Triggering and modulation of the host-parasite interplay byEchinococcus multilocularis: a review

SUMMARYAs more facts emerge regarding the ways in whichE. multilocularis-derived molecules trigger the host immune response and modulate the host-parasite interplay, it becomes possible to envisage how the parasite can survive and proliferate in its intermediate host, while in other hosts it dies out. Through effects on cells of both the innate and adaptive arms of the immune response,E. multiloculariscan orchestrate a range of outcomes that are beneficial not only to the parasite, in terms of facilitating its intrahepatic proliferation and maturation, and thus life cycle over all, but also to its intermediate host, in limiting pathology. The present review deals with the role of metacestode surface molecules as well as excretory/secretory (E/S) metabolic products of the parasite in the modulation of the host responses such as to optimize its own survival.

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The possible role of the frontal and sub-parietal gland systems of the pentastomidReighardia sternae(Diesing, 1864) in the evasion of the host immune response

Parasitology ◽

10.1017/s0031182000048587 ◽

1979 ◽

Vol 78 (1) ◽

pp. 53-66 ◽

Cited By ~ 19

Author(s):

J. Riley ◽

J. L. James ◽

A. A. Banaja

Keyword(s):

Immune Response ◽

Alternative Explanation ◽

Surface Membrane ◽

Membrane System ◽

Host Immune Response ◽

Entire Surface ◽

Strong Immune Response ◽

Concomitant Immunity ◽

Host Parasite

SUMMARYThe frontal and sub-parietal glands of the pentastomidReighardia sternaeelaborate lamellate secretion which is poured on to the cuticle. The entire surface of the cuticle, including the mouth, hook pits and reproductive apertures, is coated with secretion. Electron microscope studies indicate that the glands are continuously active, which implies a turnover of surface membranes. The postulated function of these membranes is to protect certain vital areas of the host–parasite interface, notably the pores of ion-transporting cells, from the host immune response. The available evidence suggests that pentastomids do evoke a strong immune response but since most are long-lived they must circumvent it. We believe the surface membrane system to be instrumental in this. Studies on another pentastomid,Porocephalus crotaliin rats have shown that an immune response stimulated by a primary infection will kill subsequent infections and that the surface membranes are strongly immunogenic. Obvious parallels between this situation and that of schistosome infections in mammals are discussed. An alternative explanation of concomitant immunity is proposed.

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Role of Virally-Encoded Deubiquitinating Enzymes in Regulation of the Virus Life Cycle

International Journal of Molecular Sciences ◽

10.3390/ijms22094438 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4438

Author(s):

Jessica Proulx ◽

Kathleen Borgmann ◽

In-Woo Park

Keyword(s):

Immune Response ◽

Life Cycle ◽

Deubiquitinating Enzyme ◽

Deubiquitinating Enzymes ◽

Antiviral Immune Response ◽

Cellular Processes ◽

Virus Life Cycle ◽

Infected Cells ◽

Dependent Processes

The ubiquitin (Ub) proteasome system (UPS) plays a pivotal role in regulation of numerous cellular processes, including innate and adaptive immune responses that are essential for restriction of the virus life cycle in the infected cells. Deubiquitination by the deubiquitinating enzyme, deubiquitinase (DUB), is a reversible molecular process to remove Ub or Ub chains from the target proteins. Deubiquitination is an integral strategy within the UPS in regulating survival and proliferation of the infecting virus and the virus-invaded cells. Many viruses in the infected cells are reported to encode viral DUB, and these vial DUBs actively disrupt cellular Ub-dependent processes to suppress host antiviral immune response, enhancing virus replication and thus proliferation. This review surveys the types of DUBs encoded by different viruses and their molecular processes for how the infecting viruses take advantage of the DUB system to evade the host immune response and expedite their replication.

