Immune response evaluation in Balb/c mice after crude extract of Anisakis typica sensitization

Haryadi, Linda; Suprayitno, Eddy; Aulanni’am, Aulanni’am; Hariati, Anik Martinah

doi:10.14202/vetworld.2019.1529-1534

Cited by 3 publications

(4 citation statements)

References 30 publications

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“…Likewise, oral administration of Anisakis typica CE increased significantly CD4+IFN-γ+ cells in BALB/c mice. (10) This differs with the findings of the study of Heligmosomoides polygyrus, where CD4 + CD25 + T cells did not express IFN-γ. (11) However, in vivo experiments carried out in mice using the Ascaris suum antigen PAS-1 demonstrated that CD8 + γδ + T cells were able to modulate airway allergic inflammation through the production of IFN-γ.…”

Section: Discussioncontrasting

confidence: 90%

Expansion of T regulatory lymphocytes by murine bone marrow dendritic cells previously stimulated with Anisakis simplex larval antigens

Zamora

Rodero

Ibáñez‐Escribano

et al. 2021

Mem. Inst. Oswaldo Cruz

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BACKGROUND Anisakis simplex antigens present immunomodulatory properties by the induction of tolerogenic dendritic cells (DCs) in mice. OBJECTIVES To study the capacity of DCs stimulated with A. simplex excretory-secretory (ES) or crude extract (CE) to generate T regs. To investigate in vitro effects of antigens on the metabolic activity of splenocytes induced by LPS or CpG. METHODS Phenotypic and functional characterization of T cells co-cultured with A. simplex-pulsed DCs was performed by flow cytometry. Lymphocyte mitochondrial respiratory activity was estimated by the Alamar Blue ® Assay. FINDINGS In C57BL/6J, CD4 + CD25-Foxp3 + and CD8 + CD25-Foxp3 + populations increased by CE-stimulated-DCs. In BALB/c, CE-stimulated-DCs caused the expansion of CD4 + CD25 + Foxp3 + IL-10+ and CD8 + CD25 + Foxp3 + IL-10+. IFN-γ expression raised in BALB/c CD4 + CD25 + and CD4 + CD25for CE and ES, respectively. ES-stimulated-DCs increased CD4 + CD25 + Foxp3 + and CD8 + CD25-Foxp3 + expression in T cells. The association of ES or CE with LPS produced the increase in splenocyte activity in C57BL/6J. The association of CE with CpG decreased the proliferation caused by CpG in C57BL/6J. MAIN CONCLUSIONS A. simplex increase the frequency of T regs , which in turn produce IL-10 and IFN-γ. The host genetic base is essential in the development of anti-Anisakis immune responses (Th2, Th1, T reg).

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Section: Discussioncontrasting

confidence: 90%

Expansion of T regulatory lymphocytes by murine bone marrow dendritic cells previously stimulated with Anisakis simplex larval antigens

Zamora

Rodero

Ibáñez‐Escribano

et al. 2021

Mem. Inst. Oswaldo Cruz

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“…Furthermore, A. pegreffii may induce allergies as well based on the presence of A. pegreffii -tropomyosin in the serum of patients with crustacean allergy [ 53 ]. A. pegreffii -induced allergies have also been reported in animal models [ 13 , 35 , 54 ]. A. simplex and A. pegreffii have been reported as different species with genetic differences [ 55 – 57 ] but can be distinguished only at the L4 or adult stages [ 58 ].…”

Section: Discussionmentioning

confidence: 99%

“…Acute airway inflammation models, usually induced within 3 weeks, are often characterized by airway hypersensitivity (AHR) and inflammation, but not remodeling [ 33 , 34 ]. Notably, in a 1-week model system using Anisakis crude extract allergens, the number of cells involved in the inflammatory immune response increased; however, observations of airway remodeling, indicative of asthma, were not reported [ 35 ]. Airway remodeling features, such as goblet cell proliferation, were not observed in the 2-week model as well [ 33 ].…”

Section: Introductionmentioning

confidence: 99%

Anisakis pegreffii Extract Induces Airway Inflammation with Airway Remodeling in a Murine Model System

