Vaccination as a control strategy against the coccidial parasitesEimeria,ToxoplasmaandNeospora

Parasitology ◽  
2006 ◽  
Vol 133 (S2) ◽  
pp. S145-S168 ◽  
Author(s):  
E. A. INNES ◽  
A. N. VERMEULEN
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Large Scale ◽  
Neospora Caninum ◽  
Vaccination Strategy ◽  
Host Immune System ◽  
Scale Production ◽  
Vaccination Strategies ◽  
Development Of Resistance ◽  
Causes Of Disease

The protozoan parasitesEimeriaspp.Toxoplasma gondiiandNeospora caninumare significant causes of disease in livestock worldwide andT. gondiiis also an important human pathogen. Drugs have been used with varying success to help control aspects of these diseases and commercial vaccines are available for all three groups of parasites. However, there are issues with increasing development of resistance to many of the anti-coccidial drugs used to help control avian eimeriosis and public concerns about the use of drugs in food animals. In addition there are no drugs available that can act against the tissue cyst stage of eitherT. gondiiorN. caninumand thus cure animals or people of infection. All three groups of parasites multiply within the cells of their host species and therefore cell mediated immune mechanisms are thought to be an important component of host protective immunity. Successful vaccination strategies for bothEimeriaandToxoplasmahave relied on using a live vaccination approach using attenuated parasites which allows correct processing and presentation of antigen to the host immune system to stimulate appropriate cell mediated immune responses. However, live vaccines can have problems with safety, short shelf-life and large-scale production; therefore there is continued interest in devising new vaccines using defined recombinant antigens. The major challenges in devising novel vaccines are to select relevant antigens and then present them to the immune system in an appropriate manner to enable the induction of protective immune responses. With all three groups of parasites, vaccine preparations comprising antigens from the different life cycle stages may also be advantageous. In the case ofEimeriaparasites there are also problems with strain-specific immunity therefore a cocktail of antigens from different parasite strains may be required. Improving our knowledge of the different parasite transmission routes, host-parasite relationships, disease pathogenesis and determining the various roles of the host immune response being at times host-protective, parasite protective and in causing immunopathology will help to tailor a vaccination strategy against a particular disease target. This paper discusses current vaccination strategies to help combat infections withEimeria,ToxoplasmaandNeosporaand recent research looking towards developing new vaccine targets and approaches.

An appraisal of survival strategies

Parasitology ◽  
1984 ◽  
Vol 88 (4) ◽  
pp. 575-577 ◽  
Author(s):  
N. A. Mitchison
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Survival Strategies ◽  
Host Immune System ◽  
Cellular Immunology ◽  
Host Immune Responses ◽  
Host Defence System ◽  
Bio Engineering

Only a few years ago parasite immunology looked an unattractive subject better left to the dogged specialists. Parasites and hosts had been playing chess together for a million years, and there seemed little prospect of perturbing matters in favour of the host immune system. All that has changed, for three reasons. Firstly, we have learned how to grow at least some parasites in vitro, and prospects of doing so with others are encouraging. Secondly, progress in cellular immunology has revealed the sort of loopholes in the host defence system which parasites are likely to exploit: we are learning the questions which matter about parasites as antigens. Thirdly, and most importantly, molecular genetics is being brought to bear on parasites: we can now see a real, though long-term, prospect of manufacturing practicable vaccines through bio-engineering, and more immediately it gives us the tools needed to probe the host immune responses in the form of cloned antigens.

scholarly journals Mutual Interplay of Host Immune System and Gut Microbiota in the Immunopathology of Atherosclerosis

2020 ◽  
Vol 21 (22) ◽  
pp. 8729 ◽  
Author(s):  
Chih-Fan Yeh ◽  
Ying-Hsien Chen ◽  
Sheng-Fu Liu ◽  
Hsien-Li Kao ◽  
Ming-Shiang Wu ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Cytokine Production ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Inflammasome Activation ◽  
Host Immune System ◽  
Gut Permeability ◽  
And Function ◽  
Progression Of Atherosclerosis

