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Related Concept Videos

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...
Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the exudate's...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

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
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...
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:

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Related Experiment Video

Updated: May 9, 2026

Multicellular Human Alveolar Model Composed of Epithelial Cells and Primary Immune Cells for Hazard Assessment
09:27

Multicellular Human Alveolar Model Composed of Epithelial Cells and Primary Immune Cells for Hazard Assessment

Published on: May 6, 2020

A modular cell-type focused inflammatory process network model for non-diseased pulmonary tissue.

Jurjen W Westra1, Walter K Schlage, Arnd Hengstermann

  • 1Selventa, One Alewife Center, Cambridge, MA 02140, USA.

Bioinformatics and Biology Insights
|July 12, 2013
PubMed
Summary

Cigarette smoke triggers lung inflammation by disrupting cell defenses and altering immune cell profiles. This study models these inflammatory processes to understand lung disease development.

Keywords:
biological expression language (BEL)cigarette smokegene expressioninflammationnetwork modelreverse causal reasoning (RCR)

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Area of Science:

  • Pulmonary Medicine
  • Computational Biology
  • Immunology

Background:

  • Environmental stressors like cigarette smoke (CS) induce significant inflammatory responses in the lungs.
  • Pulmonary cells are critically positioned at the body's environmental interface, making them vulnerable to inhaled toxins.

Purpose of the Study:

  • To construct a computable causal network model of pulmonary inflammatory processes induced by CS.
  • To provide a comprehensive framework for understanding CS-induced lung inflammation and disease pathogenesis.

Main Methods:

  • Combined a literature survey with computational analysis of transcriptomic data.
  • Developed the Inflammatory Process Network (IPN) model to represent key pathways.

Main Results:

  • The IPN model predicted reduced epithelial barrier defenses and increased mucus in bronchial cells exposed to CS.
  • The model also predicted an attenuated pro-inflammatory (M1) profile in alveolar macrophages following CS exposure.
  • These predictions align with previously established findings on CS effects.

Conclusions:

  • The IPN offers a robust, experimentally supported framework for studying CS-induced pulmonary inflammation.
  • The model serves as a valuable, freely accessible resource for research into pulmonary disease pathogenesis.