Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Complement System01:27

Complement System

12.6K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
12.6K
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

879
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,...
879
Antimicrobial Proteins01:23

Antimicrobial Proteins

15.4K
Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
15.4K
Bacterial Signaling01:30

Bacterial Signaling

43.2K
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...
43.2K
Colonisation of Pathogens01:25

Colonisation of Pathogens

35
Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...
35
Regulation of Bacterial Virulence01:28

Regulation of Bacterial Virulence

36
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...
36

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Type 2 and type 1 diabetes have opposing effects on the systemic murine complement alternative pathway.

iScience·2026
Same author

C4BP occludes the non-opsonic interaction of <i>Neisseria gonorrhoeae</i> with human neutrophil CEACAMs.

Infection and immunity·2026
Same author

Spinal pain and associated factors among young motorcyclists a cross-sectional study with mediating analysis.

Scientific reports·2026
Same author

COMP-PMEPA1 axis promotes epithelial-to-mesenchymal transition in breast cancer cells.

Molecular oncology·2026
Same author

C4BP occludes the non-opsonic interaction of <i>Neisseria gonorrhoeae</i> with human neutrophil CEACAMs.

bioRxiv : the preprint server for biology·2026
Same author

Nuclear cell-free DNA on the loose: an early warning signal of ischemia-reperfusion injury in kidney transplantation.

Frontiers in immunology·2026

Related Experiment Video

Updated: Mar 30, 2026

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness
12:21

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness

Published on: September 28, 2022

3.3K

Roles of Complement C1q in Pneumococcus-Host Interactions.

Vaibhav Agarwal1, Anna M Blom2

  • 1German Research Foundation- DFG Office India, 2 Nyaya Marg, Chanakyapuri, New Delhi 110021, India.

Critical Reviews in Immunology
|November 13, 2015
PubMed
Summary
This summary is machine-generated.

Streptococcus pneumoniae exploits the complement system

More Related Videos

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
06:54

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

6.5K
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

15.7K

Related Experiment Videos

Last Updated: Mar 30, 2026

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness
12:21

A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness

Published on: September 28, 2022

3.3K
Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
06:54

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

6.5K
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

15.7K

Area of Science:

  • Immunology
  • Microbiology
  • Pathogenesis

Background:

  • The human immune system, especially the complement system, defends against pathogens.
  • Pathogens evolve strategies to evade or manipulate the immune response for survival.
  • Streptococcus pneumoniae can transition from a commensal to a dangerous pathogen.

Purpose of the Study:

  • To review the role of C1q in Streptococcus pneumoniae-host interactions.
  • To understand how pneumococci subvert the complement system for colonization and invasion.

Main Methods:

  • Literature review of studies on C1q and Streptococcus pneumoniae.
  • Analysis of molecular mechanisms in pneumococcus-host immune evasion.

Main Results:

  • Pneumococci utilize C1q, a complement protein, as a molecular bridge.
  • This interaction facilitates bacterial adherence to host cells.
  • C1q is exploited by pneumococci for invasion, contrary to its defensive role.

Conclusions:

  • Streptococcus pneumoniae actively manipulates the host complement system.
  • C1q plays a critical, non-canonical role in pneumococcal pathogenesis.
  • Understanding this interaction is key to controlling pneumococcal infections.