Neutrophil and Monocyte Function in Patients with Chronic Hepatitis C Undergoing Antiviral Therapy with Regimens Containing Protease Inhibitors with and without Interferon
Real-life data showed an increased incidence of bacterial infections in patients with advanced liver disease receiving a protease inhibitor (PI)-containing antiviral regimen against hepatitis C (HCV). However, the causes of this event are unknown. We hypothesized that PIs might impair innate immune...
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| Veröffentlicht in: | PloS one 2016-11, Vol.11 (11), p.e0166631-e0166631 |
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| creator | Gambato, Martina Caro-Pérez, Noelia González, Patricia Cañete, Nuria Mariño, Zoe Lens, Sabela Bonacci, Martín Bartres, Concepció Sánchez-Tapias, José-María Carrión, José A Forns, Xavier Juan, Manel Pérez-Del-Pulgar, Sofía Londoño, María-Carlota |
| description | Real-life data showed an increased incidence of bacterial infections in patients with advanced liver disease receiving a protease inhibitor (PI)-containing antiviral regimen against hepatitis C (HCV). However, the causes of this event are unknown. We hypothesized that PIs might impair innate immune responses through the inhibition of proteases participating in the anti-bacterial functions of neutrophils and monocytes. The aims of the study were to assess phagocytic and oxidative burst capacity in neutrophils and monocytes obtained from patients receiving a PI containing-antiviral regimen, and to determine cytokine secretion after neutrophil stimulation with flagellin. Forty patients with chronic HCV (80% with cirrhosis) were enrolled in the study, 28 received triple therapy (Group A) with pegylated-interferon and ribavirin for 4 weeks followed by the addition of a PI (telaprevir, boceprevir or simeprevir), and 12 patients received an interferon-free regimen (Group B) with simeprevir and sofosbuvir. Phagocytosis and oxidative burst capacity were analyzed by flow cytometry at baseline, week 4, and week 8 of therapy. In neutrophils from Group A patients, oxidative burst rate and oxidative enzymatic activity per cell significantly decreased throughout the study period (p = 0.014 and p = 0.010, respectively). Pairwise comparisons showed a decrease between baseline and week 4 and 8 of therapy. No differences were observed after the introduction of the PI. The oxidative enzymatic activity per cell in monocytes significantly decrease during the study period (p = 0.042) due to a decrease from baseline to week 8 of therapy (p = 0.037) in patients from Group A. None of these findings were observed in Group B patients. Cytokine secretion did not significantly change during the study in both groups. In conclusion, our data suggest that the use interferon (rather than the PI) has a deleterious effect on neutrophil and monocyte phagocytic and oxidative burst capacity in this cohort of patients with HCV-related advanced liver fibrosis. |
| doi_str_mv | 10.1371/journal.pone.0166631 |
| format | Article |
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However, the causes of this event are unknown. We hypothesized that PIs might impair innate immune responses through the inhibition of proteases participating in the anti-bacterial functions of neutrophils and monocytes. The aims of the study were to assess phagocytic and oxidative burst capacity in neutrophils and monocytes obtained from patients receiving a PI containing-antiviral regimen, and to determine cytokine secretion after neutrophil stimulation with flagellin. Forty patients with chronic HCV (80% with cirrhosis) were enrolled in the study, 28 received triple therapy (Group A) with pegylated-interferon and ribavirin for 4 weeks followed by the addition of a PI (telaprevir, boceprevir or simeprevir), and 12 patients received an interferon-free regimen (Group B) with simeprevir and sofosbuvir. Phagocytosis and oxidative burst capacity were analyzed by flow cytometry at baseline, week 4, and week 8 of therapy. In neutrophils from Group A patients, oxidative burst rate and oxidative enzymatic activity per cell significantly decreased throughout the study period (p = 0.014 and p = 0.010, respectively). Pairwise comparisons showed a decrease between baseline and week 4 and 8 of therapy. No differences were observed after the introduction of the PI. The oxidative enzymatic activity per cell in monocytes significantly decrease during the study period (p = 0.042) due to a decrease from baseline to week 8 of therapy (p = 0.037) in patients from Group A. None of these findings were observed in Group B patients. Cytokine secretion did not significantly change during the study in both groups. In conclusion, our data suggest that the use interferon (rather than the PI) has a deleterious effect on neutrophil and monocyte phagocytic and oxidative burst capacity in this cohort of patients with HCV-related advanced liver fibrosis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0166631</identifier><identifier>PMID: 27861593</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Antibacterial agents ; Antiinfectives and antibacterials ; Antiviral agents ; Antiviral drugs ; Apoptosis ; Bacterial infections ; Biological response modifiers ; Biology and Life Sciences ; Bursting ; Care and treatment ; Chronic diseases ; Cirrhosis ; Cirrosi hepàtica ; Cytometry ; Disease susceptibility ; Enzymatic activity ; Fibrosis ; Flagellin ; Flow cytometry ; Gastroenterology ; Health aspects ; Hepatic cirrhosis ; Hepatitis ; Hepatitis C ; Hepatitis C virus ; Hepatology ; Hypertension ; Immune response ; Immune system ; Infection ; Infections ; Innate immunity ; Interferon ; Interferó ; Leukocytes (neutrophilic) ; Liver ; Liver cirrhosis ; Liver diseases ; Malalties cròniques ; Medical research ; Medicine and Health Sciences ; Monocytes ; Neutropenia ; Neutrophils ; Patients ; Phagocytes ; Phagocytosis ; Protease ; Protease inhibitors ; Proteases ; Proteinase inhibitors ; Ribavirin ; Therapy ; Transplants & implants</subject><ispartof>PloS one, 2016-11, Vol.11 (11), p.e0166631-e0166631</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Gambato et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>cc-by (c) Gambato, Martina et al., 2016 info:eu-repo/semantics/openAccess <a href="http://creativecommons.org/licenses/by/3.0/es">http://creativecommons.org/licenses/by/3.0/es</a></rights><rights>2016 Gambato et al 2016 Gambato et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c767t-28a8552df3e87e2c6e6b828a1eeb9a2e1f768bf67f97b09136781722bb55db913</citedby><cites>FETCH-LOGICAL-c767t-28a8552df3e87e2c6e6b828a1eeb9a2e1f768bf67f97b09136781722bb55db913</cites><orcidid>0000-0002-6533-1586</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5115763/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5115763/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,26951,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27861593$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gambato, Martina</creatorcontrib><creatorcontrib>Caro-Pérez, Noelia</creatorcontrib><creatorcontrib>González, Patricia</creatorcontrib><creatorcontrib>Cañete, Nuria</creatorcontrib><creatorcontrib>Mariño, Zoe</creatorcontrib><creatorcontrib>Lens, Sabela</creatorcontrib><creatorcontrib>Bonacci, Martín</creatorcontrib><creatorcontrib>Bartres, Concepció</creatorcontrib><creatorcontrib>Sánchez-Tapias, José-María</creatorcontrib><creatorcontrib>Carrión, José A</creatorcontrib><creatorcontrib>Forns, Xavier</creatorcontrib><creatorcontrib>Juan, Manel</creatorcontrib><creatorcontrib>Pérez-Del-Pulgar, Sofía</creatorcontrib><creatorcontrib>Londoño, María-Carlota</creatorcontrib><title>Neutrophil and Monocyte Function in Patients with Chronic Hepatitis C Undergoing Antiviral Therapy with Regimens Containing Protease Inhibitors with and without Interferon</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Real-life data showed an increased incidence of bacterial infections in patients with advanced liver disease receiving a protease inhibitor (PI)-containing antiviral regimen against hepatitis C (HCV). However, the causes of this event are unknown. We hypothesized that PIs might impair innate immune responses through the inhibition of proteases participating in the anti-bacterial functions of neutrophils and monocytes. The aims of the study were to assess phagocytic and oxidative burst capacity in neutrophils and monocytes obtained from patients receiving a PI containing-antiviral regimen, and to determine cytokine secretion after neutrophil stimulation with flagellin. Forty patients with chronic HCV (80% with cirrhosis) were enrolled in the study, 28 received triple therapy (Group A) with pegylated-interferon and ribavirin for 4 weeks followed by the addition of a PI (telaprevir, boceprevir or simeprevir), and 12 patients received an interferon-free regimen (Group B) with simeprevir and sofosbuvir. Phagocytosis and oxidative burst capacity were analyzed by flow cytometry at baseline, week 4, and week 8 of therapy. In neutrophils from Group A patients, oxidative burst rate and oxidative enzymatic activity per cell significantly decreased throughout the study period (p = 0.014 and p = 0.010, respectively). Pairwise comparisons showed a decrease between baseline and week 4 and 8 of therapy. No differences were observed after the introduction of the PI. The oxidative enzymatic activity per cell in monocytes significantly decrease during the study period (p = 0.042) due to a decrease from baseline to week 8 of therapy (p = 0.037) in patients from Group A. None of these findings were observed in Group B patients. Cytokine secretion did not significantly change during the study in both groups. In conclusion, our data suggest that the use interferon (rather than the PI) has a deleterious effect on neutrophil and monocyte phagocytic and oxidative burst capacity in this cohort of patients with HCV-related advanced liver fibrosis.