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

Inflammation01:38

Inflammation

Overview
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Immune Surveillance by NK Cells and Phagocytes01:25

Immune Surveillance by NK Cells and Phagocytes

Immune surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
Natural Killer Cells: The Fast Responders
NK cells are large granular lymphocytes found in the blood and lymphatic system. These...
Cells of the Innate Immune Response01:28

Cells of the Innate Immune Response

The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
Phagocytes
Phagocytes police the peripheral tissues by removing cellular debris and responding to the invasion of foreign substances or pathogens. Many phagocytes attack and remove microorganisms even before lymphocytes detect them. The human body has two general...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Acute Inflammation I: Cellular Phase01:26

Acute Inflammation I: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...

You might also read

Related Articles

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

Sort by
Same author

Toll-Like Receptors-Intrarenal Mechanisms beyond Immune Function: Renal-Associated TLR2 Mediates Ischemia/Reperfusion Injury in the Kidney.

Journal of the American Society of Nephrology : JASN·2023
Same author

Diabetic control and nutritional status up to 1 year after total pancreatectomy: a nationwide multicentre prospective study.

The British journal of surgery·2021
Same author

Activation of innate immunity by 14-3-3 ε, a new potential alarmin in osteoarthritis.

Osteoarthritis and cartilage·2020
Same author

Low-dose gonadotropin-releasing hormone agonist therapy (draw-back therapy) for successful long-term management of adenomyosis associated with cerebral venous and sinus thrombosis from low-dose oral contraceptive use.

Clinical and experimental obstetrics & gynecology·2018
Same author

Hybrid Laparoscopic Sacrocolpopexy for Pelvic Organ Prolapse With Severe Cystocele.

Journal of minimally invasive gynecology·2016
Same author

Surgical Treatment Outcomes in Patients With Recurrent Pregnancy Loss Attributed to Septate Uterus.

Journal of minimally invasive gynecology·2016
Same journal

A Gut-Protective TRPV1-Neuroepithelial Axis: Electroacupuncture Reverses Intestinal Damage in Diet-Induced Obesity.

Diabetes, obesity & metabolism·2026
Same journal

Impact of iGlarLixi on Glycaemic Control Depth and Variability in Asian Pacific People With Type 2 Diabetes: A Post Hoc Analysis of LixiLan-O-AP and LixiLan-L-CN.

Diabetes, obesity & metabolism·2026
Same journal

Efficacy and Safety of Intensifying Once-Weekly Insulin Icodec Treatment With Once-Weekly Semaglutide in Adults With Type 2 Diabetes: A Single-Arm, Open-Label, Treat-to-Target, Phase 3b Trial (ONWARDS 8).

Diabetes, obesity & metabolism·2026
Same journal

Potential Mediators of Efpeglenatide's Cardiovascular Benefit: An Exploratory Analysis of the AMPLITUDE-O Trial.

Diabetes, obesity & metabolism·2026
Same journal

Exercise or Fasting in Individuals With Type 2 Diabetes Receiving Once-Weekly Basal Insulin Icodec.

Diabetes, obesity & metabolism·2026
Same journal

Tirzepatide Is Associated With Improved Metabolic Outcomes in People With Type 1 Diabetes and Overweight or Obesity: A Retrospective Cohort Study.

Diabetes, obesity & metabolism·2026
See all related articles

Related Experiment Video

Updated: May 8, 2026

Bone Marrow-derived Macrophage Production
07:06

Bone Marrow-derived Macrophage Production

Published on: November 22, 2013

Macrophages control innate inflammation.

S Akira1, T Misawa, T Satoh

  • 1Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan. sakira@biken.osaka-u.ac.jp

Diabetes, Obesity & Metabolism
|September 6, 2013
PubMed
Summary
This summary is machine-generated.

Tubulin polymerization inhibitors block the NLRP3 inflammasome, a key pathway in metabolic diseases. Trib1 protein is essential for M2 macrophage differentiation, maintaining adipose tissue and preventing metabolic disorders.

Keywords:
NLRP3 inflammasomeSirtuin 2Trib1adipose tissuegoutinnate immunityinsulin resistancelipodystrophymacrophagemicrotubules

More Related Videos

Mesenchymal Stem Cell Regulation of Macrophage Phagocytosis; Quantitation and Imaging
09:10

Mesenchymal Stem Cell Regulation of Macrophage Phagocytosis; Quantitation and Imaging

Published on: July 16, 2021

Related Experiment Videos

Last Updated: May 8, 2026

Bone Marrow-derived Macrophage Production
07:06

Bone Marrow-derived Macrophage Production

Published on: November 22, 2013

Mesenchymal Stem Cell Regulation of Macrophage Phagocytosis; Quantitation and Imaging
09:10

Mesenchymal Stem Cell Regulation of Macrophage Phagocytosis; Quantitation and Imaging

Published on: July 16, 2021

Area of Science:

  • Immunology
  • Metabolic Diseases
  • Cell Biology

Background:

  • Macrophages are central to metabolic diseases like gout and type 2 diabetes.
  • The NLRP3 inflammasome, involving ASC, drives macrophage-mediated inflammation.
  • Trib1 regulates immune transcription factors and macrophage differentiation.

Purpose of the Study:

  • To identify inhibitors of NLRP3 inflammasome activation.
  • To elucidate the role of Trib1 in macrophage differentiation and metabolic homeostasis.

Main Methods:

  • Compound screening to identify tubulin polymerization inhibitors.
  • Investigating the effect of NLRP3 inflammasome inducers on NAD+ levels and Sirtuin 2 activity.
  • Analyzing microtubule-dependent mitochondrial transport in inflammasome activation.
  • Generating and studying mice lacking Trib1 in hematopoietic cells.

Main Results:

  • Tubulin polymerization inhibitors suppress NLRP3 inflammasome activation.
  • NLRP3 inflammasome activation leads to decreased NAD+ levels, Sirtuin 2 inactivation, and α-tubulin acetylation.
  • Microtubule-driven mitochondrial transport is crucial for NLRP3 inflammasome assembly.
  • Trib1 deficiency in hematopoietic cells causes lipodystrophy, hypertriglyceridemia, insulin resistance, and increased inflammation.
  • Trib1 is vital for M2-like macrophage differentiation and adipose tissue maintenance.

Conclusions:

  • Microtubule dynamics and mitochondrial transport are essential for NLRP3 inflammasome activation.
  • Trib1 is a critical regulator of tissue-resident M2 macrophage differentiation, crucial for suppressing metabolic disorders.