In North America, the tick-borne pathogens Borreliella burgdorferi (Lyme disease; LD) and Anaplasma phagocytophilum (anaplasmosis) are a significant health threat to dogs. Little is known regarding the seroprevalence of maternal antibodies (Abs) to these pathogens in young dogs. The analysis of maternal antibody (Ab) profiles is important as it could bear on the interpretation of currently available diagnostic assays and the potential for vaccine interference in pups. In this pilot study, sera from 32 client-owned dogs (6-24 weeks of age; 3 serum samples per dog) from four veterinary hospitals in the United States were screened for IgG against B. burgdorferi and A. phagocytophilum using whole cell lysate immunoblots and recombinant protein-based ELISAs. As a control, the sera were also screened for Abs to canine parvovirus and canine distemper virus using a commercially available colorimetric assay. Maternally derived Abs against B. burgdorferi including the diagnostic antigen VlsE were detected in 2 of the 32 dogs, accounting for 12.5 % of dogs from LD endemic regions, and as expected, the Ab levels declined over time. Differentiating between maternal Ab and infection-induced Ab is of importance in interpreting serological tests for tick-borne diseases in young dogs and in making decisions regarding treatment and timing of vaccination.
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http://dx.doi.org/10.1016/j.vetimm.2022.110471 | DOI Listing |
Alzheimers Dement
December 2024
Homi Bhabha National Institute, Mumbai, Maharashtra, India.
Background: Recent advances in understanding the regulatory networks implicated in Alzheimer's Disease (AD) evinces the involvement of long non-coding RNAs (lncRNAs) as crucial regulatory players. The present study explores the role played by maternally imprinted lncRNA XIST in regulating the sex-biased prevalence of AD.
Method: With whole transcriptomic sequencing data from the hippocampal RNA of post-mortem AD brains from humans and APP/PS1 mice, the altered expression of XIST in AD was studied.
Npj Viruses
December 2024
Department of Infectious Disease, Imperial College London, London, SW7 2AZ UK.
Maternal immunisation against respiratory viruses provides protection in early life, but as antibodies wane, there can be a gap in coverage. This immunity gap might be filled by inducing pathogen-specific lung tissue-resident T cells (TRM). However, the neonatal mouse lung has a different inflammatory environment to the adult lung which affects T cell recruitment.
View Article and Find Full Text PDFCureus
December 2024
Department of Midwifery, School of Health and Care Sciences, University of West Attica, Athens, GRC.
Maternal Graves' disease (GD) poses a significant risk to neonatal thyroid function due to the transplacental transfer of thyrotropin receptor antibodies (TRAbs). This systematic review aims to assess the impact of maternal GD on neonatal thyroid outcomes and identify key maternal factors influencing these outcomes. A comprehensive literature search was conducted across PubMed, Scopus, and Cochrane, resulting in the inclusion of 18 studies published from 2014 to 2024.
View Article and Find Full Text PDFBMC Pregnancy Childbirth
January 2025
Collection Biologique de L'Hôpital de La Mère Et de L'Enfant CB-HME (Mother and Child Biobank), University Hospital Center, 8 Avenue Dominique Larrey, Limoges, France.
Background: Maternal agonistic autoantibodies against the angiotensin II type 1 receptor (AT1-AAs) have been implicated in the pathophysiology of preeclampsia, but their presence in their offsprings and their possible neonatal effects have not been specifically explored. This prospective study aimed to evaluate the presence of AT1-AAs and their potential clinical effects in neonates of AT1-AAs positive mothers.
Methods: Women with preeclampsia and their neonates were included.
Sci Rep
January 2025
Department of Gastroenterology, Fifth Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
The deregulation of immune responses is what causes food allergy (FA) to occur. FA's cause is still unknown. The goal of this study is to investigate the mechanism how the impaired production of IL-10 occurs in peripheral naive B cells of patients with FA.
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