Inflammation is the key for the initiation and progression of atherosclerosis. Accumulating evidence has revealed that an altered gut microbiome (dysbiosis) triggers both local and systemic inflammation to cause chronic inflammatory diseases, including atherosclerosis. There have been some microbiome-relevant pro-inflammatory mechanisms proposed to link the relationships between dysbiosis and atherosclerosis such as gut permeability disruption, trigger of innate immunity from lipopolysaccharide (LPS), and generation of proatherogenic metabolites, such as trimethylamine N-oxide (TMAO). Meanwhile, immune responses, such as inflammasome activation and cytokine production, could reshape both composition and function of the microbiota. In fact, the immune system delicately modulates the interplay between microbiota and atherogenesis. Recent clinical trials have suggested the potential of immunomodulation as a treatment strategy of atherosclerosis. Here in this review, we present current knowledge regarding to the roles of microbiota in contributing atherosclerotic pathogenesis and highlight translational perspectives by discussing the mutual interplay between microbiota and immune system on atherogenesis.

scholarly journals Role of the microbiome in human development

Gut ◽  
2019 ◽  
Vol 68 (6) ◽  
pp. 1108-1114 ◽  
Author(s):  
Maria Gloria Dominguez-Bello ◽  
Filipa Godoy-Vitorino ◽  
Rob Knight ◽  
Martin J Blaser
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Human Development ◽  
Life Forms ◽  
Host Responses ◽  
Host Immune System ◽  
Next Generation ◽  
Host Health ◽  
Host Development

The host-microbiome supraorganism appears to have coevolved and the unperturbed microbial component of the dyad renders host health sustainable. This coevolution has likely shaped evolving phenotypes in all life forms on this predominantly microbial planet. The microbiota seems to exert effects on the next generation from gestation, via maternal microbiota and immune responses. The microbiota ecosystems develop, restricted to their epithelial niches by the host immune system, concomitantly with the host chronological development, providing early modulation of physiological host development and functions for nutrition, immunity and resistance to pathogens at all ages. Here, we review the role of the microbiome in human development, including evolutionary considerations, and the maternal/fetal relationships, contributions to nutrition and growth. We also discuss what constitutes a healthy microbiota, how antimicrobial modern practices are impacting the human microbiota, the associations between microbiota perturbations, host responses and diseases rocketing in urban societies and potential for future restoration.

scholarly journals Fungal Extracellular Vesicles as Potential Targets for Immune Interventions

mSphere ◽  
2019 ◽  
Vol 4 (6) ◽  
Author(s):  
Mateus Silveira Freitas ◽  
Vânia Luiza Deperon Bonato ◽  
Andre Moreira Pessoni ◽  
Marcio L. Rodrigues ◽  
Arturo Casadevall ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Nucleic Acids ◽  
Extracellular Vesicles ◽  
Fungal Pathogen ◽  
Fungal Infections ◽  
Pathogenic Fungi ◽  
Therapeutic Strategies ◽  
Host Immune System ◽  
Immunomodulatory Properties

ABSTRACT The release of extracellular vesicles (EVs) by fungi is a fundamental cellular process. EVs carry several biomolecules, including pigments, proteins, enzymes, lipids, nucleic acids, and carbohydrates, and are involved in physiological and pathological processes. EVs may play a pivotal role in the establishment of fungal infections, as they can interact with the host immune system to elicit multiple outcomes. It has been observed that, depending on the fungal pathogen, EVs can exacerbate or attenuate fungal infections. The study of the interaction between fungal EVs and the host immune system and understanding of the mechanisms that regulate those interactions might be useful for the development of new adjuvants as well as the improvement of protective immune responses against infectious or noninfectious diseases. In this review, we describe the immunomodulatory properties of EVs produced by pathogenic fungi and discuss their potential as adjuvants for prophylactic or therapeutic strategies.

