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Related Concept Videos

Transcytosis of IgG01:15

Transcytosis of IgG

Transcytosis is the process in which molecules are internalized by endocytosis, transported across the cell, and released through exocytosis from the opposite end of the cell. Molecules such as insulin, immunoglobulins, and certain nutrients are transferred through the recycling endosomes by recycling and transcytosis.
IgG molecules from a mother undergo transcytosis starting around 13 weeks of gestation. The amount of IgG transferred and entering the fetal blood circulation increases with...
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Development of Immunocompetence

The initiation of cell-mediated immunity can be observed as early as the third month of fetal growth, with active antibody-mediated immunity following approximately one month later.
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Subsequent T...
Microbial Interactions: Parasitism01:22

Microbial Interactions: Parasitism

Parasitism is a form of microbial interaction in which parasitic microbes exploit a host organism for nutrients and shelter, often at the host's expense. Unlike mutualistic relationships, where both organisms benefit, parasitism benefits only the parasite and harms the host.Classification of ParasitesMicrobial parasites are broadly classified based on their location relative to the host.Ectoparasites remain on the host’s surface, such as the skin or outer tissues, drawing nutrients...
Development of the Oral Microbiota01:28

Development of the Oral Microbiota

The establishment of the oral microbiome begins before birth, challenging the long-held belief that the fetal oral cavity is sterile. The presence of oral microbes such as Streptococcus and Fusobacterium in amniotic fluid suggests that microbial exposure may occur in utero, potentially through translocation from the maternal oral or gastrointestinal tract. This early colonization primes the neonatal immune system and sets the stage for subsequent microbial succession. Maternal health,...
Malaria01:29

Malaria

Malaria pathogenesis in humans reflects a delicate interplay between parasite biology and host response. Clinical illness reflects a host’s immune response to the parasite’s asexual replication cycle, which is often asymptomatic in individuals with partial immunity. From the parasite's perspective, transmission between mosquito and human with minimal host pathology is evolutionarily advantageous. Among the six Plasmodium species infecting humans, P. falciparum and P. vivax dominate in global...
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Pneumonia I: Introduction

Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...

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Related Experiment Video

Updated: Jun 14, 2026

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
08:50

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development

Published on: June 24, 2020

Parasitic Infections in Pregnancy Decrease Placental Transfer of Antipneumococcus Antibodies.

Noah D McKittrick1, David M Vu2, Indu Malhotra3

  • 1Division of Infectious Diseases, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA noahmck@stanford.edu.

Clinical and Vaccine Immunology : CVI
|April 14, 2017
PubMed
Summary
This summary is machine-generated.

Maternal parasitic infections like malaria and schistosomiasis reduce the transfer of crucial Streptococcus pneumoniae antibodies from mother to infant. This impacts newborn immunity, highlighting a critical area for prenatal care and research.

Keywords:
humoral immunityparasitesplacental antibody transferpregnancy

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Ex vivo Culture of Human Placental Explants for the Study of Viral Transmission Across the Maternal-Fetal Interface
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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
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Measuring Naturally Acquired Phagocytosis-Inducing Antibodies to Plasmodium falciparum Parasites by a Flow Cytometry-Based Assay
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Ex vivo Culture of Human Placental Explants for the Study of Viral Transmission Across the Maternal-Fetal Interface
05:22

Ex vivo Culture of Human Placental Explants for the Study of Viral Transmission Across the Maternal-Fetal Interface

Published on: December 30, 2025

Area of Science:

  • Immunology
  • Maternal-fetal medicine
  • Infectious disease

Background:

  • Maternal antibodies confer vital immunity to newborns.
  • The impact of maternal parasitic infections on antibody transfer is poorly understood.

Purpose of the Study:

  • To investigate how prenatal parasitic infections affect maternal-fetal IgG antibody transfer.
  • To compare antibody transfer in women with malaria, hookworm, or schistosomiasis versus uninfected women.

Main Methods:

  • Analysis of maternal plasma and infant cord blood from 100 pregnant Kenyan women (30 uninfected, 30 malaria, 30 hookworm, 10 schistosomiasis).
  • Multiplex fluorescent bead assay used to quantify IgG antibodies against 10 pneumococcal serotypes, diphtheria toxoid, and Haemophilus influenzae type B.

Main Results:

  • Infants of mothers with prenatal malaria, hookworm, or Schistosoma haematobium infections showed significantly reduced IgG antibody transfer for multiple Streptococcus pneumoniae serotypes.
  • No significant differences in IgG transfer ratios for diphtheria toxoid or Haemophilus influenzae type B antibodies were observed.

Conclusions:

  • Prenatal parasitic infections impair the placental transfer of maternal IgG antibodies to infants, specifically for several key Streptococcus pneumoniae serotypes.
  • This reduction in antibody transfer may compromise neonatal immunity against pneumococcal disease.