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Plos Pathogens

Publication date: 2021-11-01
Volume: 17
Publisher: Public Library of Science (PLoS)

Author:

Nogueira, Denise Silva
de Oliveira, Luciana Maria ; Oliveira Amorimid, Chiara Cassia ; Gazzinelli-Guimaraes, Ana Clara ; Barbosa, Fernando Sergio ; Silva Oliveira, Fabricio Marcus ; Kraemer, Lucas ; Mattos, Matheus ; Cardoso, Mariana Santos ; Resende, Nathalia Maria ; Climaco, Marianna de Carvalho ; Negrao-Correa, Deborah Aparecida ; Caetano Faria, Ana Maria ; Caliari, Marcelo Vidigal ; Bueno, Lilian Lacerda ; Gaze, Soraya ; Russo, Remo Castro ; Gazzinelli-Guimaraes, Pedro Henrique ; Fujiwara, Ricardo Toshio

Keywords:

ACTIVATION, B1B LYMPHOCYTES, GENERATION, IGA, IMMUNITY, INNATE LYMPHOID-CELLS, Life Sciences & Biomedicine, MAINTENANCE, Microbiology, Parasitology, PLASMA-CELLS, RESPONSES, Science & Technology, STRONGYLOIDES-VENEZUELENSIS, Virology, Animals, Ascariasis, Ascaris suum, Eosinophils, Female, Immunoglobulin A, Secretory, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Pneumonia, Toll-Like Receptor 2, Toll-Like Receptor 4, 0605 Microbiology, 1107 Immunology, 1108 Medical Microbiology, 3107 Microbiology, 3204 Immunology, 3207 Medical microbiology

Abstract:

Human ascariasis is the most prevalent but neglected tropical disease in the world, affecting approximately 450 million people. The initial phase of Ascaris infection is marked by larval migration from the host's organs, causing mechanical injuries followed by an intense local inflammatory response, which is characterized mainly by neutrophil and eosinophil infiltration, especially in the lungs. During the pulmonary phase, the lesions induced by larval migration and excessive immune responses contribute to tissue remodeling marked by fibrosis and lung dysfunction. In this study, we investigated the relationship between SIgA levels and eosinophils. We found that TLR2 and TLR4 signaling induces eosinophils and promotes SIgA production during Ascaris suum infection. Therefore, control of parasite burden during the pulmonary phase of ascariasis involves eosinophil influx and subsequent promotion of SIgA levels. In addition, we also demonstrate that eosinophils also participate in the process of tissue remodeling after lung injury caused by larval migration, contributing to pulmonary fibrosis and dysfunction in re-infected mice. In conclusion, we postulate that eosinophils play a central role in mediating host innate and humoral immune responses by controlling parasite burden, tissue inflammation, and remodeling during Ascaris suum infection. Furthermore, we suggest that the use of probiotics can induce eosinophilia and SIgA production and contribute to controlling parasite burden and morbidity of helminthic diseases with pulmonary cycles.