scholarly journals Host Alternative NADH:Ubiquinone Oxidoreductase Serves as a Susceptibility Factor to Promote Pathogenesis of Rhizoctonia solani in Plants

2019 ◽  
Vol 109 (10) ◽  
pp. 1741-1750 ◽  
Author(s):  
Ravi Kant ◽  
Kriti Tyagi ◽  
Srayan Ghosh ◽  
Gopaljee Jha
Keyword(s):  
Rhizoctonia Solani ◽  
Host Susceptibility ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Virus Induced Gene Silencing ◽  
Antioxidant Genes ◽  
Susceptibility Factor ◽  
Susceptibility Factors ◽  
Species Optimum ◽  
Isoflavone Reductase

Phytopathogens have evolved mechanisms to utilize host genes (commonly known as susceptibility factors) to promote their pathogenesis. Rhizoctonia solani is a highly destructive fungal pathogen of various plants, including rice. We previously reported rice genes that were differentially regulated during R. solani pathogenesis. In this study, we analyzed the role of tomato homologs of two rice genes, isoflavone reductase (IFR) and alternative NADH:ubiquinone oxidoreductase (NUOR), as potential susceptibility factors for R. solani. Virus-induced gene silencing of NUOR in tomato resulted in compromised susceptibility against R. solani, whereas IFR-silenced plants demonstrated susceptibility similar to that of control plants. NUOR silencing in tomato led to homogenous accumulation of reactive oxygen species (optimum range) upon R. solani infection. In addition, the expression and enzyme activity of some host defense and antioxidant genes was enhanced, whereas H2O2 content, lipid peroxidation, and electrolyte leakage were reduced in NUOR-silenced plants. Similarly, transient silencing of OsNUOR provided tolerance against R. solani infection in rice. Overall, the data presented in this study suggest that NUOR serves as a host susceptibility factor to promote R. solani pathogenesis.

Immunity to pathogenic free-living amoebae: role of humoral antibody

1980 ◽  
Vol 29 (2) ◽  
pp. 401-407 ◽  
Author(s):  
R T Cursons ◽  
T J Brown ◽  
E A Keys ◽  
K M Moriarty ◽  
D Till
Keyword(s):  
New Zealand ◽  
Immunoglobulin M ◽  
Host Susceptibility ◽  
Free Living ◽  
Protective Mechanisms ◽  
Susceptibility Factors ◽  
Human Sera ◽  
Normal Human ◽  
Health Districts

Pathogenic free-living amoebae are common in nature, but few clinical infections by these amoebae have been reported. This has prompted studies of host susceptibility factors in humans. A survey of normal human sera from three New Zealand Health Districts was made; antibodies to pathogenic free-living amoebae were found in all sera, with titers ranging from 1:5 to 1:20 for Naegleria spp. and from 1:20 to 1:80 for Acanthamoeba spp. The antibodies belonged mainly to immunoglobulin G and immunoglobulin M classes. The presence of a specific neutralizing factor against Acanthamoeba spp. but not Naegleria spp. was demonstrated. Possible protective mechanisms are discussed.

scholarly journals Obesity-Induced Dysbiosis Exacerbates IFN-γ Production and Pulmonary Inflammation in the Mycobacterium tuberculosis Infection

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1732
Author(s):  
Sandra Patricia Palma Albornoz ◽  
Thais Fernanda de Campos Fraga-Silva ◽  
Ana Flávia Gembre ◽  
Rômulo Silva de Oliveira ◽  
Fernanda Mesquita de Souza ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Gut Microbiota ◽  
Inflammatory Diseases ◽  
Pulmonary Inflammation ◽  
Host Susceptibility ◽  
Chronic Infections ◽  
Mycobacterium Tuberculosis Infection ◽  
Pulmonary Damage ◽  
Ifn Γ

