Abstract
BackgroundGestational zinc deficiency has been confirmed to impair the infant immune function. However, knowledge about effects of maternal mild zinc deficiency during pregnancy on hepatitis B vaccine responsiveness in offspring is limited. In this report, we aimed to examine how maternal zinc deficiency during pregnancy influences humoral and cellular immune responses to hepatitis B vaccination in offspring of BALB/c mice.Methodology/Principal FindingsFrom day 1 of pregnancy upon delivery, maternal mice were given a standard diet (30 mg/kg/day zinc), zinc deficient diet (8 mg/kg/day zinc), or combination of zinc deficient diet (8 mg/kg/day zinc in the first 2 weeks of gestation) and zinc supplement diet (150 mg/kg/day zinc for the last week of pregnancy), respectively. Newborn pups of these maternal mice were immunized with hepatitis B vaccine at postnatal weeks 0, 2 and 4. Then, splenocytes and blood samples from the offspring mice were harvested for detection of serum zinc concentrations, humoral and cell-mediated immune responses, expression of cytokines using ELISA, CCK-8 and flow cytometric analysis. Results from the present study demonstrated that gestational zinc deficiency inhibited antibody responses, and decreased the proliferative capacity of T cells in offsprings immunized with hepatitis B vaccine. Additionally, HBsAg-specific cytokines analysis revealed that gestational zinc deficiency could inhibit secretion of IFN-γ from splenocytes, and decrease IFN-γ expression of CD4+ and CD8+ T cells.Conclusions/SignificanceGestational zinc deficiency can weaken the humoral and cell-mediated immune responses to hepatitis B vaccine via decreasing B cell counts and hepatitis B virus-specific immunoglobulin G production, as well as reducing T cell proliferation, CD4+/CD8+ T cell ratio, and Th1-type immune responses.
Highlights
Hepatitis B virus (HBV) is an important cause of chronic viral infection, with an approximately 400 million chronic carriers in the world [1]
Results from the present study demonstrated that gestational zinc deficiency inhibited antibody responses, and decreased the proliferative capacity of T cells in offsprings immunized with hepatitis B vaccine
We demonstrated that newborn pups whose mothers suffered from gestational zinc deficiency failed to develop an adequate immunoglobulin G (IgG) level and T cell proliferation response to HBV vaccine
Summary
Hepatitis B virus (HBV) is an important cause of chronic viral infection, with an approximately 400 million chronic carriers in the world [1]. The HBV vaccination program has successfully decreased the HBV carrier rate in infants from ,10% to 1% [5,6,7] and dramatically reduced the incidence of hepatocellular carcinoma in children [8]. The mechanisms underlying the hypo- or nonresponsiveness to HBV vaccine are not fully understood, immunodeficiency has been caused by gestational zinc deprivation [12]. The offspring of maternal zinc deficiency during pregnancy might be susceptible to HBV vaccine hypo- or nonresponsiveness. Knowledge about effects of maternal mild zinc deficiency during pregnancy on hepatitis B vaccine responsiveness in offspring is limited. We aimed to examine how maternal zinc deficiency during pregnancy influences humoral and cellular immune responses to hepatitis B vaccination in offspring of BALB/c mice
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