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Mycobacterium tuberculosis adhesins: potential biomarkers as anti-tuberculosis therapeutic and diagnostic targets

Microbiology ◽

10.1099/mic.0.082206-0 ◽

2014 ◽

Vol 160 (9) ◽

pp. 1821-1831 ◽

Cited By ~ 22

Author(s):

Viveshree S. Govender ◽

Saiyur Ramsugit ◽

Manormoney Pillay

Keyword(s):

Immune Response ◽

Mycobacterium Tuberculosis ◽

Control Strategies ◽

Host Cells ◽

Tuberculosis Control ◽

Surface Molecules ◽

Host Pathogen Interaction ◽

Bacterial Aggregation ◽

Insight Into

Adhesion to host cells is a precursor to host colonization and evasion of the host immune response. Conversely, it triggers the induction of the immune response, a process vital to the host’s defence against infection. Adhesins are microbial cell surface molecules or structures that mediate the attachment of the microbe to host cells and thus the host–pathogen interaction. They also play a crucial role in bacterial aggregation and biofilm formation. In this review, we discuss the role of adhesins in the pathogenesis of the aetiological agent of tuberculosis, Mycobacterium tuberculosis. We also provide insight into the structure and characteristics of some of the characterized and putative M. tuberculosis adhesins. Finally, we examine the potential of adhesins as targets for the development of tuberculosis control strategies.

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Immunity and its role in periodontal diseases

Romanian Journal of Stomatology ◽

10.37897/rjs.2017.1.4 ◽

2017 ◽

Vol 63 (1) ◽

pp. 24-27

Author(s):

Irina Dumitrache ◽

Keyword(s):

Immune Response ◽

Chronic Disease ◽

Periodontal Disease ◽

Clinical Efficacy ◽

Periodontal Diseases ◽

Adult Population ◽

Host Immune Response ◽

Immunomodulatory Therapy ◽

Common Chronic Disease

Periodontal disease is one of the most common chronic disease, with a prevalence between 5% and 30% in adult population aged 25-75. In the pathogenesis of periodontal disease, the host immune response has a great importance and in the last years it has been underlined the role of immunomodulatory therapy in the management of periodontal disease. Septilin is a herbal immunomodulatory with clinical efficacy proven in the periodontal disease.

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Role of Host Immune Response and Viral Load in the Differential Outcome of Pandemic H1N1 (2009) Influenza Virus Infection in Indian Patients

PLoS ONE ◽

10.1371/journal.pone.0013099 ◽

2010 ◽

Vol 5 (10) ◽

pp. e13099 ◽

Cited By ~ 54

Author(s):

Vidya A. Arankalle ◽

Kavita S. Lole ◽

Ravi P. Arya ◽

Anuradha S. Tripathy ◽

Ashwini Y. Ramdasi ◽

...

Keyword(s):

Immune Response ◽

Influenza Virus ◽

Viral Load ◽

Virus Infection ◽

Influenza Virus Infection ◽

Host Immune Response ◽

Pandemic H1n1 ◽

Differential Outcome ◽

Pandemic H1n1 2009

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Experimental life cycle of Lagochilascaris minor Leiper, 1909

Revista do Instituto de Medicina Tropical de São Paulo ◽

10.1590/s0036-46651992000400003 ◽

1992 ◽

Vol 34 (4) ◽

pp. 277-287 ◽

Cited By ~ 34

Author(s):

Dulcinéa Maria Barbosa Campos ◽

Lindomar G. Freire Filha ◽

Miguel Alípio Vieira ◽

Julieta Machado Paçô ◽

Moacir A. Maia

Keyword(s):

Life Cycle ◽

Intermediate Host ◽

Subcutaneous Tissue ◽

Cervical Region ◽

Parasite Development ◽

Mature Stage ◽

Post Inoculation ◽

Skeletal Musculature ◽

Third Stage

The life cycle of Lagochilascaris minor was studied using material collected from human lesion and applying the experimental model: rodents (mice, hamsters), and carnivorae (cats, dogs). In mice given infective eggs, orally, hatch of the third stage larvae was noted in the gut wall, with migration to liver, lungs, skeletal musculature and subcutaneous tissue becoming, soon after, encysted. In cats infected with skinned carcasses of mice (60 to 235 days of infection) it was observed: hatch of third stage larvae from the nodules (cysts) in the stomach, migration through the oesophagus, pharynx, trachea, related tissues (rhino-oropharynx), and cervical lymphonodes developing to the mature stage in any of these sites on days 9-20 post inoculation (P.I.). There was no parasite development up to the mature stage in cats inoculated orally with infective eggs, which indicates that the life cycle of this parasite includes an obligatory intermediate host. In one of the cats (fed carcass of infected mice) necropsied on day 43 P.I., it was observed the occurence of the self-infective cycle of L. minor in the lung tissues and in the cervical region which was characterized by the finding of eggs in different stages of development, third stage larvae and mature worms. It's believed that some component of the carnivorae gastrointestinal tracts may preclude the development of third stage larvae from L. minor eggs what explains the interruption of the life cycle in animals fed infective eggs. It's also pointed out the role of the intermediate host in the first stages of the life cycle of this helminth.

