Objective:: To investigate the transmission of anti-Staphylococcus aureus (Sa) IgG, IgG1 and IgG2 via placental transfer and the transfer of IgA via the colostrum according to maternal Sa carrier status at delivery.
Methods:: We evaluated anti-Sa IgG, IgG1 and IgG2 in maternal and cord sera and IgA in colostrum from a case (n=49, Sa+) and a control group (n=98, Sa-).
Results:: Of the 250 parturients analyzed for this study, 49 were nasally colonized with S. aureus (prevalence of 19.6%). Ninety-eight non-colonized subjects were selected for the control group. The anti-Sa IgG, IgG1 and IgG2 levels and the IgG avidity indexes in the maternal and cord sera did not differ between the groups, with a low transfer ratio of anti-Sa IgG to the newborns in both groups. The anti-Sa IgG2 titers were significantly higher than the IgG1 titers in the maternal and cord sera. Inversely, the transfer ratios were higher for anti-Sa IgG1 compared with IgG2; however, no differences between the groups were detected. The Sa-specific IgA levels and avidity indexes in the colostrum were equivalent between groups.
Conclusions:: Maternal Sa nasal colonization at delivery is not associated with higher antibody levels in the mother or newborns. The high titers of anti-Sa IgG2 found in the cord serum indicate a greater reactivity with non-protein antigens, which may further contribute to the susceptibility to staphylococcal infections at birth. The presence of IgA in the colostrum with avidity to S. aureus reinforces the importance of breastfeeding shortly after birth.
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http://dx.doi.org/10.6061/clinics/2016(12)02 | DOI Listing |
Equine Vet J
January 2025
School of Biodiversity, One Health and Veterinary Medicine, University of Glasgow, Glasgow, UK.
Background: Foals suffer from total failure to transfer passive immunity (TFTPI) when serum immunoglobulin (IgG) is <4 g/L, and partial failure to transfer passive immunity (PFTPI) when serum IgG is 4-8 g/L.
Objectives: To explore risk factors for poor serum IgG concentration.
Study Design: Retrospective observational study.
Immunity
January 2025
Department of Microbiology and Immunology, The University of Melbourne, Peter Doherty Institute for Infection and Immunity, Melbourne, VIC 3000, Australia. Electronic address:
The mechanisms underpinning susceptibility to influenza virus infection, resulting in life-threatening disease, are not well understood. In this issue of Immunity, Chakraborty et al. demonstrate that sialylated IgG suppresses NF-κB-driven inflammatory responses in the lungs by inducing repressor element-1 silencing transcription factor (REST) to prevent excessive inflammation without impacting viral replication.
View Article and Find Full Text PDFPLoS One
January 2025
Faculdade de Medicina da Universidade de São Paulo, Instituto de Medicina Tropical, São Paulo, Brazil.
Background: Most longitudinal studies of COVID-19 incidence have used unlinked samples. The city of Manaus, Brazil, has a blood donation program which allows sample linkage, and was struck by two large COVID-19 epidemic waves between mid-2020 and early 2021.
Methods: We estimated the changing force of infection, i.
J Med Virol
January 2025
Department of Rheumatology and Immunology, The Affiliated Suqian First People's Hospital of Nanjing Medical University, Suqian, Jiangsu, China.
Varicella, a highly contagious disease caused by the varicella-zoster virus (VZV), remains prevalent in China despite the introduction of the varicella vaccine in 1997. The current vaccination protocol in China involves a voluntary, self-funded single-dose regimen. This study aims to investigate the longevity of immune response in Chinese children following two-dose varicella vaccination administered at different intervals, with the objective of optimizing vaccination strategies.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Shanxi Genetic Engineering Center for Experimental Animal Models, The Fifth Hospital (Shanxi Provincial People's Hospital) of Shanxi Medical University, Taiyuan, Shanxi, China.
Phospholipase A2 receptor 1 (PLA2R1) exists in many animals and plays an important role in membranous nephropathy. In this study, we aimed to evaluate a PLA2R1 knock-in rat model with repaired kidney function to study the molecular mechanisms of membranous nephropathy. We constructed the PLA2R1 knockout [PLA2R1(-)] model and PLA2R1 knock in [PLA2R1(+)] model in rats.
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