Related Experiment Video
Updated: Aug 8, 2026

Using Eggs from Schistosoma mansoni as an In vivo Model of Helminth-induced Lung Inflammation
Published on: June 5, 2012
Chemokine expression dynamics in mycobacterial (type-1) and schistosomal (type-2) antigen-elicited pulmonary
1Departments of Pathology and Laboratory Medicine, Veterans Affairs Medical Center, 2215 Fuller Rd., Ann Arbor, MI 48105, USA.
Insights
This study reveals distinct chemokine profiles in mouse lungs during type-1 and type-2 granuloma formation. Cytokine depletions show chemokine expression is regulated by specific cytokines.
Area of Science:
- Immunology
- Molecular Biology
- Pathology
Background:
- Granulomas are key inflammatory structures in response to persistent stimuli.
- Type-1 and type-2 immune responses involve distinct cytokine profiles and cellular players.
- Chemokines are crucial for directing immune cell migration to inflammatory sites.
Purpose of the Study:
- To characterize the transcriptomic profiles of 24 chemokines during type-1 and type-2 granuloma development in mouse lungs.
- To investigate the temporal expression patterns of chemokines in response to different antigenic challenges.
- To determine the role of key cytokines, such as interferon-gamma and tumor necrosis factor-alpha, in regulating chemokine expression.
Main Methods:
- Induction of type-1 (mycobacterial antigen) and type-2 (Schistosoma mansoni egg antigen) granulomas in mouse lungs.
- Quantitative real-time PCR to measure chemokine transcript expression over 8 days.
- Measurement of chemokine protein levels where feasible.
- In vivo cytokine depletion experiments using neutralizing antibodies.
Main Results:
- Bead challenge significantly upregulated 18 of 24 chemokines, with distinct patterns for type-1 and type-2 responses.
- Chemokines were categorized into type-1-dominant, type-2-dominant, co-dominant, and constitutive expression groups.
- CXC and some CC chemokines showed early peak expression (1-2 days), while others peaked later.
- Interferon-gamma neutralization primarily affected monokine induced by gamma-interferon (MIG) expression.
- Tumor necrosis factor-alpha neutralization led to a significant reduction in various chemokines.
Conclusions:
- Type-1 and type-2 granulomas exhibit characteristic and distinct chemokine expression profiles.
- Chemokine expression is temporally regulated and coordinated during granuloma formation.
- Cytokine-mediated regulation, particularly by interferon-gamma and tumor necrosis factor-alpha, plays a significant role in controlling chemokine profiles.
Abstract:
Transcript expression of 24 chemokines (CKs) was examined throughout 8 days in mouse lungs with type-1 (Th1) or type-2 (Th2) cytokine-mediated granulomas induced by bead-immobilized mycobacterial purified protein derivative or Schistosoma mansoni egg antigens. Where possible, CK protein levels were also measured. In addition, we examined effects of in vivo cytokine depletions. Findings were as follows: 1) bead challenge induced increases in 18 of 24 CK transcripts with type-1 and type-2 responses displaying different patterns. CKs fell into four categories: a) type-1-dominant (gamma-interferon-inducible protein (IP-10), monokine induced by INF-gamma (MIG), macrophage inflammatory protein-2 (MIP-2), lipopolysaccharide-induced chemokine (LIX), rodent growth-related oncogene homologue (KP), macrophage inflammatory protein-1alpha (MIP-1alpha) and -1beta (MIP-1beta), lymphotactin), b) type-2-dominant (eotaxin, monocyte chemotactic protein-2 (MCP-2) and -3 (MCP-3), liver and activation-regulated chemokine (LARC), T cell activation protein-3 (TCA-3), c) type-1 and type-2 co-dominant (MCP-1, MCP-5, monocyte-derived chemokine (MDC), thymus and activation-related chemokine (TARC), C10), and d) constitutive (lungkine, secondary lymphoid-tissue chemokine (SLC), EBI1-ligand chemokine (ELC), fractalkine, macrophage inflammatory protein-1gamma (MIP1-gamma), and stromal cell derived factor-1alpha (SDF1-alpha). 2) CKs displayed characteristic temporal patterns. CXC (IP-10, MIG, MIP-2, LIX, KC) and certain CC (MCP-1, MCP-5, MIP-1alpha, MIP-1beta) CKs were produced maximally within 1 to 2 days. Others (MCP-2, MCP-3, eotaxin, lymphotactin, LARC, TCA-3) displayed peak expression later. 3) Interferon-gamma neutralization profoundly abrogated MIG, but had little effect on other CKs. Tumor necrosis factor-alpha neutralization caused up to 50% reduction in a range of CKs. These findings indicate that type-1 and type-2 granulomas display characteristic CK profiles with coordinated expression that is under cytokine-mediated regulation.
More Related Videos
Related Concept Videos
Pulmonary Tuberculosis II
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
Tuberculosis
Chronic Inflammation: Introduction

