic><topic>Biochemistry</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cell Biology</topic><topic>Cellular stress response</topic><topic>Chaperonin 60 - chemistry</topic><topic>Chaperonin 60 - therapeutic use</topic><topic>Clinical trials</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>COVID-19 - blood</topic><topic>COVID-19 - complications</topic><topic>COVID-19 Drug Treatment</topic><topic>Cytokine Release Syndrome - blood</topic><topic>Cytokine Release Syndrome - complications</topic><topic>Cytokine Release Syndrome - drug therapy</topic><topic>Cytokine storm</topic><topic>Cytokines</topic><topic>Female</topic><topic>Granzyme B</topic><topic>Heat shock proteins</topic><topic>Hsp60 protein</topic><topic>Humans</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammation - blood</topic><topic>Inflammation - complications</topic><topic>Inflammation - drug therapy</topic><topic>Interleukin 10</topic><topic>Interleukin-10 - blood</topic><topic>Interleukin-6 - blood</topic><topic>Intravenous administration</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Mechanical ventilation</topic><topic>Middle Aged</topic><topic>Neurosciences</topic><topic>ORIGINAL PAPER</topic><topic>Patients</topic><topic>Peptides</topic><topic>Perforin</topic><topic>Rheumatoid arthritis</topic><topic>SARS-CoV-2 - drug effects</topic><topic>T-Lymphocytes, Regulatory - drug effects</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hernandez-Cedeño, M.</creatorcontrib><creatorcontrib>Venegas-Rodriguez, R.</creatorcontrib><creatorcontrib>Peña-Ruiz, R.</creatorcontrib><creatorcontrib>Bequet-Romero, M.</creatorcontrib><creatorcontrib>Santana-Sanchez, R.</creatorcontrib><creatorcontrib>Penton-Arias, E.</creatorcontrib><creatorcontrib>Martinez-Donato, G.</creatorcontrib><creatorcontrib>Guillén-Nieto, G.</creatorcontrib><creatorcontrib>del Carmen Dominguez-Horta, María</creatorcontrib><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>Calcium & Calcified Tissue Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell stress & chaperones</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hernandez-Cedeño, M.</au><au>Venegas-Rodriguez, R.</au><au>Peña-Ruiz, R.</au><au>Bequet-Romero, M.</au><au>Santana-Sanchez, R.</au><au>Penton-Arias, E.</au><au>Martinez-Donato, G.</au><au>Guillén-Nieto, G.</au><au>del Carmen Dominguez-Horta, María</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CIGB-258, a peptide derived from human heat-shock protein 60, decreases hyperinflammation in COVID-19 patients</atitle><jtitle>Cell stress & chaperones</jtitle><stitle>Cell Stress and Chaperones</stitle><addtitle>Cell Stress Chaperones</addtitle><date>2021-05-01</date><risdate>2021</risdate><volume>26</volume><issue>3</issue><spage>515</spage><epage>525</epage><pages>515-525</pages><issn>1355-8145</issn><eissn>1466-1268</eissn><abstract>Hyperinflammation distinguishes COVID-19 patients who develop a slight disease or none, from those progressing to severe and critical conditions. CIGB-258 is a therapeutic option for the latter group of patients. This drug is an altered peptide ligand (APL) derived from the cellular stress protein 60 (HSP60). In preclinical models, this peptide developed anti-inflammatory effects and increased regulatory T cell (Treg) activity. Results from a phase I clinical trial with rheumatoid arthritis (RA) patients indicated that CIGB-258 was safe and reduced inflammation. The aim of this study was to examine specific biomarkers associated with hyperinflammation, some cytokines linked to the cytokine storm granzyme B and perforin in a cohort of COVID-19 patients treated with this peptide. All critically ill patients were under invasive mechanical ventilation and received the intravenous administration of 1 or 2 mg of CIGB-258 every 12 h. Seriously ill patients were treated with oxygen therapy receiving 1 mg of CIGB-258 every 12 h and all patients recovered from their severe condition. Biomarker levels associated with hyperinflammation, such as interleukin (IL)-6, IL-10, tumor necrosis factor (TNF-a), granzyme B, and perforin, significantly decreased during treatment. Furthermore, we studied the ability of CIGB-258 to induce Tregs in COVID-19 patients and found that Tregs were induced in all patients studied. Altogether, these results support the therapeutic potential of CIGB-258 for diseases associated with hyperinflammation.</abstract><cop>Dordrecht</cop><pub>Springer Science + Business Media</pub><pmid>33629254</pmid><doi>10.1007/s12192-021-01197-2</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-0616-7376</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell stress & chaperones, 2021-05, Vol.26 (3), p.515-525 |
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| language | eng |
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| source | Jstor Complete Legacy; MEDLINE; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Adult Aged Aged, 80 and over Anti-Inflammatory Agents - chemistry Anti-Inflammatory Agents - therapeutic use Arthritis Biochemistry Biomarkers Biomedical and Life Sciences Biomedicine Cancer Research Cell Biology Cellular stress response Chaperonin 60 - chemistry Chaperonin 60 - therapeutic use Clinical trials Coronaviruses COVID-19 COVID-19 - blood COVID-19 - complications COVID-19 Drug Treatment Cytokine Release Syndrome - blood Cytokine Release Syndrome - complications Cytokine Release Syndrome - drug therapy Cytokine storm Cytokines Female Granzyme B Heat shock proteins Hsp60 protein Humans Immunology Inflammation Inflammation - blood Inflammation - complications Inflammation - drug therapy Interleukin 10 Interleukin-10 - blood Interleukin-6 - blood Intravenous administration Lymphocytes Lymphocytes T Male Mechanical ventilation Middle Aged Neurosciences ORIGINAL PAPER Patients Peptides Perforin Rheumatoid arthritis SARS-CoV-2 - drug effects T-Lymphocytes, Regulatory - drug effects Tumor Necrosis Factor-alpha - blood Tumor necrosis factor-TNF Tumor necrosis factor-α Young Adult |
| title | CIGB-258, a peptide derived from human heat-shock protein 60, decreases hyperinflammation in COVID-19 patients |
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