Related Experiment Video

Updated: Aug 5, 2026

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
09:01

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection

Published on: December 11, 2013

Yersinia YopJ inhibits pro-inflammatory molecule expression in human bronchial epithelial cells

Limei Zhou1, Alan Tan, Marc B Hershenson

  • 1Department of Pediatrics, University of Chicago, Chicago, IL 60637-1470, USA.

Respiratory Physiology & Neurobiology
|April 28, 2004
PubMed

Insights

Yersinia outer protein-J (YopJ) inhibits pro-inflammatory responses in lung epithelial cells. This virulence factor blocks key signaling pathways, reducing the expression of immune-related genes and potentially impacting airway disease pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Pro-inflammatory molecule expression in human bronchial epithelial cells contributes to airway disease pathogenesis.
  • Yersinia outer protein-J (YopJ) is a bacterial virulence effector known to inhibit mitogen-activated protein (MAP) kinase kinases (MKKs).

Purpose of the Study:

  • To investigate the hypothesis that YopJ attenuates epithelial cell pro-inflammatory molecule expression.
  • To elucidate the molecular mechanisms by which YopJ affects inflammatory signaling in lung epithelial cells.

Main Methods:

  • Co-transfection of 16HBE14o-cells with Yersinia pseudotuberculosis YopJ cDNA or an empty vector.
  • Assessing the activation of key signaling molecules including ERK-2, JNK-1, and IKK-beta.
  • Evaluating the transactivation of NF-kappaB and AP-1 promoter sequences and the transcription of IL-8, RANTES, and ICAM-1.

Main Results:

  • YopJ expression significantly reduced the activation of ERK-2, JNK-1, and IKK-beta.
  • YopJ blocked the transactivation of NF-kappaB and AP-1 promoter sequences.
  • Expression of YopJ decreased the transcription of key pro-inflammatory genes: IL-8, RANTES, and ICAM-1.

Conclusions:

  • YopJ expression effectively inhibits the innate immune response in lung epithelial cells, a primary site for Yersinia pestis infection.
  • MAP kinases play a crucial role in regulating pro-inflammatory molecule expression in bronchial epithelial cells, and YopJ's inhibitory action supports this.
  • YopJ's ability to suppress epithelial cell inflammatory responses offers insights into bacterial pathogenesis and host-pathogen interactions in respiratory infections.

More Related Videos

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment09:00

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Published on: June 24, 2020

Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth08:36

Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth

Published on: May 31, 2024

Related Concept Videos

Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs01:25

Antiasthma Drugs: Mast Cell Stabilizers and Anti-IgE Drugs

Asthma is a chronic respiratory condition for which new therapeutic avenues, including anti-inflammatory drugs like mast cell stabilizers and anti-IgE treatments, continue to be developed.
Mast cell stabilizers, such as cromolyn (also known as sodium cromoglycate) and nedocromil (Tilade), are effective drugs in asthma management. These stabilizers hinder histamine release by skillfully obstructing the activation of mast cells and other cellular entities. Notably, they navigate this task without...
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,...
Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:
Inhibitors of Bacterial Protein Synthesis01:25

Inhibitors of Bacterial Protein Synthesis

Aminoglycosides constitute a highly potent class of bactericidal antibiotics that exert their antimicrobial effects by targeting the bacterial ribosome, specifically disrupting protein synthesis. These polycationic molecules consist of amino-modified sugars linked via glycosidic bonds to an aminocyclitol core such as 2-deoxystreptamine or streptamine. Their strong positive charges facilitate tight binding to the negatively charged phosphate backbone of ribosomal RNA (rRNA), primarily at the 16S...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...