What Can Parasites Tell Us About the Pathogenesis and Treatment of Asthma and Allergic Diseases

Bohnacker, Sina; Troisi, Fabiana; Jiménez, Marta de los Reyes; Bieren, Julia Esser‐von

doi:10.3389/fimmu.2020.02106

Cited by 18 publications

(16 citation statements)

References 113 publications

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“…[6][7][8] Helminths have developed several mechanisms to modulate the immune response of hosts, thereby inhibiting the occurrence of asthma. 9,10 Helminth infection or helminth-derived molecules induce regulatory T cells (Tregs), [11][12][13] IL-10-producing regulatory B cells, 14,15 dendritic cells, 16 and alternatively activated macrophages 17 to prevent allergic airway inflammation in asthmatic mice. In comparison with helminth infection or most macromolecules derived from parasites, we have identified a small-molecule peptide from Schistosoma japonicum (S. japonicum) and it named as SJMHE1; it could induce CD4 + CD25 + Treg cells 18 and suppress the delayed-type hypersensitivity in mice.…”

Section: Introductionmentioning

confidence: 99%

SJMHE1 Peptide from Schistosoma japonicum Inhibits Asthma in Mice by Regulating Th17/Treg Cell Balance via miR-155

Li¹,

Shan²,

Zhu³

et al. 2021

JIR

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Helminths and their products can regulate immune response and offer new strategies to control and alleviate inflammation, including asthma. We previously found that a peptide named as SJMHE1 from Schistosoma japonicum can suppress asthma in mice. This study mainly investigated the molecular mechanism of SJMHE1 in inhibiting asthma inflammation. Methods: SJMHE1 was administered to mice with OVA-induced asthma via subcutaneous injection, and its effects were detected by testing the airway inflammation of mice. The Th cell distribution was analyzed by flow cytometry. Th-related transcription factor and cytokine expression in the lungs of mice were analyzed using quantitative real-time PCR (qRT-PCR). The expression of miR-155 and levels of phosphorylated STAT3 and STAT5 were also determined after SJMHE1 treatment in mice by qRT-PCR and Western blot analysis. The in vitro mouse CD4 + T cells were transfected with lentivirus containing overexpressed or inhibited miR-155, and the proportion of Th17, Treg cells, CD4 + p-STAT3 + , and CD4 + p-STAT5 + cells were analyzed by flow cytometry. Results: SJMHE1 ameliorated the airway inflammation of asthmatic mice, upregulated the proportion of Th1 and Treg cells, and the expression of Th1 and Treg-related transcription factor and cytokines. Simultaneously, SJMHE1 treatment reduced the percentage of Th2 and Th17 cells and the expression of Th2 and Th17-related transcription factor and cytokines. SJMHE1 treatment decreased the expression of miR-155 and p-STAT3 but increased p-STAT5 expression. In vitro, the percentage of Th17 and CD4 + p-STAT3 + cells increased in CD4 + T cells transfected over-expression of miR-155, but SJMHE1 inhibited the miR-155-mediated increase of Th17 cells. Furthermore, SJMHE1 increased the proportion of Treg and CD4 + p-STAT5 + cells after transfected over-expression or inhibition of miR-155. Conclusion: SJMHE1 regulated the balance of Th17 and Treg cells by modulating the activation of STAT3 and STAT5 via miR-155 in asthma. SJMHE1 might be a promising treatment for asthma.

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Section: Introductionmentioning

confidence: 99%

SJMHE1 Peptide from Schistosoma japonicum Inhibits Asthma in Mice by Regulating Th17/Treg Cell Balance via miR-155

Li¹,

Shan²,

Zhu³

et al. 2021

JIR

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“…For example, schistosome glutathione S-transferase (P28GST) improves intestinal inflammation in experimental colitis and Fasciola hepatica mitigates experimental autoimmune encephalomyelitis (EAE) and MS. 77 Similarly, ES-62, a glycoprotein from the filarial nematode Acanthocheilonema vitae, is a potent pharmacological molecule that can be used for asthma, lung fibrosis and RA. 78 Likewise, metabolism and weight regulation are in part immunologically regulated, hence helminth infections such as Nippostrongylus brasiliensis and S. mansoni, once again display a therapeutic perspective since it was shown that they prevent glucose intolerance through adipose tissue eosinophils and type 2 macrophages activation. 37 Furthermore, a number of animal studies have evidenced that helminth infections (S. mansoni, Trichinella spiralis and Filaria spp.,) and helminth derived products can prevent onset or cure T1D, possibly by repressing Th1 immune response.…”

