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Anthelminthic Agents

Anthelminthic Agents

Anthelmintic drugs differ significantly from antiparasitic therapies targeting protozoa, primarily due to differences in parasite biology. Whereas most protozoal treatments act on proliferating cells, anthelmintics are typically directed against mature, nonproliferative helminths. The therapeutic approach considers the helminth's reliance on neuromuscular coordination, glucose metabolism, and microtubular integrity for survival, reproduction, and localization within the host. Most anthelmintics...

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Updated: May 2, 2026

Cultivation of Heligmosomoides Polygyrus: An Immunomodulatory Nematode Parasite and its Secreted Products

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Published on: April 6, 2015

Antihelminthic niclosamide modulates dendritic cells activation and function.

Chieh-Shan Wu¹, Yi-Rong Li², Jeremy J W Chen³

¹Department of Dermatology, Kaohsiung Veterans General Hospital, Taiwan, ROC; Department of Dermatology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Taiwan, ROC; Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Taiwan, ROC.

Cellular Immunology

|February 25, 2014

Summary

Niclosamide, an antihelminthic drug, was found to suppress dendritic cell (DC) activation. This immunomodulatory effect suggests potential therapeutic applications for niclosamide in treating inflammatory and autoimmune diseases.

Keywords:

Contact hypersensitivity (CHS)Cytokine Dendritic cells Niclosamide T cell proliferation

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Area of Science:

Immunology
Pharmacology

Background:

Dendritic cells (DCs) bridge innate and adaptive immunity, making them key targets for immunomodulatory drugs.
Niclosamide is an FDA-approved antihelminthic agent with potential immunomodulatory properties.

Purpose of the Study:

To investigate the effects of niclosamide on the activation of lipopolysaccharide (LPS)-stimulated murine bone marrow-derived dendritic cells (DCs).

Main Methods:

Examined niclosamide's impact on cytokine/chemokine expression, MHC and costimulatory molecules in LPS-activated DCs.
Assessed niclosamide-treated DCs' ability to stimulate T cell proliferation and IFN-γ production in vitro.
Evaluated niclosamide's effect on contact hypersensitivity (CHS) in vivo.
Investigated the role of MAPK and NF-κB signaling pathways.

Main Results:

Niclosamide reduced pro-inflammatory cytokine and chemokine expression in LPS-activated DCs.
Niclosamide altered MHC and costimulatory molecule expression and antigen uptake by DCs.
Niclosamide-treated DCs exhibited diminished capacity to stimulate T cell proliferation and IFN-γ production.
Niclosamide attenuated in vivo contact hypersensitivity response.
Niclosamide inhibited LPS-induced activation of MAPK-ERK, JNK, and NF-κB pathways.

Conclusions:

Niclosamide effectively manipulates dendritic cell function by inhibiting their activation.
These findings highlight niclosamide's immunopharmacological role and its potential for treating chronic inflammatory and DC-mediated autoimmune diseases.