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Related Concept Videos

Introduction to Fibroblasts01:09

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
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...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...

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Related Experiment Video

Updated: Jul 1, 2026

Chronic Salmonella Infection Induced Intestinal Fibrosis
08:40

Chronic Salmonella Infection Induced Intestinal Fibrosis

Published on: September 22, 2019

Microbiota-fibroblasts interactions in multi-organ fibrosis.

Caiyu Qi1, Zhen Lin2, Yuyang Gan2

  • 1Department of Plastic and Aesthetic Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD 21210, USA.

Microbiological Research
|June 29, 2026
PubMed
Summary
This summary is machine-generated.

The human microbiome influences fibrosis by regulating fibroblast activity. Targeting these microbiota-fibroblast interactions offers a new therapeutic strategy for chronic fibrotic diseases.

Keywords:
Commensal microbiotaFibroblasts plasticityGut-organ crosstalkMicrobiota-host interactionsOrgan fibrosisPrecision medicine

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Murine Dermal Fibroblast Isolation by FACS
06:04

Murine Dermal Fibroblast Isolation by FACS

Published on: January 7, 2016

Area of Science:

  • Microbiology
  • Pathology
  • Immunology

Background:

  • Fibrosis is a key feature of chronic diseases, involving fibroblast activation and extracellular matrix deposition.
  • The human microbiome and host interact as a system, with microbial signals influencing tissue remodeling.
  • Emerging research highlights the role of the microbiota-fibroblast axis in fibrotic diseases.

Purpose of the Study:

  • To review the microbiota-fibroblast axis and its role in regulating fibroblast activation and fibrogenesis.
  • To explore how microbial signals from various niches contribute to fibrosis across multiple organs.
  • To organize these interactions within interconnected regulatory networks and evaluate therapeutic potential.

Main Methods:

  • Literature review integrating evidence from multiple microbial niches (oral, gut, lung).
  • Analysis of direct and indirect mechanisms of microbiota-host interactions in fibrosis.
  • Evaluation of correlative evidence linking microbial dysbiosis to fibrosis progression.

Main Results:

  • Microbial components (bacteria, viruses, metabolites) regulate fibroblast activation and fibrogenesis.
  • Interactions across organ systems (e.g., gut-liver, oral-heart) contribute to fibrosis.
  • Microbial dysbiosis is linked to the progression of fibrotic diseases.

Conclusions:

  • The microbiota-fibroblast axis is a critical regulator of fibrotic diseases.
  • Targeting microbial-host interactions presents a promising therapeutic avenue for fibrotic conditions.
  • A holobiont perspective is essential for understanding and treating fibrosis.