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Related Concept Videos

Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
Transduction01:16

Transduction

Among the three main modes of HGT—transformation, conjugation, and transduction—transduction is unique in that it is mediated by bacteriophages, or bacterial viruses.Transduction occurs in two ways. Generalized transduction occurs during the lytic cycle of a bacteriophage infection. In this process, bacteriophages infect bacterial cells, replicate within them, and ultimately cause cell lysis, releasing newly assembled virions. Occasionally, random fragments of the bacterial genome are...
Infection01:20

Infection

When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
The chain begins with pathogens: bacteria, viruses, fungi, prions, or parasites such as protozoa helminths. These can be present on the skin as transient or resident flora, or they can be acquired from the environment. Identifying and treating the type of infection and...
Stringent Response in E. coli01:23

Stringent Response in E. coli

Bacterial growth is closely tied to nutrient availability, with cells proliferating exponentially under favorable conditions and entering a stationary phase when resources become scarce. This transition is mediated by a regulatory mechanism known as the stringent response, which allows bacteria to adapt to nutrient deprivation by modulating gene expression and metabolic activity.During nutrient scarcity, intracellular amino acid levels decline. It results in the accumulation of uncharged tRNAs...
Colonisation of Pathogens01:25

Colonisation of Pathogens

Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...

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Related Experiment Video

Updated: Jun 9, 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

TLR-mediated preterm birth in response to pathogenic agents.

Jessica E Thaxton1, Tania A Nevers, Surendra Sharma

  • 1Department of Pediatrics, Women and Infants' Hospital of Rhode Island-Warren Alpert Medical School of Brown University, Providence, RI 02905, USA.

Infectious Diseases in Obstetrics and Gynecology
|September 10, 2010
PubMed
Summary

Maternal infections can cause preterm birth by triggering immune responses. This study explores how Toll-like receptors and pathogenic entry routes contribute to adverse immune reactions, leading to premature delivery.

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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

Published on: July 26, 2017

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Last Updated: Jun 9, 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

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
09:51

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

Published on: July 26, 2017

Area of Science:

  • Reproductive immunology
  • Maternal-fetal medicine
  • Infectious disease immunology

Background:

  • Rising incidence of preterm birth in developed nations.
  • Maternal infections are a probable cause of preterm birth.
  • Immune dysregulation at the maternal-fetal interface is critical.

Purpose of the Study:

  • To highlight maternal infection factors triggering preterm birth.
  • To discuss the role of Toll-like receptors (TLRs) in uterine immunity.
  • To explore pathogenic entry routes causing preterm birth.

Main Methods:

  • Review of immune pathways involved in pregnancy.
  • Analysis of Toll-like receptor (TLR) activation in response to pathogens.
  • Examination of cytokine storm and cell-mediated mechanisms.

Main Results:

  • Specific Toll-like receptor (TLR) activations induce distinct immune cascades leading to preterm birth.
  • Pathogenic entry via cytokine storm or unknown cell-mediated pathways can trigger preterm birth.
  • Adverse immune responses to foreign agents disrupt maternal-fetal balance.

Conclusions:

  • Maternal infections significantly contribute to preterm birth through immune dysregulation.
  • Understanding TLR signaling and pathogenic routes is key to preventing preterm birth.
  • Further research into cell-mediated mechanisms is warranted.