Related Experiment Video

Updated: Aug 19, 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

Fetal and neonatal inflammatory response and adverse outcome

L Cornette1

  • 1Peter Congdon Neonatal Unit, Clarendon Wing - C Floor, Leeds General Infirmary, Great George Street, Leeds LS2 9NS, UK. luc.cornette@lth.nhs.uk

Seminars in Fetal & Neonatal Medicine
|February 5, 2005
PubMed

Insights

Fetal/neonatal inflammatory responses interact with hypoxia-ischemia, potentially causing brain injury. Further research is needed to understand links between inflammation and adverse neurodevelopmental outcomes.

Area of Science:

  • Perinatology
  • Neonatology
  • Neuroscience

Background:

  • Fetal/neonatal inflammatory response is a critical factor in perinatal health.
  • Inflammation and hypoxia-ischemia are implicated in neonatal brain injury.
  • Neurodevelopmental assessment is complex and requires careful consideration.

Purpose of the Study:

  • To define fetal/neonatal inflammatory response and its link to neurotoxicity.
  • To examine the interaction between infection/inflammation and hypoxia-ischemia.
  • To investigate the relationship between inflammatory response and adverse neurodevelopmental outcomes.

Main Methods:

  • Literature review of existing evidence.
  • Analysis of the interplay between inflammatory mediators and hypoxic-ischemic events.
  • Exploration of factors influencing neurodevelopmental assessment.

Main Results:

  • Evidence suggests a significant link between inflammatory responses and adverse neurodevelopmental outcomes.
  • Cytokine release plays a role in brain injury following infection/inflammation and hypoxia-ischemia.
  • Multiple variables require further investigation to fully elucidate this relationship.

Conclusions:

  • Inflammation is a key factor in fetal/neonatal brain injury.
  • Understanding the timing, nature, and contributing factors of inflammation is crucial.
  • Further research into anti-insult strategies, extra-cranial morbidity, genetics, and environmental influences is warranted.

More Related Videos

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Related Concept Videos

Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Development of Immunocompetence01:22

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.
The initial cells that migrate from the fetal thymus settle within the skin and epithelial tissues lining the mouth, digestive tract, and in females, the uterus and vagina. These cells, including skin-based dendritic cells, serve as antigen-presenting cells, playing a key role in T cell activation.
Subsequent T...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...