Comparison of ISG15, IL28B and USP18 mRNA levels in peripheral blood mononuclear cells of chronic hepatitis B virus infected patients and healthy individuals.

Hepatitis B viruses IFN-lambda-3 protein ISG15 protein Immunity USP18

Journal

Gastroenterology and hepatology from bed to bench
ISSN: 2008-2258
Titre abrégé: Gastroenterol Hepatol Bed Bench
Pays: Iran
ID NLM: 101525875

Informations de publication

Date de publication:
2019
Historique:
entrez: 6 4 2019
pubmed: 6 4 2019
medline: 6 4 2019
Statut: ppublish

Résumé

The purpose of this study was to evaluate the expression level of Interferon-stimulated Gene 15 (ISG15), Interleukin28B (IL28B) or IFN-lambda-3 and Ubiquitin specific peptidase 18 (USP18) genes in Peripheral Blood Mononuclear Cells (PBMCs) of patients with chronic active and inactive hepatitis B in comparison with healthy individuals. Despite the presence of the vaccine for hepatitis B virus (HBV), it remains a public health challenge. The effort to uncover the immune genes attributed to infection outcome is going through. This Cross-sectional study was conducted on hepatitis B infected patients that were admitted to the Clinic of Liver diseases, Shiraz, January-November 2016. Patients were divided into two groups including active and inactive chronic regarding relevant World Gastroenterology Organization Global Guideline. They were mono-infected with HBV, and HCV or HIV co-infection was excluded from the study. Gene expression analysis was performed on fresh PBMCs samples with the help of Real-time PCR method. Interleukin 28B gene expression showed no statistically significant difference between the three studied groups (P>0.05). The expression level of ISG15 was significantly higher in the healthy control group compared to active (P= 0.0068) and inactive chronic subjects (P<0.0001). Similarly, USP18 expression level in the control group was also significantly higher compared to the active (P= 0.0228) and inactive chronic patients (P=0. 0226). The results of this study showed that the expression level of ISG15 and USP18 but not IL28B were higher in healthy individuals than in those infected with HBV. This difference expression may highlight the role of ISG15 and USP18 in the immune-related mechanism of HBV infection.

Sections du résumé

AIM OBJECTIVE
The purpose of this study was to evaluate the expression level of Interferon-stimulated Gene 15 (ISG15), Interleukin28B (IL28B) or IFN-lambda-3 and Ubiquitin specific peptidase 18 (USP18) genes in Peripheral Blood Mononuclear Cells (PBMCs) of patients with chronic active and inactive hepatitis B in comparison with healthy individuals.
BACKGROUND BACKGROUND
Despite the presence of the vaccine for hepatitis B virus (HBV), it remains a public health challenge. The effort to uncover the immune genes attributed to infection outcome is going through.
METHODS METHODS
This Cross-sectional study was conducted on hepatitis B infected patients that were admitted to the Clinic of Liver diseases, Shiraz, January-November 2016. Patients were divided into two groups including active and inactive chronic regarding relevant World Gastroenterology Organization Global Guideline. They were mono-infected with HBV, and HCV or HIV co-infection was excluded from the study. Gene expression analysis was performed on fresh PBMCs samples with the help of Real-time PCR method.
RESULTS RESULTS
Interleukin 28B gene expression showed no statistically significant difference between the three studied groups (P>0.05). The expression level of ISG15 was significantly higher in the healthy control group compared to active (P= 0.0068) and inactive chronic subjects (P<0.0001). Similarly, USP18 expression level in the control group was also significantly higher compared to the active (P= 0.0228) and inactive chronic patients (P=0. 0226).
CONCLUSION CONCLUSIONS
The results of this study showed that the expression level of ISG15 and USP18 but not IL28B were higher in healthy individuals than in those infected with HBV. This difference expression may highlight the role of ISG15 and USP18 in the immune-related mechanism of HBV infection.

Identifiants

pubmed: 30949318
pmc: PMC6441482

Types de publication

Journal Article

Langues

eng

Pagination

38-45

Déclaration de conflit d'intérêts

The authors declare that they have no conflict of interest.

