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

The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

3.6K
Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
3.6K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

5.0K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
5.0K
Aging01:26

Aging

1.1K
Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...
1.1K

You might also read

Related Articles

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

Sort by
Same author

Digital and computational innovations for posttraumatic stress disorder: How digital technologies can improve diagnosis, risk stratification, and individualized treatment.

Journal of traumatic stress·2026
Same author

Cyclical alcohol craving is linked with estradiol-based modulation of ventral tegmental area functional connectivity and is blunted by childhood maltreatment.

Biological psychiatry. Cognitive neuroscience and neuroimaging·2026
Same author

Moving toward precision in pneumonia through lung histopathology Sub-phenotyping.

American journal of respiratory and critical care medicine·2026
Same author

A novel engineered skin closes full thickness burn wounds: A case report.

JPRAS open·2026
Same author

Capsule and PspA Cooperatively Confer Resistance of <i>Streptococcus pneumoniae</i> to the Human Defensin HNP-1.

International journal of molecular sciences·2026
Same author

Personalized fMRI-Guided TMS Targeting the Threat Neurocircuitry in PTSD: A Randomized Clinical Trial.

The American journal of psychiatry·2026

Related Experiment Video

Updated: May 3, 2026

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages
09:09

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages

Published on: April 20, 2018

24.1K

Elevated A20 contributes to age-dependent macrophage dysfunction in the lungs.

Cecilia A Hinojosa1, Ramya Akula Suresh Babu1, Md M Rahman2

  • 1Center for Airway Inflammation, Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.

Experimental Gerontology
|January 21, 2014
PubMed
Summary

Elevated A20 levels in aged mice impair macrophage function, contributing to inflamm-aging. Fish oil supplementation reversed this, enhancing bacterial resistance and suggesting age-dependent macrophage dysfunction is reversible.

Keywords:
AgingInfectionInflammationInnate immunityMacrophagePneumonia

More Related Videos

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure
08:54

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure

Published on: October 22, 2019

8.6K
Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo
06:29

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo

Published on: May 5, 2023

3.3K

Related Experiment Videos

Last Updated: May 3, 2026

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages
09:09

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages

Published on: April 20, 2018

24.1K
In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure
08:54

In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure

Published on: October 22, 2019

8.6K
Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo
06:29

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo

Published on: May 5, 2023

3.3K

Area of Science:

  • Immunology
  • Aging Research
  • Molecular Biology

Background:

  • Advanced age is linked to chronic inflammation (inflamm-aging) and impaired macrophage function, termed age-dependent macrophage dysfunction (ADMD).
  • ADMD is characterized by reduced pro-inflammatory cytokine response and phagocytosis, partly due to impaired NFκB and MAPK signaling.
  • This dysfunction is associated with poor activation of key signaling pathways following Toll-like receptor stimulation.

Purpose of the Study:

  • To test the hypothesis that elevated A20 production during inflamm-aging causes ADMD.
  • To investigate the role of A20, a suppressor of NFκB and MAPK signaling, in age-related macrophage dysfunction.
  • To explore potential therapeutic interventions for ADMD.

Main Methods:

  • Comparative analysis of A20 and CYLD expression in lung tissues and alveolar macrophages (AM) from young, mature, and aged C57BL/6 mice using Western blots and immunohistochemistry.
  • Assessment of TRAF6 polyubiquitination in AM after co-incubation with Streptococcus pneumoniae.
  • In vitro studies using J774A.1 macrophage cell line and primary AM to investigate A20 inducibility by TNFα and IL-6, and the effect of A20 overexpression on cytokine production and phagocytosis.
  • Evaluation of the impact of dietary fish oil supplementation in aged mice on lung A20 levels and resistance to S. pneumoniae challenge.

Main Results:

  • A20 levels were significantly elevated in the lungs and AM of aged mice, while CYLD levels decreased.
  • AM from aged mice exhibited diminished TRAF6 polyubiquitination upon bacterial challenge.
  • A20 production was inducible by TNFα in macrophages, and its overexpression led to reduced IL-6 production in response to S. pneumoniae.
  • Fish oil supplementation in aged mice reduced lung A20 levels and significantly enhanced bacterial clearance, improving resistance to S. pneumoniae infection.

Conclusions:

  • Elevated A20, partly induced by TNFα, contributes to age-dependent macrophage dysfunction (ADMD).
  • The study identifies A20 as a key mediator in the impaired immune response associated with aging.
  • ADMD is potentially reversible, as demonstrated by the therapeutic effect of fish oil supplementation.