</description><subject>Analysis</subject><subject>Antibacterial agents</subject><subject>Antiinfectives and antibacterials</subject><subject>Antiviral agents</subject><subject>Antiviral drugs</subject><subject>Apoptosis</subject><subject>Bacterial infections</subject><subject>Biological response modifiers</subject><subject>Biology and Life Sciences</subject><subject>Bursting</subject><subject>Care and treatment</subject><subject>Chronic diseases</subject><subject>Cirrhosis</subject><subject>Cirrosi hepàtica</subject><subject>Cytometry</subject><subject>Disease susceptibility</subject><subject>Enzymatic activity</subject><subject>Fibrosis</subject><subject>Flagellin</subject><subject>Flow cytometry</subject><subject>Gastroenterology</subject><subject>Health aspects</subject><subject>Hepatic cirrhosis</subject><subject>Hepatitis</subject><subject>Hepatitis C</subject><subject>Hepatitis C virus</subject><subject>Hepatology</subject><subject>Hypertension</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Infection</subject><subject>Infections</subject><subject>Innate immunity</subject><subject>Interferon</subject><subject>Interferó</subject><subject>Leukocytes (neutrophilic)</subject><subject>Liver</subject><subject>Liver cirrhosis</subject><subject>Liver diseases</subject><subject>Malalties cròniques</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Monocytes</subject><subject>Neutropenia</subject><subject>Neutrophils</subject><subject>Patients</subject><subject>Phagocytes</subject><subject>Phagocytosis</subject><subject>Protease</subject><subject>Protease 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Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Recercat</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gambato, Martina</au><au>Caro-Pérez, Noelia</au><au>González, Patricia</au><au>Cañete, Nuria</au><au>Mariño, Zoe</au><au>Lens, Sabela</au><au>Bonacci, Martín</au><au>Bartres, Concepció</au><au>Sánchez-Tapias, José-María</au><au>Carrión, José A</au><au>Forns, Xavier</au><au>Juan, Manel</au><au>Pérez-Del-Pulgar, Sofía</au><au>Londoño, María-Carlota</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neutrophil and Monocyte Function in Patients with Chronic Hepatitis C Undergoing Antiviral Therapy with Regimens Containing Protease Inhibitors with and without Interferon</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-11-18</date><risdate>2016</risdate><volume>11</volume><issue>11</issue><spage>e0166631</spage><epage>e0166631</epage><pages>e0166631-e0166631</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Real-life data showed an increased incidence of bacterial infections in patients with advanced liver disease receiving a protease inhibitor (PI)-containing antiviral regimen against hepatitis C (HCV). However, the causes of this event are unknown. We hypothesized that PIs might impair innate immune responses through the inhibition of proteases participating in the anti-bacterial functions of neutrophils and monocytes. The aims of the study were to assess phagocytic and oxidative burst capacity in neutrophils and monocytes obtained from patients receiving a PI containing-antiviral regimen, and to determine cytokine secretion after neutrophil stimulation with flagellin. Forty patients with chronic HCV (80% with cirrhosis) were enrolled in the study, 28 received triple therapy (Group A) with pegylated-interferon and ribavirin for 4 weeks followed by the addition of a PI (telaprevir, boceprevir or simeprevir), and 12 patients received an interferon-free regimen (Group B) with simeprevir and sofosbuvir. Phagocytosis and oxidative burst capacity were analyzed by flow cytometry at baseline, week 4, and week 8 of therapy. In neutrophils from Group A patients, oxidative burst rate and oxidative enzymatic activity per cell significantly decreased throughout the study period (p = 0.014 and p = 0.010, respectively). Pairwise comparisons showed a decrease between baseline and week 4 and 8 of therapy. No differences were observed after the introduction of the PI. The oxidative enzymatic activity per cell in monocytes significantly decrease during the study period (p = 0.042) due to a decrease from baseline to week 8 of therapy (p = 0.037) in patients from Group A. None of these findings were observed in Group B patients. Cytokine secretion did not significantly change during the study in both groups. In conclusion, our data suggest that the use interferon (rather than the PI) has a deleterious effect on neutrophil and monocyte phagocytic and oxidative burst capacity in this cohort of patients with HCV-related advanced liver fibrosis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27861593</pmid><doi>10.1371/journal.pone.0166631</doi><tpages>e0166631</tpages><orcidid>https://orcid.org/0000-0002-6533-1586</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-11, Vol.11 (11), p.e0166631-e0166631 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1841403070 |
| source | DOAJ Directory of Open Access Journals; Recercat; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Analysis Antibacterial agents Antiinfectives and antibacterials Antiviral agents Antiviral drugs Apoptosis Bacterial infections Biological response modifiers Biology and Life Sciences Bursting Care and treatment Chronic diseases Cirrhosis Cirrosi hepàtica Cytometry Disease susceptibility Enzymatic activity Fibrosis Flagellin Flow cytometry Gastroenterology Health aspects Hepatic cirrhosis Hepatitis Hepatitis C Hepatitis C virus Hepatology Hypertension Immune response Immune system Infection Infections Innate immunity Interferon Interferó Leukocytes (neutrophilic) Liver Liver cirrhosis Liver diseases Malalties cròniques Medical research Medicine and Health Sciences Monocytes Neutropenia Neutrophils Patients Phagocytes Phagocytosis Protease Protease inhibitors Proteases Proteinase inhibitors Ribavirin Therapy Transplants & implants |
| title | Neutrophil and Monocyte Function in Patients with Chronic Hepatitis C Undergoing Antiviral Therapy with Regimens Containing Protease Inhibitors with and without Interferon |
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