Interactions between mosses (Bryophyta) and fungi

2006 ◽  
Vol 84 (10) ◽  
pp. 1509-1519 ◽  
Author(s):  
Marie L. Davey ◽  
Randolph S. Currah
Keyword(s):  
Host Cell ◽  
Mycorrhizal Fungi ◽  
Host Responses ◽  
Fungal Propagules ◽  
Parasite Relationship ◽  
Cellular Specificity ◽  
Host Parasite ◽  
Highly Evolved

A taxonomically diverse suite of fungi interacts with bryophytes as pathogens, parasites, saprobes, and commensals. Necrotrophic pathogens such as Tephrocybe palustris (Peck) Donk and Nectria mnii Döbbeler form patches of moribund gametophytes in otherwise healthy mats of mosses. These pathogens exhibit different methods of host cell disruption; N. mnii appears to displace the host cell protoplast with intracellular hyphae, while T. palustris causes host protoplast degeneration. Host responses to infection by bryopathogens are also variable. Host–pathogen relationships can be highly evolved, as in Bryophytomyces sphagni (Navashin) Cif., in which fungal propagules replace the bryophyte spores, and exploit the explosive dispersal mechanisms of the Sphagnum host. Bryophilous parasites tend to exhibit high tissue or cellular specificity with varying host specificity. For example, Octospora similis (Kirchstein) Benkert infects the rhizoids of species of Bryum, and Discinella schimperi (Navashin) Redhead specifically colonizes the mucilage producing cells of stems of Sphagnum squarrosum Crome. Eocronartium muscicola (Pers.) Fitzp. demonstrates a highly evolved host–parasite relationship in which the basidiocarp displaces the sporophyte and is fed directly by the gametophyte through specialized transfer tissues. Fungi such as Oidiodendron maius Barron are capable of decomposing moss cell walls that are generally resistant to decomposition because of their polyphenolic component. Mycorrhizal fungi, including Glomus, Suillus, and Endogone, have not been observed to form functional, nutrient-exchanging mycorrhizal interfaces with bryophytes, rather, they function as saprobes on moribund and senescent gametophytes. Finally, endophytic fungi may provide bryophyte hosts with greater tolerance to extreme pH or promote vegetative growth. In vivo observation of bryophyte–fungus interactions has provided insight into the types of interactions that occur; however to further understand the physiology, anatomy, and etiology of these interactions, it is necessary to culture bryophilous fungi in vitro and create artificial axenic systems for study.

Cellular and immunological basis of the host-parasite relationship during infection withNeospora caninum

Parasitology ◽  
2006 ◽  
Vol 133 (3) ◽  
pp. 261-278 ◽  
Author(s):  
A. HEMPHILL ◽  
N. VONLAUFEN ◽  
A. NAGULESWARAN
Keyword(s):  
Host Cell ◽  
Cell Biology ◽  
Neospora Caninum ◽  
Host Cells ◽  
Term Survival ◽  
Prevention Of Infection ◽  
Parasite Relationship ◽  
Potential Applications

Neospora caninumis an apicomplexan parasite that is closely related toToxoplasma gondii, the causative agent of toxoplasmosis in humans and domestic animals. However, in contrast toT. gondii, N. caninumrepresents a major cause of abortion in cattle, pointing towards distinct differences in the biology of these two species. There are 3 distinct key features that represent potential targets for prevention of infection or intervention against disease caused byN. caninum. Firstly, tachyzoites are capable of infecting a large variety of host cellsin vitroandin vivo. Secondly, the parasite exploits its ability to respond to alterations in living conditions by converting into another stage (tachyzoite-to-bradyzoite orvice versa). Thirdly, by analogy withT. gondii, this parasite has evolved mechanisms that modulate its host cells according to its own requirements, and these must, especially in the case of the bradyzoite stage, involve mechanisms that ensure long-term survival of not only the parasite but also of the host cell. In order to elucidate the molecular and cellular bases of these important features ofN. caninum, cell culture-based approaches and laboratory animal models are being exploited. In this review, we will summarize the current achievements related to host cell and parasite cell biology, and will discuss potential applications for prevention of infection and/or disease by reviewing corresponding work performed in murine laboratory infection models and in cattle.

