Fasciola hepatica co-infection enhances Th1 immune response in the adventitial layer of non-fertile Echinococcus granulosus cysts

AbstractCystic echinococcosis is a zoonotic disease caused by the metacestode of Echinococcus granulosus sensu lato. The disease is characterized by the development of cystic structures inside viscera of the intermediate host, mainly liver and lungs. These cysts are formed by three layers: germinal, laminated, and adventitial layer, the latter being the local host immune response. Metacestodes that develop protoscoleces, the infective stage to the definitive host, are termed fertile, whereas cysts that do not produce protoscoleces are termed non-fertile. Sheep usually harbor fertile cysts while cattle usually harbor non-fertile cysts. Adventitial layers with fibrotic resolution are associated to fertile cysts, whereas a granulomatous reaction is associated with non-fertile cysts. The aim of this study was to analyze cellular distribution in the adventitial layer of fertile and non-fertile E. granulosus sensu stricto cysts found in liver and lungs of cattle and sheep. A total of 418 cysts were analyzed, 203 from cattle (8 fertile and 195 non-fertile) and 215 from sheep (64 fertile and 151 non-fertile). Fertile cysts from cattle showed mixed patterns of response, with fibrotic resolution and presence of granulomatous response in direct contact with the laminated layer, while sheep fertile cysts always displayed fibrotic resolution next to the laminated layer. Cattle non-fertile cysts display a granulomatous reaction in direct contact with the laminated layer, whereas sheep non-fertile cysts display a granulomatous reaction, but in direct contact with the fibrotic resolution. This shows that cattle and sheep cystic echinococcosis cysts have distinct local immune response patterns, which are associated to metacestode fertility.

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Lymphocyte Populations in the Adventitial Layer of Hydatid Cysts in Cattle: Relationship With Cyst Fertility Status and Fasciola Hepatica Co-Infection

Veterinary Pathology ◽

10.1177/0300985819875721 ◽

2019 ◽

Vol 57 (1) ◽

pp. 108-114 ◽

Cited By ~ 1

Author(s):

Mauricio Jiménez ◽

Caroll Stoore ◽

Christian Hidalgo ◽

Felipe Corrêa ◽

Marcela Hernández ◽

...

Keyword(s):

Immune Response ◽

B Cells ◽

Hydatid Cyst ◽

Cystic Echinococcosis ◽

B Lymphocyte ◽

Fasciola Hepatica ◽

Hydatid Cysts ◽

T And B Cells ◽

Intermediate Hosts ◽

Adventitial Layer

Cystic echinococcosis is a worldwide zoonosis caused by the cestode Echinococcus granulosus. Two types of hydatid cysts occur in intermediate hosts: fertile cysts that generate protoscoleces from the germinal layer of the cyst, and infertile cysts that do not produce protoscoleces and are unable to continue the life cycle of the parasite. The adventitial layer, a host-derived fibrous capsule surrounding the hydatid cyst, is suggested to play an important role in local immune regulation during infection and in fertility of the cysts. Fasciola hepatica, another important parasite of cattle, induces a characteristic Th2-like immune response that could modulate the immune response against E. granulosus. Natural co-infection of both parasites is common in cattle, but no reports describe the local immune response against E. granulosus with F. hepatica infection in the same host. This study analyzed the number and distribution of T and B cells in the adventitial layer of liver and lung cysts and the relationship with cyst fertility and F. hepatica co-infection. T lymphocytes were the predominant cell type in the adventitial layer of infertile hydatid cysts and were more numerous in infertile hydatid cysts. B lymphocyte numbers were not associated with hydatid cyst fertility. Mast cells were infrequent in the adventitial layer. The number of T and B cells was not associated with F. hepatica co-infection. The present study contributes to the understanding of local immune responses in bovine cystic echinococcosis.

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MiR-374b-5p Regulates T Cell Differentiation and Is Associated with rEg.P29 Immunity

BioMed Research International ◽

10.1155/2020/8024763 ◽

2020 ◽

Vol 2020 ◽

pp. 1-11

Author(s):

Dongjie Li ◽

Xiancai Du ◽

Mingxing Zhu ◽

Songhao Yang ◽

Wei Zhao

Keyword(s):

Flow Cytometry ◽

Immune Response ◽

T Cells ◽

Cell Differentiation ◽

Echinococcus Granulosus ◽

Secondary Infection ◽

T Cell Differentiation ◽

Mrna Levels ◽

Th17 Differentiation ◽

Th1 Immune Response

Cystic echinococcosis (CE) is a zoonotic disease caused by Echinococcus granulosus (Eg) infection. Our previous study confirmed that recombinant Eg.P29 (rEg.P29) could protect against echinococcus granulosus secondary infection in sheep and mice. The aim of the study was to investigate the association between immunoprotection of rEg.P29 vaccine and mmu-miR-374b-5p (miR-374b-5p) and study the immunity influence of miR-374b-5p on CD4+ T cells in mice spleen. MiR-374b-5p level was significantly increased after the second-week and the fourth week of vaccination with rEg.P29. Overexpression of miR-374b-5p increased IFN-γ, IL-2, IL-17A mRNA levels and decreased IL-10 mRNA levels in CD4+ T cells. Moreover, the inhibition of miR-374b-5p decreased IFN-γ and IL-17A and increased IL-10 mRNA levels in CD4+ T cells; this was further confirmed by the flow cytometry. The vaccination of rEg.P29 enhanced miR-374b-5p expression that was associated with a higher Th1 and Th17 immune response, a lower IL-10 mRNA production with miR-374b-5p overexpression, a lower Th1 immune response, and a higher IL-10 mRNA levels with miR-374b-5p inhibitions. To sum up, these data suggest that miR-374b-5p may participate in rEg.P29 immunity by regulating Th1 and Th17 differentiation.