Experimental Otitis Media in Chinchillas

1980 ◽  
Vol 89 (3_suppl) ◽  
pp. 344-350 ◽  
Author(s):  
Daniel M. Lewis ◽  
Samuel J. Meadema ◽  
James L. Schram ◽  
David J. Lim
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Otitis Media ◽  
Middle Ear ◽  
Primary Infection ◽  
Intramuscular Injection ◽  
Bacterial Suspension ◽  
Immune Mechanisms ◽  
Development Of Resistance ◽  
Type 3

Otitis media was induced in chinchillas by intrabullar injection of type 3 Streptococcus pneumoniae. It was found that the severity of a primary infection was related to the dose of bacteria injected, and animals that had recovered from a primary infection were resistant to reinfection with type 3 S pneumoniae. Middle ear effusions from infected animals contained antibodies to type 3 pneumococcal polysaccharide, whereas the sera of these animals lacked this antibody, suggesting that resistance to reinfection was due to local immune mechanisms. This idea was tested by immunizing chinchillas by various routes. Animals immunized with formalin-killed type 3 S pneumoniae by intramuscular injection (to stimulate the systemic immune system) or by intranasal inoculation (to stimulate the secretory immune system) were found to be susceptible to infection with type 3 pneumococcus, while animals immunized by inoculation of bacterial suspension directly into the middle ear were resistant to infection. In addition, we found that ampicillin treatment of a primary infection blocks the development of resistance since antibiotic-treated animals were susceptible to reinfection with the type 3 pneumococcus. These results indicate that chinchillas develop an immunity to pneumococcal otitis media following recovery from primary infection and that this immunity is mediated primarily by local immune mechanisms rather than systemic immune responses.

Leishmanial selenoproteins and the host immune system: towards new therapeutic strategies?

2020 ◽  
Vol 114 (7) ◽  
pp. 541-544
Author(s):  
Sajad Rashidi ◽  
Kurosh Kalantar ◽  
Paul Nguewa ◽  
Gholamreza Hatam
Keyword(s):  
Immune System ◽  
Adverse Effects ◽  
Immune Responses ◽  
Immune Cells ◽  
Therapeutic Strategies ◽  
Host Immune System ◽  
Host Immune Responses ◽  
Leishmania Parasites

Abstract Optimum levels of selenoproteins are essential for starting and managing the host immune responses against pathogens. According to the expression of selenoproteins in Leishmania parasites, and since high levels of selenoproteins lead to adverse effects on immune cells and their functions, Leishmania parasites might then express selenoproteins such as selenomethionine in their structure and/or secretions able to challenge the host immune system. Finally, this adaptation may lead to evasion of the parasite from the host immune system. The expression of selenoproteins in Leishmania parasites might then induce the development of infection. We therefore suggest these molecules as new therapeutic candidates for the treatment of leishmaniasis.

scholarly journals Inflammasome Activation in Bovine Peripheral Blood-Derived Macrophages Is Associated with Actin Rearrangement

Animals ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 655
Author(s):  
Amin Tahoun ◽  
Kirsty Jensen ◽  
Hanem El-Sharkawy ◽  
David Gally ◽  
Amira M. Rizk ◽  
...  
Keyword(s):  
Cell Death ◽  
Immune System ◽  
Immune Responses ◽  
Defense Mechanism ◽  
Inflammasome Activation ◽  
Host Immune System ◽  
Bovine Macrophage ◽  
The Relationship ◽  
Actin Localization ◽  
Actin Rearrangement

Inflammation is critical for infection control and acts as an arsenal defense mechanism against invading microbes through activation of the host immune system. It works via its inflammasome components to sense the dangerous invading microorganism and send messages to the immune system to destroy them. To date, the function of bovine macrophage inflammasome and its relationship with actin has not been identified. This study aimed to investigate the activation of bovine inflammasome by phase one flagellin from Salmonella typhimurium and its interaction with actin. Bovine monocyte-derived macrophages were prepared and challenged with S. typhimurium SL1344 phase one flagellin. The results demonstrated the relationship between the flagellin-based activation of inflammasome and actin rearrangement. The flagellin-based activation of inflammasome promoted the activation and co-localization of F-actin and the inflammasome complex. Actin was remodeled to different degrees according to the stage of inflammasome activation. The actin redistribution varied from polymerization to filopodia, while at the stage of pyroptotic cell death, actin was broken down and interacted with activated inflammasome complexes. In conclusion, flagellin-dependent inflammasome activation and actin localization to the inflammasome at the stage of pyroptotic cell death may be of importance for appropriate immune responses, pending further studies to explore the exact cross-linking between the inflammasome complex and actin.

scholarly journals Immunity against Helminths: Interactions with the Host and the Intercurrent Infections

