Related Experiment Video

Updated: May 26, 2026

Intravitreal Injection and Quantitation of Infection Parameters in a Mouse Model of Bacterial Endophthalmitis
07:24

Intravitreal Injection and Quantitation of Infection Parameters in a Mouse Model of Bacterial Endophthalmitis

Published on: February 6, 2021

Role of Toll-like receptor (TLR) 2 in experimental Bacillus cereus endophthalmitis

Billy D Novosad1, Roger A Astley, Michelle C Callegan

  • 1Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.

Plos One
|December 14, 2011
PubMed

Insights

Toll-like receptor 2 (TLR2) significantly influences Bacillus cereus endophthalmitis. Mice lacking TLR2 showed reduced inflammation and better retinal preservation, indicating TLR2

Area of Science:

  • Ophthalmology
  • Immunology
  • Microbiology

Background:

  • Bacillus cereus causes severe, rapid intraocular infections (endophthalmitis) characterized by explosive inflammation.
  • The mechanisms driving this intense immune response, particularly the role of pathogen recognition receptors, remain unclear.
  • Toll-like receptors (TLRs) are crucial for detecting pathogens; TLR2 is a known receptor for Gram-positive bacteria.

Purpose of the Study:

  • To investigate the role of Toll-like receptor 2 (TLR2) in the host's immune response to Bacillus cereus endophthalmitis.
  • To determine if TLR2 influences the severity of inflammation, bacterial growth, and retinal damage during B. cereus infection.

Main Methods:

  • Experimental endophthalmitis was induced in wild-type and TLR2-deficient (TLR2(-/-)) mice.
  • Key parameters assessed included bacterial load, inflammatory cell infiltration (PMNs), cytokine/chemokine levels, retinal function, and histology.
  • Ocular myeloperoxidase activity was measured to quantify neutrophil infiltration.

Main Results:

  • Bacterial growth rates were similar in both wild-type and TLR2(-/-) mice.
  • TLR2(-/-) mice exhibited significantly reduced intraocular inflammation, with less inflammatory cell infiltration and preserved retinal architecture compared to wild-type mice.
  • Retinal function was better preserved in TLR2(-/-) mice, and pro-inflammatory cytokine levels (TNFα, IFNγ, IL6, KC) were lower.

Conclusions:

  • Toll-like receptor 2 (TLR2) plays a critical role in mediating the acute inflammatory response during Bacillus cereus endophthalmitis.
  • Absence of TLR2 leads to diminished cytokine production and inflammatory cell recruitment, resulting in less ocular damage and improved retinal function.
  • TLR2 is a key component in the initial recognition and subsequent inflammatory cascade following B. cereus infection in the eye.

More Related Videos

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling09:51

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

Published on: July 26, 2017

Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages08:34

Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages

Published on: February 22, 2017

Related Concept Videos

Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
Clathrin-Mediated Endocytosis of LDL
One well-characterized example of receptor-mediated endocytosis is the...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
Bacterial Toxins01:12

Bacterial Toxins

Bacterial toxins are sophisticated virulence factors that enable pathogenic bacteria to interact with, invade, and damage host tissues. These toxins fall broadly into two types: protein exotoxins, which are secreted into the environment and target specific host receptors, and lipopolysaccharide endotoxins, which are structural components of the bacterial outer membrane released primarily during bacterial lysis or membrane shedding. Exotoxins generally act more selectively, binding to cell...
Formation of Lipopolysaccharides01:19

Formation of Lipopolysaccharides

Lipopolysaccharides (LPS) are crucial components of the outer membrane of Gram-negative bacteria, serving both structural and functional roles. It contributes to membrane stability and protects bacteria from host immune responses. LPS is composed of three major regions—lipid A, a core oligosaccharide, and an O antigen. The biosynthesis and assembly of LPS involve a highly coordinated set of enzymatic reactions and transport mechanisms. Additionally, LPS is recognized as an endotoxin, triggering...
Bacterial Signaling01:30

Bacterial Signaling

Bacterial signaling can occur within bacteria (intracellular) or between bacteria (intercellular). At times, a group of bacteria behaves like a community. To achieve this, they engage in quorum sensing, the perception of higher cell density that causes changes in gene expression. Quorum sensing involves both extracellular and intracellular signaling. The signaling cascade starts with a molecule called an autoinducer (AI). Individual bacteria produce AIs that move out of the bacterial cell...