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Biological Underpinnings of Health Alterations in Women With PTSD: A Sex Disparity

Biological Research For Nursing ◽

10.1177/1099800405276709 ◽

2005 ◽

Vol 7 (1) ◽

pp. 44-54 ◽

Cited By ~ 22

Author(s):

Jessica M. Gill ◽

Sarah L. Szanton ◽

Gayle G. Page

Keyword(s):

Posttraumatic Stress Disorder ◽

Immune Response ◽

Major Depressive Disorder ◽

Stress Disorder ◽

Neuroendocrine System ◽

Major Depressive ◽

Fourfold Increase ◽

Sex Disparity ◽

Th1 Immune Response

Women develop posttraumatic stress disorder (PTSD) at twice the rate of men, even though fewer women than men experience traumatic events over their lifetimes. Current studies of individuals with PTSD provide evidence of alterations in the neuroendocrine system that involve levels and activity of cortisol and DHEA and changes in immune function that predispose these individuals toward an innate (Th1) immune response. Yet few studies have addressed the possible role of these biologic alterations in women’s increased vulnerability to developing PTSD. In addition, current studies are limited in their ability to link biologic alterations to the observed fourfold increase in medical conditions in women with PTSD as compared to women without PTSD. And finally, few studies have addressed the biologic impact of co-occurring major depressive disorder (MDD) in individuals with PTSD. This critical review provides an update on neuroendocrine and immune perturbations associated with PTSD with and without cooccurring MDD to suggest links to health and possible mechanisms underlying the observed sex disparity in the development of PTSD.

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Early Hepatic Changes and Immune Response in Goats Vaccinated with a Recombinant Glutathione Transferase Sigma Class and Challenged with Fasciola hepatica

Journal of Comparative Pathology ◽

10.1016/j.jcpa.2012.11.146 ◽

2013 ◽

Vol 148 (1) ◽

pp. 82

Author(s):

R. Zafra ◽

I.L. Pacheco ◽

L. Buffoni ◽

A. Escamilla ◽

A. Martínez-Moreno ◽

...

Keyword(s):

Immune Response ◽

Glutathione Transferase ◽

Fasciola Hepatica

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The Pivotal Role of Signal Regulatory Protein α in Exacerbating Pulmonary Fibrosis Complicated with Bacterial Infection

Journal of Immune Research ◽

10.26420/jimmunres.2021.1039 ◽

2021 ◽

Vol 7 (1) ◽

Author(s):

Yamaguchi R ◽

◽

Sakamoto A ◽

Haraguchi M ◽

Narahara S ◽

...

Keyword(s):

Immune Response ◽

Pulmonary Fibrosis ◽

Bacterial Infection ◽

Signaling Pathway ◽

Regulatory Protein ◽

Interferon Regulatory Factor ◽

Regulatory Factor ◽

Interferon Regulatory Factor 1 ◽

Th1 Immune Response

The pathogenesis of pulmonary fibrosis remains unknown. However, bacterial infections in patients with idiopathic pulmonary fibrosis are a serious complication that exacerbate the disease. Serum levels of Surfactant Protein D (SPD) are known to be elevated in patients with pulmonary fibrosis, but the role of SPD in pulmonary fibrosis complicated with bacterial infection is unknown. Lipopolysaccharide upregulates Interleukin (IL)-12p40 expression and IL-12p40 promotes Interferon Gamma (IFNγ) production to induce the T helper cell 1 (Th1) immune response via Signal Transducers and Activators of Transcription 4 (STAT4) signaling. A lack of IFNγ shifts the immune response from Th1 to Th2. IL-4 is a profibrotic Th2 cytokine that activates fibroblasts. Granulocyte-macrophage colony-stimulating factor induced by IL-1 and TNFα during the Th1 immune response upregulates Signal Regulatory Protein α (SIRPα) expression. Interferon Regulatory Factor 1 (IRF1) functions as the promoter activator of IL-12p40 after stimulation with LPS. SPD is a ligand for SIRPα, and SPD/SIRPα ligation activates the Mitogen-Activated Protein Kinase (MAPK)/Extracellular Signal-Related Kinase (ERK) signal cascade; ERK downregulates Interferon Regulatory Factor 1 (IRF1) expression. Consequently, the SPD/SIRPα signaling pathway decreases IL-12p40 production in human macrophages after exposure to LPS. IL-12p40 is a key immunoregulatory factor in bacterial infection that promotes production of IFNγ by T lymphocytes. Pulmonary fibroblasts are activated by IL-4/IL-4R ligation. IFNγ induces IRF1 via STAT1 signaling, and IRF1 acts as the promoter repressor of IL-4 to attenuate its production. IFNγ also inhibits IL-4R expression. A reduction in IFNγ induced by IL-12p40 deficiency via the SPD/SIRPα signaling pathway enhances IL-4 and IL-4R expression to augment the activity of fibroblasts. This finding indicates that pulmonary fibrosis is exacerbated by SPD/SIRPα signaling during bacterial infection.

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