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Inhalation Anthrax

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Anthrax is a zoonotic disease caused by Bacillus anthracis, a Gram-positive, spore-forming bacterium. It primarily affects herbivorous animals but can be transmitted to humans through skin contact, ingestion, or inhalation of spores.Cutaneous anthrax, the most common form, typically results from direct contact with bacterial spores through skin abrasions and is generally less severe. Gastrointestinal anthrax results from eating undercooked or contaminated meat. It affects the mouth, throat, or...

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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation

Published on: July 6, 2019

Anthrax lethal toxin-induced gene expression changes in mouse lung.

Eric K Dumas¹, Philip M Cox, Charles O'Connor Fullenwider

¹Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, 1100 N. Lindsay, Oklahoma City, OK 73104, USA. dumase@omrf.org

|November 1, 2011

Summary

This summary is machine-generated.

Anthrax Lethal Toxin (LeTx) causes vascular leakage and pulmonary edema. This study reveals LeTx alters gene expression in mouse lungs, particularly immune-related genes, offering new insights into anthrax pathogenesis.

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Area of Science:

Toxicology
Molecular Biology
Immunology

Background:

Bacillus anthracis Lethal Toxin (LeTx) is a key virulence factor.
LeTx causes systemic toxicity, vascular leakage, and pulmonary edema in animal models.
Understanding LeTx-induced gene expression changes in lung tissue is crucial.

Purpose of the Study:

To investigate gene expression changes in mouse lungs following systemic LeTx exposure.
To compare LeTx effects on susceptible (A/J) and less susceptible (C57BL/6) mouse strains.
To identify genes associated with vascular leakage and immune responses.

Main Methods:

Systemic administration of wild-type and mutant LeTx to A/J and C57BL/6 mice.
Gene expression profiling of lung tissue 6 hours post-exposure.
Differential gene expression analysis between toxin-exposed and control groups.

Main Results:

LeTx induced significant up- and down-regulation of genes in mouse lungs.
A/J mice exhibited more differentially expressed genes than C57BL/6 mice.
LeTx modulated genes involved in vascular permeability and unexpectedly altered immune gene expression (lymphoid up, myeloid down).

Conclusions:

LeTx significantly impacts lung gene expression, with strain-dependent susceptibility.
Altered expression of vascular permeability and immune-related genes provides new avenues for research.
Findings offer novel insights into anthrax-induced vascular leakage and pulmonary edema mechanisms.