Références

Mol Cell Biol. 1999 Apr;19(4):3029-38
pubmed: 10082570
Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13825-30
pubmed: 12374864
Mol Cell Biol. 2006 Jan;26(2):472-9
pubmed: 16382139
Semin Liver Dis. 2007 May;27(2):152-60
pubmed: 17520515
J Gastrointestin Liver Dis. 2007 Dec;16(4):403-6
pubmed: 18193122
J Immunol. 2008 Nov 1;181(9):6467-72
pubmed: 18941237
Nat Genet. 2009 Oct;41(10):1100-4
pubmed: 19749758
Biochim Biophys Acta. 2010 May;1802(5):485-96
pubmed: 20153823
J Gen Virol. 2010 Sep;91(Pt 9):2238-48
pubmed: 20505011
Gut. 2010 Aug;59(8):1111-9
pubmed: 20639253
J Immunol. 2010 Oct 1;185(7):4311-8
pubmed: 20810994
Cell. 2010 Oct 15;143(2):187-90
pubmed: 20946978
J Infect Dis. 2010 Dec 1;202(11):1749-53
pubmed: 20977343
Liver Int. 2011 Sep;31(8):1118-26
pubmed: 21745278
Gastroenterology. 2012 Mar;142(3):513-520.e1
pubmed: 22108195
Occup Med (Lond). 2011 Dec;61(8):531-40
pubmed: 22114089
Tissue Antigens. 2012 Apr;79(4):302-5
pubmed: 22239156
Vaccine. 2012 Mar 9;30(12):2212-9
pubmed: 22273662
Cancer Immunol Immunother. 2012 Sep;61(9):1433-9
pubmed: 22310928
Aliment Pharmacol Ther. 2012 Jul;36(2):104-14
pubmed: 22612303
Oncol Lett. 2011 Sep 1;2(5):871-877
pubmed: 22866143
Cell Death Dis. 2012 Nov 15;3:e419
pubmed: 23152055
Clin Res Hepatol Gastroenterol. 2013 Nov;37(5):491-5
pubmed: 23433963
PLoS One. 2013;8(2):e58071
pubmed: 23469142
Nat Med. 2013 Jul;19(7):859-68
pubmed: 23836236
Hepat Mon. 2013 Jul 03;13(7):e8351
pubmed: 24066001
Rev Med Virol. 2014 Sep;24(5):332-42
pubmed: 24806972
Mater Sociomed. 2014 Apr;26(2):129-33
pubmed: 24944540
Yonsei Med J. 2015 May;56(3):625-33
pubmed: 25837166
Viral Immunol. 2015 Nov;28(9):504-8
pubmed: 26485346
Int J Clin Exp Med. 2015 Oct 15;8(10):17140-50
pubmed: 26770308
Nat Commun. 2016 May 19;7:11496
pubmed: 27193971
PLoS One. 2016 May 26;11(5):e0156496
pubmed: 27227879
Nat Rev Immunol. 2016 Aug;16(8):509-23
pubmed: 27374637
J Clin Gastroenterol. 2016 Oct;50(9):691-703
pubmed: 27623512
Oncotarget. 2016 Oct 18;7(42):67777-67787
pubmed: 27626177
J Hepatol. 2017 May;66(5):897-909
pubmed: 28043874
Gastroenterol Hepatol Bed Bench. 2017 Fall;10(4):272-277
pubmed: 29379591
Gastroenterol Hepatol Bed Bench. 2017 Winter;10(Suppl1):S38-S43
pubmed: 29511470
Nature. 1979 Jun 7;279(5713):523-5
pubmed: 571963
J Gen Virol. 1995 Jul;76 ( Pt 7):1749-61
pubmed: 9049380

Auteurs

Seyed Mohammad Ali Hashemi (SMA)

Department of Bacteriology and Virology, Shiraz University of Medical Sciences, Shiraz, Iran.

Jamal Sarvari (J)

Department of Bacteriology and Virology, Shiraz University of Medical Sciences, Shiraz, Iran.
Gastroenterohepatology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Mohammad Reza Fattahi (MR)

Gastroenterohepatology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Razieh Dowran (R)

Department of Bacteriology and Virology, Shiraz University of Medical Sciences, Shiraz, Iran.

Amin Ramezani (A)

Institute for Cancer Research, Shiraz University of Medical Sciences, Shiraz, Iran.

Seyed Younes Hosseini (SY)

Department of Bacteriology and Virology, Shiraz University of Medical Sciences, Shiraz, Iran.

Classifications MeSH