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Related Concept Videos

Complement System01:27

Complement System

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 membrane...
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Pulmonary Tuberculosis II

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Pulmonary Tuberculosis I

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Cystic Fibrosis: Pathogenesis

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Related Experiment Video

Updated: May 18, 2026

A 3D Human Lung Tissue Model for Functional Studies on Mycobacterium tuberculosis Infection
10:10

A 3D Human Lung Tissue Model for Functional Studies on Mycobacterium tuberculosis Infection

Published on: October 5, 2015

Complement factor C7 contributes to lung immunopathology caused by Mycobacterium tuberculosis.

Kerry J Welsh1, Cole T Lewis, Sydney Boyd

  • 1Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, Houston, TX 77030, USA.

Clinical & Developmental Immunology
|September 14, 2012
PubMed
Summary

Complement C7 deficiency impacts host immune response to Mycobacterium tuberculosis (MTB). C7-deficient mice showed altered lung pathology and increased certain immune cells, suggesting C7

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08:48

Separation and Fractionation of Culture Filtrate Proteins (CFPs) from Mycobacterium tuberculosis

Published on: July 11, 2025

Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Mycobacterium tuberculosis (MTB) poses a significant global health challenge.
  • The complement system plays a role in host defense against MTB, but terminal complement factors are understudied.
  • Complement C7's specific function in MTB infection is not well understood.

Purpose of the Study:

  • To investigate the role of complement C7 in host immune response and pathology during MTB infection.
  • To assess the impact of C7 deficiency on bacterial burden, lung histopathology, and cytokine profiles.

Main Methods:

  • Aerosol challenge of C7-deficient and wild-type mice with MTB Erdman.
  • Assessment of bacterial burden (colony-forming units) in liver and lungs at 30 and 60 days post-infection.
  • Histopathological analysis of lungs, including cell counts (lymphocytes, macrophages, CD4+ cells) and cytokine expression (IFN-γ, TNF-α).
  • Evaluation of MTB proliferation and cytokine production in isolated macrophages.

Main Results:

  • C7-deficient mice had significantly lower liver bacterial burden at day 30 but no difference in lung bacterial burden.
  • At day 60, C7-deficient mice exhibited reduced lung consolidation, increased lymphocytes and CD4+ cells, and decreased macrophages.
  • Increased lung expression of IFN-γ and TNF-α was observed in C7-deficient mice at day 60.
  • No differences in MTB proliferation within macrophages from C7-deficient versus wild-type mice were found.

Conclusions:

  • Complement C7 plays a role in the immunopathology of Mycobacterium tuberculosis infection.
  • C7 deficiency alters the host's cellular and cytokine response in the lungs during MTB infection.
  • Further research is warranted to elucidate the precise mechanisms of C7 in MTB-induced immunopathology.