Related Experiment Video

Updated: Nov 7, 2025

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

3.5K

Mycobacterium PPE31 Contributes to Host Cell Death

Siyuan Feng1,2, Zhongsi Hong1, Guoliang Zhang3

  • 1Center for Infection and Immunity, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhongshan School of Medicine, Sun Yat-sen University, Zhuhai, China.

Frontiers in Cellular and Infection Microbiology
|April 30, 2021
PubMed

Insights

The PPE31 gene is crucial for mycobacterial virulence and survival. Deleting it impairs infectivity and reduces inflammatory responses in host cells, impacting innate immunity.

Area of Science:

  • Microbiology
  • Immunology
  • Genetics

Background:

  • Genome-wide mutagenesis reveals numerous genes essential for mycobacterial infectivity and survival.
  • The precise roles and mechanisms of these genes within host environments remain largely uncharacterized.

Purpose of the Study:

  • To investigate the function of the PPE31 gene in mycobacterial virulence.
  • To elucidate PPE31's role in modulating host innate immune responses during infection.

Main Methods:

  • CRISPR interference was used to create a knockdown of the PPE31 gene in Mycobacterium marinum.
  • PPE31 mutant strains were generated in both Mycobacterium marinum and Mycobacterium tuberculosis.
  • In vitro assays assessed acid resistance, macrophage inflammatory mediator expression, host cell death (JNK signaling), and intracellular survival.
  • In vivo studies evaluated the survival of Mycobacterium marinum in zebrafish.

Main Results:

  • Deletion of PPE31 reduced acid resistance in both M. marinum and M. tuberculosis.
  • Macrophages infected with PPE31 mutants exhibited reduced inflammatory mediator expression and decreased JNK-dependent host cell death.
  • PPE31 mutants showed significantly reduced survival within macrophages and decreased infectivity in a zebrafish model.
  • Loss of PPE31 in M. tuberculosis increased sensitivity to acid stress.

Conclusions:

  • PPE31 is a significant virulence-associated factor in mycobacteria.
  • The PPE31 gene plays a critical role in modulating innate immune responses, contributing to mycobacterial survival and pathogenesis.
  • Targeting PPE31 could be a potential strategy for controlling mycobacterial infections.
Keywords:
JNK signalingMycobacterium tuberculosisPPE31cell deathvirulence factors

More Related Videos

Visualization of Macrophage Lytic Cell Death During Mycobacterial Infection in Zebrafish Embryos via Intravital Microscopy06:49

Visualization of Macrophage Lytic Cell Death During Mycobacterial Infection in Zebrafish Embryos via Intravital Microscopy

Published on: January 9, 2019

6.5K
Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses08:38

Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses

Published on: February 22, 2019

6.1K

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.3K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
7.0K
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.7K
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
8.3K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.8K