NOD1 signaling regulates early tissue inflammation during helminth infection.

Autor:	Lopes CA; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA., Leal-Silva T; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Vieira-Santos F; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Nascimento Souza JL; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Oliveira CCA; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Oliveira FMS; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Kraemer L; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Magalhaes L; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Bara-Garcia P; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA., Kang B; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA., Zamboni D; Laboratory of Innate Immunity and Microbial Pathogenesis, Department of Cellular and Molecular Biology, University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil., Russo RC; Laboratory of Pulmonary Immunology and Mechanics, Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Fujiwara RT; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Nutman TB; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA., Gazzinelli-Guimaraes P; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA; Department of Microbiology, Immunology and Tropical Medicine, George Washington School of Medicine and Health Sciences, Washington DC, USA. Electronic address: pedro.gazzinelliguimaraes@gwu.edu., Bueno LL; Laboratory of Immunobiology and Control of Parasites, Department of Parasitology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.. Electronic address: llbueno@icb.ufmg.br.
Jazyk:	angličtina
Zdroj:	Mucosal immunology [Mucosal Immunol] 2024 Dec 09. Date of Electronic Publication: 2024 Dec 09.
DOI:	10.1016/j.mucimm.2024.12.004
Abstrakt:	The role of innate receptors in initiating the early inflammatory response to helminth larval stages in affected tissues during their life cycle within the host remains poorly understood. Given its pivotal role in detecting microbial elements and eliciting immune responses, exploring the NOD1 receptor could offer crucial insights into immune responses to parasitic infections. By using the larval ascariasis model, the acute model for early Ascaris sp. infection in humans, we report that NOD1 signaling markedly regulates pulmonary tissue inflammation during Ascaris larval migration. Here we show that Ascaris-infected NOD1-deficient mice exhibited a pronounced decrease in macrophage and eosinophil recruitment to the lungs. This diminished cellular recruitment to the lung correlated with impaired production of a mixed cytokine profile including IFN-γ, IL-1β, IL-5, IL-10, IL-17 and IL-33. The attenuated inflammatory response observed in the absence of NOD1 signaling during infection was associated with a notable amelioration in lung dysfunction compared to WT-infected mice. Systemically, NOD1 signaling was also associated with Ascaris-specific IgG2b antibody responses. In summary, our findings highlight a pathogenic role for NOD1 signaling in Ascaris-induced tissue inflammation, underlying hematopoietic cell recruitment and regulating downstream inflammatory cascades associated with the host's innate immune responses in the tissue triggered by helminth larval migration. Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2024. Published by Elsevier Inc.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu