Aa
cytokines on acute hbv
Z Gastroenterol 2013; 51 - P_5_45
DOI: 10.1055/s-0032-1332159
Serum cytokines and HBsAg decline in patients with acute Hepatitis B Virus (HBV) infection
AA Markova 1, J Jaroszewicz 2, M Rogalska-Taranta 1, C Falk 3, SB Wiegand 1, K Port 1, B Maasoumy 1, B Calle Serrano 1, R Flisiak 2, MP Manns 1, H Wedemeyer 1, M Cornberg 1
1Hannover Medical School, Department of Gastroenterology, Hepatology and Endocrinology, Hanover, Germany
2Medical University of Bialystok, Department of Infectious Diseases and Hepatology, Bialystok, Poland
3Hannover Medical School, Institute of Transplantat Immunology, IFB-Tx, Hanover, Germany
Congress Abstract
Background: HBsAg loss and seroconversion is the ultimate goal of therapy for chronic HBV infection. However, HBsAg loss is a rare event even with antiviral therapy. In contrast, the majority of adults with acute HBV infection achieve HBsAg loss. The analysis of the natural course of acute HBV infection may help to define correlates of immune control of HBV. The aim of this study was to analyse serum cytokines and their association with dynamics of HBsAg clearance during acute HBV infection.
Methods: A panel of 15 serum cytokines and chemokines was assessed in 15 patients with symptomatic acute HBV infection who were followed longitudinally up to 10 months after the onset of infection (56 samples, median 4 time points per patient). Cytokines/chemokines were measured using the Luminex-based multiplex technology (BioRad). HBsAg was quantified with the Abbott Architect assay. Cytokine concentrations were associated with a) early versus late acute HBV infection and b) with the decline of HBsAg. The early phase of acute HBV infection was defined by high ALT levels (>500 IU/ml) and the late phase of acute HBV infection by normal ALT and HBV DNA 500 IU/day) or slow (decrease <500 IU/day).
Results: HBsAg decline parallels HBV DNA decrease during acute HBV infection (R=0.93, p<0.0001). 14/15 patients lost HBsAg (1 lost-to follow-up). A significant difference (p<0.01) of serum cytokine concentrations between early and late acute HBV infection was observed for IP-10 (CXCL10; 8762 vs. 512 pg/ml), IFN-γ (55 vs. 36 pg/ml), MIP-1β (CCL4; 106 vs. 18 pg/ml), IL-6 (4.5 vs. 2.1 pg/ml), IL-8 (CXCL8; 23 vs. 4 pg/ml), TNF-α (18 vs. 12 pg/ml) while for MIP-1α (CCL3), IL-4, IL-10, IL-15, the difference was less pronounced but still significant (p<0.05). Serum levels of IL-2, IL-5, IL-7, IL-12p70 and IL-17 showed no significant difference between early and late acute HBV infection. The following cytokines/chemokines were significantly higher in patients with a fast HBsAg decline versus slow HBsAg decline during the first 30 days after presentation: IP-10 (CXCL10; p=0.02), IL-2 (p=0.02), MIP-1α (CCL3; p=0.006), MIP-1β (CCL4; p=0.02), TNF-α (p=0.009), IL-6 (p=0.006), IFN-γ (p=0.008), IL-10 (p=0.003).
Conclusions: We identified specific serum cytokines and chemokines that were significantly different between early and late acute HBV infection suggesting a role in the pathogenesis. In addition, specific cytokines and chemokines were also associated with a faster HBsAg decline during acute HBV infection. Our data may be important to define markers of immune control and for the design of new therapeutic concepts to increase the rate of HBsAg loss.
