Related Experiment Video

Updated: May 12, 2026

Following in Real Time the Impact of Pneumococcal Virulence Factors in an Acute Mouse Pneumonia Model Using Bioluminescent Bacteria
11:32

Following in Real Time the Impact of Pneumococcal Virulence Factors in an Acute Mouse Pneumonia Model Using Bioluminescent Bacteria

Published on: February 23, 2014

The Spr1875 protein confers resistance to the microglia-mediated killing of Streptococcus pneumoniae

Samuele Peppoloni1, Bruna Colombari, Concetta Beninati

  • 1Dipartimento di Medicina Diagnostica, Clinica e di Sanità Pubblica, Università di Modena e Reggio Emilia (Unimore), 41125 Modena, Italy. samuele.peppoloni@unimore.it

Microbial Pathogenesis
|April 17, 2013
PubMed

Insights

Streptococcus pneumoniae

Area of Science:

  • Microbiology
  • Immunology
  • Neuroscience

Background:

  • Streptococcus pneumoniae is a leading cause of bacterial meningitis.
  • Microglia are the primary immune cells of the central nervous system.
  • The role of specific pneumococcal surface proteins in host-pathogen interactions with microglia is not fully understood.

Purpose of the Study:

  • To investigate the role of the novel pneumococcal surface protein Spr1875 in the interaction between Streptococcus pneumoniae and microglia.
  • To determine if Spr1875 influences bacterial survival and killing within microglia.

Main Methods:

  • Utilized an in vitro infection model using the BV2 microglial cell line.
  • Compared the wild-type S. pneumoniae strain DP1004 with its isogenic spr1875-deleted mutant (Δspr1875).
  • Assessed bacterial phagocytosis, intracellular killing (antibiotic protection assay), and phagosome maturation.

Main Results:

  • Both S. pneumoniae strains were efficiently phagocytosed by microglia.
  • The wild-type strain (DP1004) exhibited greater resistance to intracellular killing and microglial-mediated killing compared to the Δspr1875 mutant.
  • Spr1875 deletion impaired bacterial survival within microglia.

Conclusions:

  • The pneumococcal surface protein Spr1875 influences the interaction between Streptococcus pneumoniae and microglia.
  • Spr1875 contributes to bacterial resistance against microglial clearance mechanisms.
  • Spr1875 may play a significant role in the pathogenesis of pneumococcal meningitis.

More Related Videos

Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae09:12

Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae

Published on: January 17, 2014

Constructing Mutants in Serotype 1 Streptococcus pneumoniae strain 519/4306:06

Constructing Mutants in Serotype 1 Streptococcus pneumoniae strain 519/43

Published on: September 11, 2020

Related Concept Videos

Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
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...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...