Plasmodium falciparumgrowth inhibition by human plateletsin vitro

Parasitology ◽  
1989 ◽  
Vol 99 (3) ◽  
pp. 317-322 ◽  
Author(s):  
F. Peyron ◽  
B. Polack ◽  
D. Lamotte ◽  
L. Kolodie ◽  
P. Ambroise-Thomas
Keyword(s):  
Growth Inhibition ◽  
Human Platelets ◽  
Activated Platelets ◽  
Erythrocyte Lysis ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Host Parasite ◽  
Oxygen Metabolites

SummaryPlatelets take an active part in immunological processes as well as in haemostasis, especially in the host-parasite relationship. Our aim is to assess the growth ofPlasmodium falciparum, cultured in human erythrocytes in the presence of fresh washed human platelets, since thrombocytopaenia is frequently observed during malarial infections. Our results show that platelets induce a dose-related growth inhibition ofP. falciparum. Both proliferation and maturation of intraerythrocytic stages of the parasite are inhibited. This growth inhibition is triggered by the parasite itself as neither specific antibodies nor any other components are needed to activate platelets. Activated platelets are directly toxic since complement is not involved. Furthermore, inhibition is not mediated by erythrocyte lysis or by toxic oxygen metabolites. Platelets induce an inhibition ofP.falciparumgrowth, at leastin vitro, although the importance of their role playedin vivoin malarial immunity has yet to be evaluated.

scholarly journals Host-Parasite Relationship in Cystic Echinococcosis: An Evolving Story

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Alessandra Siracusano ◽  
Federica Delunardo ◽  
Antonella Teggi ◽  
Elena Ortona
Keyword(s):  
Cystic Echinococcosis ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Recent Developments ◽  
Host Parasite ◽  
Human Cystic Echinococcosis

The larval stage ofEchinococcus granulosuscauses cystic echinococcosis, a neglected infectious disease that constitutes a major public health problem in developing countries. Despite being under constant barrage by the immune system,E. granulosusmodulates antiparasite immune responses and persists in the human hosts with detectable humoral and cellular responses against the parasite.In vitroandin vivoimmunological approaches, together with molecular biology and immunoproteomic technologies, provided us exciting insights into the mechanisms involved in the initiation ofE. granulosusinfection and the consequent induction and regulation of the immune response. Although the last decade has clarified many aspects of host-parasite relationship in human cystic echinococcosis, establishing the full mechanisms that cause the disease requires more studies. Here, we review some of the recent developments and discuss new avenues in this evolving story ofE. granulosusinfection in man.

scholarly journals Intracellular localisation of Mycobacterium tuberculosis affects efficacy of the antibiotic pyrazinamide

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Pierre Santucci ◽  
Daniel J. Greenwood ◽  
Antony Fearns ◽  
Kai Chen ◽  
Haibo Jiang ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Host Cell ◽  
Combination Chemotherapy ◽  
In Vitro Activity ◽  
In Vivo Efficacy ◽  
Human Macrophages ◽  
Ion Microscopy ◽  
Intracellular Localisation

AbstractTo be effective, chemotherapy against tuberculosis (TB) must kill the intracellular population of the pathogen, Mycobacterium tuberculosis. However, how host cell microenvironments affect antibiotic accumulation and efficacy remains unclear. Here, we use correlative light, electron, and ion microscopy to investigate how various microenvironments within human macrophages affect the activity of pyrazinamide (PZA), a key antibiotic against TB. We show that PZA accumulates heterogeneously among individual bacteria in multiple host cell environments. Crucially, PZA accumulation and efficacy is maximal within acidified phagosomes. Bedaquiline, another antibiotic commonly used in combined TB therapy, enhances PZA accumulation via a host cell-mediated mechanism. Thus, intracellular localisation and specific microenvironments affect PZA accumulation and efficacy. Our results may explain the potent in vivo efficacy of PZA, compared to its modest in vitro activity, and its critical contribution to TB combination chemotherapy.