DOI: 10.1055/s-0032-1332159
Serum cytokines and HBsAg decline in patients with acute Hepatitis B Virus (HBV) infection
AA Markova 1, J Jaroszewicz 2, M Rogalska-Taranta 1, C Falk 3, SB Wiegand 1, K Port 1, B Maasoumy 1, B Calle Serrano 1, R Flisiak 2, MP Manns 1, H Wedemeyer 1, M Cornberg 1
1Hannover Medical School, Department of Gastroenterology, Hepatology and Endocrinology, Hanover, Germany
2Medical University of Bialystok, Department of Infectious Diseases and Hepatology, Bialystok, Poland
3Hannover Medical School, Institute of Transplantat Immunology, IFB-Tx, Hanover, Germany
Congress Abstract
Background: HBsAg loss and seroconversion is the ultimate goal of therapy for chronic HBV infection. However, HBsAg loss is a rare event even with antiviral therapy. In contrast, the majority of adults with acute HBV infection achieve HBsAg loss. The analysis of the natural course of acute HBV infection may help to define correlates of immune control of HBV. The aim of this study was to analyse serum cytokines and their association with dynamics of HBsAg clearance during acute HBV infection.
Methods: A panel of 15 serum cytokines and chemokines was assessed in 15 patients with symptomatic acute HBV infection who were followed longitudinally up to 10 months after the onset of infection (56 samples, median 4 time points per patient). Cytokines/chemokines were measured using the Luminex-based multiplex technology (BioRad). HBsAg was quantified with the Abbott Architect assay. Cytokine concentrations were associated with a) early versus late acute HBV infection and b) with the decline of HBsAg. The early phase of acute HBV infection was defined by high ALT levels (>500 IU/ml) and the late phase of acute HBV infection by normal ALT and HBV DNA 500 IU/day) or slow (decrease <500 IU/day).
Results: HBsAg decline parallels HBV DNA decrease during acute HBV infection (R=0.93, p<0.0001). 14/15 patients lost HBsAg (1 lost-to follow-up). A significant difference (p<0.01) of serum cytokine concentrations between early and late acute HBV infection was observed for IP-10 (CXCL10; 8762 vs. 512 pg/ml), IFN-γ (55 vs. 36 pg/ml), MIP-1β (CCL4; 106 vs. 18 pg/ml), IL-6 (4.5 vs. 2.1 pg/ml), IL-8 (CXCL8; 23 vs. 4 pg/ml), TNF-α (18 vs. 12 pg/ml) while for MIP-1α (CCL3), IL-4, IL-10, IL-15, the difference was less pronounced but still significant (p<0.05). Serum levels of IL-2, IL-5, IL-7, IL-12p70 and IL-17 showed no significant difference between early and late acute HBV infection. The following cytokines/chemokines were significantly higher in patients with a fast HBsAg decline versus slow HBsAg decline during the first 30 days after presentation: IP-10 (CXCL10; p=0.02), IL-2 (p=0.02), MIP-1α (CCL3; p=0.006), MIP-1β (CCL4; p=0.02), TNF-α (p=0.009), IL-6 (p=0.006), IFN-γ (p=0.008), IL-10 (p=0.003).
Conclusions: We identified specific serum cytokines and chemokines that were significantly different between early and late acute HBV infection suggesting a role in the pathogenesis. In addition, specific cytokines and chemokines were also associated with a faster HBsAg decline during acute HBV infection. Our data may be important to define markers of immune control and for the design of new therapeutic concepts to increase the rate of HBsAg loss.
as to ip 10 i have check it already, mine is very low around 20-30pg/ml and around 90pg/ml when i have hbsag decline.
few studies indicate an ip10>350pg/ml to have hbsag decline on tdf (dont know if there are studies on etv or other nucs, ip 10 and hbsag decline)
i was looking at this because in case i go at redlabs to check nagalase in the future maybe i will check cytokines too and the most important are those correlated to th1 immune response
maybe all wasted money on th1 cytokines because not easy to be changed except nagalase (respondes to gcmaf) and il17 (responds to high dose vit d3)
IFN-γ, TNF-α, il2
to this i will add il17, which is correlated with liver damage and chronicty on cronic hbv (on the few studies we have).i will add nagalase and nk cells CD16 and CD56
Th2 cells are able to synthesize the Th2 cytokines IL-4, IL-5 and IL-10
maybe all wasted money on th1 cytokines because not easy to be changed except nagalase (respondes to gcmaf) and il17 (responds to high dose vit d3)
IFN-γ, TNF-α, il2
to this i will add il17, which is correlated with liver damage and chronicty on cronic hbv (on the few studies we have).i will add nagalase and nk cells CD16 and CD56
Th2 cells are able to synthesize the Th2 cytokines IL-4, IL-5 and IL-10
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