Related Experiment Video

Updated: Jul 17, 2026

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells
09:25

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Published on: August 19, 2016

Dynamic tethering of M protein drives pathological inflammation during group A Streptococcus infections

Ananya Dash1, Stephanie Guerra1, Doris L LaRock1

  • 1Department of Microbiology and Immunology, Atlanta, Georgia, United States of America.

Plos Pathogens
|July 15, 2026
PubMed

Insights

Group A Streptococcus M protein is released by the SpeB protease, contributing to inflammation and bacterial survival during invasive infections. This proteolytic release mechanism is crucial for pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Bacterial Pathogenesis

Background:

  • M protein is a key virulence factor of Group A Streptococcus (GAS), mediating superficial and invasive infections and immune sequelae like rheumatic heart disease.
  • M protein is typically anchored to the GAS surface but can be found free during infection, suggesting a release mechanism impacting immune interactions.

Purpose of the Study:

  • To investigate the mechanism of M protein release from the GAS surface.
  • To determine the distinct roles of surface-bound versus secreted M protein in disease pathogenesis.

Main Methods:

  • Identification of the protease responsible for cleaving M protein from the GAS surface.
  • Engineering GAS strains with either surface-locked or constitutively secreted M protein.
  • Evaluation of disease contribution, inflammation, and neutrophil response in a mouse model of invasive infection.

Main Results:

  • The GAS protease SpeB cleaves M protein, releasing a stable, nearly full-length fragment.
  • Secreted M protein, but not surface-locked M protein, drives inflammation and neutrophil influx in an invasive infection mouse model.
  • M protein release enhances bacterial survival, indicating its importance in GAS pathogenesis.

Conclusions:

  • Proteolytic cleavage by SpeB is a mechanism for releasing M protein from GAS.
  • Secreted M protein plays a critical role in driving inflammation and bacterial survival during invasive infections.
  • Regulation of surface protein localization via proteolysis is a significant factor in bacterial pathogenesis.

More Related Videos

A Pre-Clinical Model of Synovitis Using Ex vivo Human Synovial Tissue with Preserved Function and Architecture08:32

A Pre-Clinical Model of Synovitis Using Ex vivo Human Synovial Tissue with Preserved Function and Architecture

Published on: March 20, 2026

Related Concept Videos

Adherens Junctions01:24

Adherens Junctions

Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
The endothelial cells...
Streptococcal Pharyngitis01:27

Streptococcal Pharyngitis

Streptococcal pharyngitis, commonly known as “strep throat,” is an acute infection of the oropharyngeal tissues caused by the Gram‑positive Group A Streptococcus (Streptococcus pyogenes). Transmission occurs primarily through respiratory droplets expelled during coughing, sneezing, or talking.Mechanisms of Host Entry and Immune EvasionUpon entering the host, S. pyogenes adheres to the mucosal epithelial cells of the pharynx via surface proteins, notably lipoteichoic acid and the antiphagocytic...
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...
Bacterial Meningitis01:24

Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.Routes of Entry...
Determinants of Bacterial Pathogenicity and Virulence01:20

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...