scholarly journals Host-parasite relationship during Epistylis sp. (Ciliophora: Epistylididae) infestation in farmed cichlid and pimelodid fish

2016 ◽  
Vol 51 (5) ◽  
pp. 520-526 ◽  
Author(s):  
Santiago Benites de Pádua ◽  
Maurício Laterça Martins ◽  
Gustavo Moraes Ramos Valladão ◽  
Laura Utz ◽  
Fernando José Zara ◽  
...  
Keyword(s):  
The Body ◽  
Farmed Fish ◽  
Hydropic Degeneration ◽  
Ulcer Disease ◽  
Opportunistic Bacteria ◽  
Parasite Relationship ◽  
Hemorrhagic Ulcer ◽  
Host Parasite ◽  
Portal Of Entry

Abstract: The objective of this work was to describe the host-Epistylis sp. relationship during infestation on farmed fish. Five Nile tilapia (Oreochromis niloticus) and ten hybrid surubim catfish (Pseudoplatystoma reticulatum x P. corruscans), all diseased, were used for in vivo morphological analysis of sessile peritrichs by contrast microscopy. Fragments of infected tissues were subjected to histological processing and scanning electron microscopy. Epistylis sp. caused hemorrhagic ulcer disease, and cichlids were more prone to develop infestations throughout the body surface due to the attachment of the colonies to the scales, which did not occur with pimelodids. Multifocal granulomatous dermatitis was observed, associated with the hydropic degeneration of the epithelium and to ulcerative areas of necrosis. Microscopic examination showed the presence of bacterial microflora associated to Epistylis sp. peduncles. Therefore, this species can be considered a portal of entry for opportunistic bacteria.

scholarly journals Intracellular localisation of Mycobacterium tuberculosis affects antibiotic efficacy

2020 ◽  
Author(s):  
Pierre Santucci ◽  
Daniel J. Greenwood ◽  
Antony Fearns ◽  
Kai Chen ◽  
Haibo Jiang ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Host Cell ◽  
Combination Chemotherapy ◽  
Human Macrophage ◽  
Ion Microscopy ◽  
Antibiotic Efficacy ◽  
Subcellular Level ◽  
Intracellular Localisation

AbstractTo be effective, chemotherapy against tuberculosis (TB) must kill the intracellular population of Mycobacterium tuberculosis (Mtb). However, how host cell environments affect antibiotic accumulation and efficacy remains elusive. Pyrazinamide (PZA) is a key antibiotic against TB, yet its behaviour is not fully understood. Here, by using correlative light, electron, and ion microscopy to image PZA at the subcellular level, we investigated how human macrophage environments affect PZA activity. We discovered that PZA accumulates heterogeneously between individual bacteria in multiple host cell environments. Crucially, Mtb phagosomal localisation and acidification increase PZA accumulation and efficacy. By imaging two antibiotics commonly used in combined TB therapy, we showed that bedaquiline (BDQ) significantly enhances PZA accumulation by a host cell mediated mechanism. Thus, intracellular localisation and specific microenvironments affect PZA accumulation and efficacy; explaining the potent in vivo efficacy compared to its modest in vitro activity and the critical contribution to TB combination chemotherapy.

Chagas Disease Chemotherapy: What Do We Know So Far?