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Emmanuelle Moreau ◽  
Alain Chauvin
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Chronic Infection ◽  
Inflammatory Diseases ◽  
Economic Importance ◽  
Host Immune System ◽  
Helminth Parasites ◽  
Strong Immune Response ◽  
Helminth Infections

Helminth parasites are of considerable medical and economic importance. Studies of the immune response against helminths are of great interest in understanding interactions between the host immune system and parasites. Effector immune mechanisms against tissue-dwelling helminths and helminths localized in the lumen of organs, and their regulation, are reviewed. Helminth infections are characterized by an association of Th2-like and Treg responses. Worms are able to persist in the host and are mainly responsible for chronic infection despite a strong immune response developed by the parasitized host. Two types of protection against the parasite, namely, premune and partial immunities, have been described. Immune responses against helminths can also participate in pathogenesis. Th2/Treg-like immunomodulation allows the survival of both host and parasite by controlling immunopathologic disorders and parasite persistence. Consequences of the modified Th2-like responses on co-infection, vaccination, and inflammatory diseases are discussed.

Modulation of immune responses to parasitoids by polydnaviruses

Parasitology ◽  
1998 ◽  
Vol 116 (S1) ◽  
pp. S57-S64 ◽  
Author(s):  
N. E. Beckage
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Body Cavity ◽  
The Body ◽  
Parasitoid Wasps ◽  
Host Immune System ◽  
Gene Products ◽  
Successful Development ◽  
Phenoloxidase Activity ◽  
Permanent Cell

SummaryParasitoids are parasites that invariably kill their host. Polydnaviruses are injected by parasitoid wasps into the body cavity of their insect host and cause immunosuppression, allowing the parasitoid to develop in the absence of encapsulation. One of the targets of the polydnaviruses are the haemocytes of the host, which undergo significant changes in response to entry of the virus. In some systems, haemocyte apoptosis is induced, or haemocyte clumping may be seen; in others, the cells round up and fail to adhere to a substrate. Effects on haemocytes may be transitory or permanent (cell death). Various polydnavirus gene products have been identified that interfere with normal haemocyte function. Phenoloxidase activity also is inhibited during parasitism, and the effect is inducible by polydnavirus. In some systems, venom components may act synergistically with polydnavirus in mediating the virally-induced effects on the host immune system. Polydnaviruses are powerful influences on the host immune system, which serve to permit successful development of the parasitoid without triggering the host immune response.

scholarly journals Cross-Reactive Immune Responses as Primary Drivers of Malaria Chronicity

2013 ◽  
Vol 82 (1) ◽  
pp. 140-151 ◽  
Author(s):  
Eili Y. Klein ◽  
Andrea L. Graham ◽  
Manuel Llinás ◽  
Simon Levin
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Malaria Infection ◽  
Antigenic Variation ◽  
Cross Reactivity ◽  
Primary Response ◽  
Small Subset ◽  
Host Immune System ◽  
Primary Role ◽  
Content Type

ABSTRACTThe within-host dynamics of an infection with the malaria parasitePlasmodium falciparumare the result of a complex interplay between the host immune system and parasite. Continual variation of theP. falciparumerythrocyte membrane protein (PfEMP1) antigens displayed on the surface of infected red blood cells enables the parasite to evade the immune system and prolong infection. Despite the importance of antigenic variation in generating the dynamics of infection, our understanding of the mechanisms by which antigenic variation generates long-term chronic infections is still limited. We developed a model to examine the role of cross-reactivity in generating infection dynamics that are comparable to those of experimental infections. The hybrid computational model we developed is attuned to the biology of malaria by mixing discrete replication events, which mimics the synchrony of parasite replication and invasion, with continuous interaction with the immune system. Using simulations, we evaluated the dynamics of a single malaria infection over time. We then examined three major mechanisms by which the dynamics of a malaria infection can be structured: cross-reactivity of the immune response to PfEMP1, differences in parasite clearance rates, and heterogeneity in the rate at which antigens switch. The results of our simulations demonstrate that cross-reactive immune responses play a primary role in generating the dynamics observed in experimentally untreated infections and in lengthening the period of infection. Importantly, we also find that it is the primary response to the initially expressed PfEMP1, or small subset thereof, that structures the cascading cross-immune dynamics and allows for elongation of the infection.

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