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Role of DNA repair in host immune response and inflammation

Mutation Research/Reviews in Mutation Research ◽

10.1016/j.mrrev.2014.11.004 ◽

2015 ◽

Vol 763 ◽

pp. 246-257 ◽

Cited By ~ 15

Author(s):

Fabrícia Lima Fontes ◽

Daniele Maria Lopes Pinheiro ◽

Ana Helena Sales de Oliveira ◽

Rayssa Karla de Medeiros Oliveira ◽

Tirzah Braz Petta Lajus ◽

...

Keyword(s):

Immune Response ◽

Dna Repair ◽

Host Immune Response

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Review on the Role of Host Immune Response in Protection and Immunopathogenesis during Cutaneous Leishmaniasis Infection

Journal of Immunology Research ◽

10.1155/2020/2496713 ◽

2020 ◽

Vol 2020 ◽

pp. 1-12

Author(s):

Teshager Dubie ◽

Yasin Mohammed

Keyword(s):

Immune Response ◽

Cutaneous Leishmaniasis ◽

Proinflammatory Cytokines ◽

Parasitic Infection ◽

Host Immune Response ◽

Immune Defense ◽

Host Cells ◽

Infected Host ◽

Major Public Health Problem

Cutaneous leishmaniasis (CL) is a major public health problem worldwide and spreads to human via the bite of sand flies during blood meal. Following its inoculation, the promastigotes are immediately taken up by phagocytic cells and these leishmania-infected host cells produce proinflammatory cytokines that activate other immune cells and these infected host cells produce more cytokines and reactive nitrogen and oxygen species for efficient control of leishmania infection. Many experimental studies showed that resistance to infection with leishmania paraites is associated with the production of proinflammatory cytokines and activation of CD4+ Th1 response. On the other hand, vulnerability to this parasitic infection is correlated to production of T helper 2 cytokines that facilitate persistence of parasites and disease progression. In addition, some studies have also indicated that CD8+ T cells play a vital role in immune defense through cytokine production and their cytotoxic activity and excessive production of proinflammatory mediators promote amplified recruitment of cells. This could be correlated with excessive inflammatory reaction and ultimately resulted in tissue destruction and development of immunopathogenesis. Thus, there are contradictions regarding the role of immune responses in protection and immunopathogenesis of CL disease. Therefore, the aim of this paper was to review the role of host immune response in protection and its contribution to disease severity for CL infection. In order to obtain more meaningful data regarding the nature of immune response to leishmania, further in-depth studies focused on immune modulation should be conducted to develop better therapeutic strategies.

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Malaria and red cell genetic defects

Blood ◽

10.1182/blood.v74.4.1213.1213 ◽

1989 ◽

Vol 74 (4) ◽

pp. 1213-1221 ◽

Cited By ~ 75

Author(s):

RL Nagel ◽

EF Jr Roth

Keyword(s):

Culture System ◽

Potential Role ◽

Dna Analysis ◽

Red Cell ◽

Metabolic Products ◽

Recombinant Technology ◽

Host Parasite ◽

Made In

Abstract The study of inherited RBC resistance to malaria has increased our knowledge of the biochemistry and physiology of the host-parasite interaction and suggested potential sites for therapeutic intervention. Discovery by Jensen and Trager of the in vitro culture system for P falciparum has facilitated research in this area. Known RBC defects may affect invasion, growth, or merozoite liberation (Fig 1). Significant advances made in understanding mechanisms underlying protection against malaria should not obscure the fact that the data are far from complete. More knowledge is needed about the influence of the erythrocyte cytoskeleton on invasion and growth of parasites as well as the potential role of phospholipids, erythrocyte enzymes other than G6PD, or other metabolic products. Application of DNA analysis and recombinant technology may have an increasing impact on study of the interaction of RBC defects with malarial parasites.

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