2021 ◽  
Vol 27 ◽  
Author(s):  
Aline Araujo Zuma ◽  
Wanderley de Souza
Keyword(s):  
Host Cell ◽  
Chagas Disease ◽  
Chronic Phase ◽  
Cell Types ◽  
Neglected Tropical Disease ◽  
Cell Type ◽  
Cure Rate ◽  
New Compounds

: Chagas disease is a Neglected Tropical Disease (NTD), and although endemic in Latin America, affects around 6-7 million people infected worldwide. The treatment of Chagas disease is based on benznidazole and nifurtimox, which are the only available drugs. However, they are not effective during the chronic phase and cause several side effects. Furthermore, BZ promotes cure in 80% of the patients in the acute phase, but the cure rate drops to 20% in adults in the chronic phase of the disease. In this review, we present several studies published in the last six years, which describes the antiparasitic potential of distinct drugs, from the synthesis of new compounds aiming to target the parasite, as well as the repositioning and the combination of drugs. We highlight several compounds for having shown results that are equivalent or superior to BZ, which means that they should be further studied, either in vitro or in vivo. Furthermore, we stand out the differences in the effects of BZ on the same strain of T. cruzi, which might be related to methodological differences such as parasite and cell ratios, host cell type and the time of adding the drug. In addition, we discuss the wide variety of strains and also the cell types used as a host cell, which makes it difficult to compare the trypanocidal effect of the compounds.

scholarly journals Macromolecular Synthesis Shutoff Resistance by Myeloid Cells Is Critical to IRF7-Dependent Systemic Interferon Alpha/Beta Induction after Alphavirus Infection

2019 ◽  
Vol 93 (24) ◽  
Author(s):  
Nishank Bhalla ◽  
Christina L. Gardner ◽  
Sierra N. Downs ◽  
Matthew Dunn ◽  
Chengqun Sun ◽  
...  
Keyword(s):  
Host Cell ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Cell Types ◽  
Macromolecular Synthesis ◽  
Transcription Inhibition ◽  
Antiviral Responses ◽  
Alphavirus Infection

ABSTRACT Alphavirus infection of fibroblastic cell types in vitro inhibits host cell translation and transcription, leading to suppression of interferon alpha/beta (IFN-α/β) production. However, the effect of infection upon myeloid cells, which are often the first cells encountered by alphaviruses in vivo, is unclear. Previous studies demonstrated an association of systemic IFN-α/β production with myeloid cell infection efficiency. Murine infection with wild-type Venezuelan equine encephalitis virus (VEEV), a highly myeloid-cell-tropic alphavirus, results in secretion of very high systemic levels of IFN-α/β, suggesting that stress responses in responding cells are active. Here, we infected myeloid cell cultures with VEEV to identify the cellular source of IFN-α/β, the timing and extent of translation and/or transcription inhibition in infected cells, and the transcription factors responsible for IFN-α/β induction. In contrast to fibroblast infection, myeloid cell cultures infected with VEEV secreted IFN-α/β that increased until cell death was observed. VEEV inhibited translation in most cells early after infection (<6 h postinfection [p.i.]), while transcription inhibition occurred later (>6 h p.i.). Furthermore, the interferon regulatory factor 7 (IRF7), but not IRF3, transcription factor was critical for IFN-α/β induction in vitro and in sera of mice. We identified a subset of infected Raw 264.7 myeloid cells that resisted VEEV-induced translation inhibition and secreted IFN-α/β despite virus infection. However, in the absence of IFN receptor signaling, the size of this cell population was diminished. These results indicate that IFN-α/β induction in vivo is IRF7 dependent and arises in part from a subset of myeloid cells that are resistant, in an IFN-α/β-dependent manner, to VEEV-induced macromolecular synthesis inhibition. IMPORTANCE Most previous research exploring the interaction of alphaviruses with host cell antiviral responses has been conducted using fibroblast lineage cell lines. Previous studies have led to the discovery of virus-mediated activities that antagonize host cell antiviral defense pathways, such as host cell translation and transcription inhibition and suppression of STAT1 signaling. However, their relevance and impact upon myeloid lineage cell types, which are key responders during the initial stages of alphavirus infection in vivo, have not been well studied. Here, we demonstrate the different abilities of myeloid cells to resist VEEV infection compared to nonmyeloid cell types and begin to elucidate the mechanisms by which host antiviral responses are upregulated in myeloid cells despite the actions of virus-encoded antagonists.

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