Section: Concluding Remarks and Future Perspectivesmentioning

confidence: 99%

How the gut parasitome affects human health

Ianiro

Iorio

Porcari

et al. 2022

Therap Adv Gastroenterol

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The human gut microbiome (GM) is a complex ecosystem that includes numerous prokaryotic and eukaryotic inhabitants. The composition of GM can influence an array of host physiological functions including immune development. Accumulating evidence suggest that several members of non-bacterial microbiota, including protozoa and helminths, that were earlier considered as pathogens, could have a commensal or beneficial relationship with the host. Here we examine the most recent data from omics studies on prokaryota-meiofauna-host interaction as well as the impact of gut parasitome on gut bacterial ecology and its role as ‘immunological driver’ in health and disease to glimpse new therapeutic perspectives.

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“…Helminth parasites typically employ multiple mechanisms to suppress host defense and to establish a chronic infection with type 2 immunity ( 231 , 232 ). One way the helminths can achieve this outcome are various immunomodulatory products that they release upon infection.…”

Section: Innate Immunity In Shaping Allergen-specific Sensitization T...mentioning

confidence: 99%

Inhalant Mammal-Derived Lipocalin Allergens and the Innate Immunity

Virtanen

2022

Front. Allergy

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A major part of important mammalian respiratory allergens belongs to the lipocalin family of proteins. By this time, 19 respiratory mammalian lipocalin allergens have been registered in the WHO/IUIS Allergen Nomenclature Database. Originally, lipocalins, small extracellular proteins (molecular mass ca. 20 kDa), were characterized as transport proteins but they are currently known to exert a variety of biological functions. The three-dimensional structure of lipocalins is well-preserved, and lipocalin allergens can exhibit high amino acid identities, in several cases more than 50%. Lipocalins contain an internal ligand-binding site where they can harbor small principally hydrophobic molecules. Another characteristic feature is their capacity to bind to specific cell-surface receptors. In all, the physicochemical properties of lipocalin allergens do not offer any straightforward explanations for their allergenicity. Allergic sensitization begins at epithelial barriers where diverse insults through pattern recognition receptors awaken innate immunity. This front-line response is manifested by epithelial barrier-associated cytokines which together with other components of immunity can initiate the sensitization process. In the following, the crucial factor in allergic sensitization is interleukin (IL)-4 which is needed for stabilizing and promoting the type 2 immune response. The source for IL-4 has been searched widely. Candidates for it may be non-professional antigen-presenting cells, such as basophils or mast cells, as well as CD4+ T cells. The synthesis of IL-4 by CD4+ T cells requires T cell receptor engagement, i.e., the recognition of allergen peptides, which also provides the specificity for sensitization. Lipocalin and innate immunity-associated cell-surface receptors are implicated in facilitating the access of lipocalin allergens into the immune system. However, the significance of this for allergic sensitization is unclear, as the recognition by these receptors has been found to produce conflicting results. As to potential adjuvants associated with mammalian lipocalin allergens, the hydrophobic ligands transported by lipocalins have not been reported to enhance sensitization while it is justified to suppose that lipopolysaccharide plays a role in it. Taken together, type 2 immunity to lipocalin allergens appears to be a harmful immune response resulting from a combination of signals involving both the innate and adaptive immunities.

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What Can Parasites Tell Us About the Pathogenesis and Treatment of Asthma and Allergic Diseases

Cited by 18 publications

References 113 publications

SJMHE1 Peptide from Schistosoma japonicum Inhibits Asthma in Mice by Regulating Th17/Treg Cell Balance via miR-155

SJMHE1 Peptide from Schistosoma japonicum Inhibits Asthma in Mice by Regulating Th17/Treg Cell Balance via miR-155

How the gut parasitome affects human health

Inhalant Mammal-Derived Lipocalin Allergens and the Innate Immunity

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