Choi

Kim

et al. 2021

BioMed Research International

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Exposure of the respiratory system to the Anisakis pegreffii L3 crude extract (AE) induces airway inflammation; however, the mechanism underlying this inflammatory response remains unknown. AE contains allergens that promote allergic inflammation; exposure to AE may potentially lead to asthma. In this study, we aimed to establish a murine model to assess the effects of AE on characteristic features of chronic asthma, including airway hypersensitivity (AHR), airway inflammation, and airway remodeling. Mice were sensitized for five consecutive days each week for 4 weeks. AHR, lung inflammation, and airway remodeling were evaluated 24 h after the last exposure. Lung inflammation and airway remodeling were assessed from the bronchoalveolar lavage fluid (BALF). To confirm the immune response in the lungs, changes in gene expression in the lung tissue were assessed with reverse transcription-quantitative PCR. The levels of IgE, IgG1, and IgG2a in blood and cytokine levels in the BALF, splenocyte, and lung lymph node (LLN) culture supernatant were measured with ELISA. An increase in AHR was prominently observed in AE-exposed mice. Epithelial proliferation and infiltration of inflammatory cells were observed in the BALF and lung tissue sections. Collagen deposition was detected in lung tissues. AE exposure increased IL-4, IL-5, and IL-13 expression in the lung, as well as the levels of antibodies specific to AE. IL-4, IL-5, and IL-13 were upregulated only in LLN. These findings indicate that an increase in IL-4+ CD4+ T cells in the LLN and splenocyte resulted in increased Th2 response to AE exposure. Exposure of the respiratory system to AE resulted in an increased allergen-induced Th2 inflammatory response and AHR through accumulation of inflammatory and IL-4+ CD4+ T cells and collagen deposition. It was confirmed that A. pegreffii plays an essential role in causing asthma in mouse models and has the potential to cause similar effects in humans.

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“…The allergenicity of two important allergens, Ani s 1 and Ani s 9, was investigated by repeated intranasal administration of the allergens [ 62 ], revealing a high ability to induce Th2 (IL-4, IL-5, IL-13 and IL-25) and Th17 (IL-6, IL-17, IL-25 and CXCL1) responses in the lung. Later, the allergenic potential of Anisakis typica was tested by oral administration of crude extract to BALB/c mice [ 63 ]. Results showed the elicitation of patterns not entirely related to food antigen allergy, showing Th1/Th2-related cytokines with mixed pattern tending to inflammation.…”

Section: In Vivo Modelsmentioning

confidence: 99%

What Do In Vitro and In Vivo Models Tell Us about Anisakiasis? New Tools Still to Be Explored

et al. 2022

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Anisakiasis is a zoonosis caused by the ingestion of raw or undercooked seafood infected with third-stage larvae (L3) of the marine nematode Anisakis. Based on L3 localization in human accidental hosts, gastric, intestinal or ectopic (extra-gastrointestinal) anisakiasis can occur, in association with mild to severe symptoms of an allergic nature. Given the increasing consumption of fish worldwide, the European Food Safety Authority declared Anisakis as an emerging pathogen. Despite its importance for public health and economy, the scientific literature is largely characterized by taxonomic, systematic and ecological studies, while investigations on clinical aspects, such as the inflammatory and immune response during anisakiasis, using a proper model that simulates the niche of infection are still very scarce. The aims of this review are to describe the clinical features of anisakiasis, to report the main evidence from the in vivo and in vitro studies carried out to date, highlighting limitations, and to propose future perspectives in the study field of anisakiasis.

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Immune response evaluation in Balb/c mice after crude extract of Anisakis typica sensitization

Cited by 3 publications

References 30 publications

Expansion of T regulatory lymphocytes by murine bone marrow dendritic cells previously stimulated with Anisakis simplex larval antigens

Expansion of T regulatory lymphocytes by murine bone marrow dendritic cells previously stimulated with Anisakis simplex larval antigens

Anisakis pegreffii Extract Induces Airway Inflammation with Airway Remodeling in a Murine Model System

What Do In Vitro and In Vivo Models Tell Us about Anisakiasis? New Tools Still to Be Explored

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