Effect of Nippostrongylus brasiliensis L3 ES on inflammatory mediator gene transcription in lipopolysaccharide lung inflammation

Zhao, M; Brown, D M; MacCallum, Janis; Proudfoot, Lorna

Abstract

The anti-inflammatory properties of parasitic helminths have been largely linked to their excretory-secretory (ES) products. Some studies have noted a lack of TNF-alpha production and limited recruitment of neutrophils into the lungs after Nippostrongylus brasiliensis infection. We previously reported that instillation of ES from L3 larvae of N. brasiliensis to the lungs could inhibit the recruitment of neutrophils on a background of LPS-induced inflammation. A similar reduction in neutrophil recruitment was observed in this study. This reduction was associated with the significant inhibition in gene transcription of the adhesion molecule, ICAM-1, and the chemokine, MIP-2 in bronchoalveolar lavage (BAL) cells. The LPS-stimulated gene transcription of the pro-inflammatory cytokines TNF-alpha and IL-1beta was also significantly reduced by L3 ES. Inducible nitric oxide synthase (iNOS) is normally elevated in classically activated macrophages, however, in this case gene transcription of iNOS was inhibited by L3 ES and may suggest a phenotype change to anti-inflammatory. The general inhibition of pro-inflammatory mediators observed in this study suggests that infective stage L3 larvae excrete and/or secrete inhibitory products capable of modifying the normally potent LPS inflammatory response.

• Journal Article Type: Article
• Acceptance Date: Oct 3, 2008
• Online Publication Date: Oct 13, 2008
• Publication Date: Dec 12, 2008
• Deposit Date: Jun 28, 2017
• Journal: Parasite Immunology
• Print ISSN: 0141-9838
• Electronic ISSN: 1365-3024
• Publisher: Wiley
• Peer Reviewed: Peer Reviewed
• Volume: 31
• Issue: 1
• Pages: 50-56
• DOI: https://doi.org/10.1111/j.1365-3024.2008.01073.x
• Keywords: anti‐inflammatory; bronchoalveolar lavage (BAL); chemokines; cytokines; lung; Nippostrongylus brasiliensis
• Public URL: http://researchrepository.napier.ac.uk/Output/953887