Host Immunity and Inflammation to Pulmonary Helminth Infections

Abstract

Helminths, including nematodes, cestodes and trematodes, are complex parasitic organisms that infect at least one billion people globally living in extreme poverty. Helminthic infections are associated with severe morbidity particularly in young children who often harbor the highest burden of disease. While each helminth species completes a distinct life cycle within the host, several helminths incite significant lung disease. This impact on the lungs occurs either directly from larval migration and host immune activation or indirectly from a systemic inflammatory immune response. The impact of helminths on the pulmonary immune response involves a sophisticated orchestration and activation of the host innate and adaptive immune cells. The consequences of activating pulmonary host immune responses are variable with several helminthic infections leading to severe, pulmonary compromise while others providing immune tolerance and protection against the development of pulmonary diseases. Further delineation of the convoluted interface between helminth infection and the pulmonary host immune responses is critical to the development of novel therapeutics that are critically needed to prevent the significant global morbidity caused by these parasites.

Impact of parasitic infection with Ascaris lumbricoides on pulmonary function tests in asthmatic and non-asthmatic children

“…This result points to the fact that the impact of Ascaris infection was associated with increased level of WBC, eosinophils and IgE in a similar profile to that change of asthmatic, but this impact was unrelated to PFT. Children immune responses to this parasitic infection resulted in increased level of WBC, eosinophils and total IgE, a result came in agreement with what were pointed by previous studies,an individual immune response to the presences of helminthic parasites led to elevated level of IgE, eosinophilia,mastocytosis and interleukin 4,5 and 13 as well as presence of parasites in the tissue might induce localized Th2 response that characterized by formation of inflammatory infiltrate rich with eosinophils [ 29 , 30 ].…”

Detrimental role of IL-33/ST2 pathway sustaining a chronic eosinophil-dependent Th2 inflammatory response, tissue damage and parasite burden during Toxocara canis infection in mice

“…In several helminth infections, IL-4, IL-13 and IL-5 producing Th2 cells are related to the most important effector mechanisms in adaptive pulmonary immunity against helminths [ 41 ]. In our study, ST2 -/- mice decreased the concentration of IL-5 and increased IL-33, IL-13 and IL-17 in the initial stage of infection, and with 63dpi in addition to IL-33 and IL-17, also increased IL-1β concentration.…”

Airway Epithelial Innate Immunity

“…Similarities in clinical presentation between parasite infections of the lungs and allergic asthma have long been noted, but a molecular relationship between the two was only established in recent decades. In particular, IL-13 and its upstream and downstream signaling pathways have been demonstrated to be essential both for resistance to parasites and for full expression of the allergic asthma phenotype (Frey et al, 2020;Weatherhead et al, 2020;Hammad and Lambrecht, 2021). Upregulated expression of the secreted mucin MUC5AC is a prominent effector response in both clinical settings (Fahy and Dickey, 2010).…”