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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

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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.
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Inflammatory Response I: Vascular and Cellular01:30

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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,...
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Inflammation01:38

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T Cell Types and Functions01:24

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

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The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
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Differentiation of Common Myeloid Progenitor Cells01:15

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Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
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Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation
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Effects of multiple pro-inflammatory stimuli

Julia Heiter1,2, Matthew W Kemp3, Owen B Spiller4

  • 1Division of Mental Health and Neuroscience, Maastricht University Medical Center, Maastricht, Netherlands.

Frontiers in Immunology
|June 5, 2023
PubMed
Summary

Chorioamnionitis from Ureaplasma parvum or lipopolysaccharide exposure harms fetal gut development. Inflammation and nerve changes worsen with longer or repeated exposure, potentially impacting infant health.

Keywords:
chorioamnionitisenteric nervous systemintestinal inflammationnecrotizing enterocolitispreterm fetal ileum

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Area of Science:

  • Perinatal medicine
  • Developmental biology
  • Gastroenterology

Background:

  • Chorioamnionitis is a frequent complication of preterm birth.
  • It is linked to increased risks of intestinal inflammation and necrotizing enterocolitis in neonates.
  • Intestinal inflammation can disrupt the development of the enteric nervous system.

Purpose of the Study:

  • To investigate the effects of chorioamnionitis, induced by Ureaplasma parvum and/or lipopolysaccharide (LPS), on fetal ileal inflammation and enteric nervous system (ENS) development.
  • To determine if repeated or chronic exposure to inflammatory stimuli impacts these outcomes.
  • To model early-life inflammation at a gestational age equivalent to 60% of term.

Main Methods:

  • Ovine fetuses were exposed to chronic Ureaplasma parvum and/or LPS via intra-amniotic injections at varying durations before delivery.
  • Intestinal inflammation was assessed by quantifying inflammatory cell markers (CD3, myeloperoxidase).
  • ENS structural changes were evaluated by assessing neuronal nuclei and glial cell (astrocyte-like) populations.

Main Results:

  • LPS exposure increased inflammatory cell infiltration.
  • Repetitive LPS or combined Ureaplasma parvum/LPS exposure significantly elevated intestinal inflammation.
  • Neuronal cell nuclei decreased across all intervention groups, most notably with repetitive LPS.
  • Astrocyte-like glial cells increased following LPS exposure (2 days prior) or chronic Ureaplasma parvum exposure.

Conclusions:

  • Exposure to chorioamnionitis in fetal development leads to significant intestinal inflammation and structural alterations in the ENS.
  • The severity of these inflammatory and structural changes is dose- and duration-dependent.
  • These findings highlight potential long-term functional consequences for infants exposed to prenatal inflammation.