The microbiota of the gut–lung axis affects local and far-reaching immune responses and might also trigger chronic and inflammatory diseases. We hypothesized that gut dysbiosis induced by obesity, which coexists in countries with a high tuberculosis burden, aggravates the host susceptibility and the pulmonary damage tolerance. To assess our hypothesis, we used a model of high-fat diet (HFD)-induced obesity, followed by infection of C57BL/6 mice with Mycobacterium tuberculosis. We showed that obesity increased the susceptibility, the pulmonary inflammation and IFN-γ levels in M. tuberculosis-infected mice. During the comorbidity obesity and tuberculosis, there is an increase of Bacteroidetes and Firmicutes in the lungs, and an increase of Firmicutes and butyrate in the feces. Depletion of gut microbiota by antibiotic treatment in the obese infected mice reduced the frequencies of CD4+IFN-γ+IL-17− cells and IFN-γ levels in the lungs, associated with an increase of Lactobacillus. Our findings reinforce the role of the gut–lung axis in chronic infections and suggest that the gut microbiota modulation may be a potential host-directed therapy as an adjuvant to treat TB in the context of IFN-γ-mediated immunopathology.

scholarly journals Intestinal Microbiota as an Alternative Therapeutic Target for Epilepsy

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Jiaying Wu ◽  
Yuyu Zhang ◽  
Hongyu Yang ◽  
Yuefeng Rao ◽  
Jing Miao ◽  
...  
Keyword(s):  
Immune Responses ◽  
Intestinal Microbiota ◽  
Neurological Disorders ◽  
Digestive System ◽  
Hygiene Hypothesis ◽  
Host Susceptibility ◽  
Immune Disorders ◽  
The Central Nervous System ◽  
Symbiotic Microbiota

Epilepsy is one of the most widespread serious neurological disorders, and an aetiological explanation has not been fully identified. In recent decades, a growing body of evidence has highlighted the influential role of autoimmune mechanisms in the progression of epilepsy. The hygiene hypothesis draws people’s attention to the association between gut microbes and the onset of multiple immune disorders. It is also believed that, in addition to influencing digestive system function, symbiotic microbiota can bidirectionally and reversibly impact the programming of extraintestinal pathogenic immune responses during autoimmunity. Herein, we investigate the concept that the diversity of parasitifer sensitivity to commensal microbes and the specific constitution of the intestinal microbiota might impact host susceptibility to epilepsy through promotion of Th17 cell populations in the central nervous system (CNS).

scholarly journals Oxidative stress promotes liver cancer metastasis via a PKA-activated RNF25/ECAD/YAP circuit

2022 ◽  
Author(s):  
Zhao Huang ◽  
Li Zhou ◽  
Jiufei Duan ◽  
Siyuan Qin ◽  
Yu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Metastasis ◽  
Anoikis Resistance ◽  
Antioxidant Genes ◽  
Redox Sensor ◽  
Stress Signals ◽  
Hcc Cells

Abstract Loss of E-cadherin (ECAD), often caused by epigenetic inactivation, is closely associated with tumor metastasis. However, how ECAD is regulated in response to oxidative stress during tumorigenesis is largely unknown. Here we identify RNF25 as a new E3 ligase of ECAD, whose activation by oxidative stress leads to ECAD protein degradation in hepatocellular carcinoma (HCC). Loss of ECAD activates YAP, which in turn promotes the transcription of RNF25, thus forming a positive feedback loop to sustain the ECAD downregulation. YAP activation mitigates oxidative stress in detached HCC cells by upregulating antioxidant genes, protecting detached HCC cells from ferroptosis, resulting in anoikis resistance. Mechanistically, we found that protein kinase A (PKA) senses oxidative stress by redox modification in its β catalytic subunit (PRKACB) at Cys200 and Cys344, which increases its kinase activity towards RNF25 phosphorylation at Ser450, facilitating RNF25-mediated degradation of ECAD. Moreover, RNF25 expression is associated with HCC metastasis and depletion of RNF25 is sufficient to diminish HCC invasion and metastasis in vitro and in vivo. Together, these results identify a dual role of RNF25 as a critical regulator of ECAD protein turnover, promoting both anoikis resistance and metastasis, and PKA is a necessary redox sensor to enable this process. Our study provides mechanistic insight into how tumor cells sense oxidative stress signals to spread while escaping cell death.

scholarly journals Oomycetes Seek Help from the Plant: Phytophthora infestans Effectors Target Host Susceptibility Factors

2016 ◽  
Vol 9 (5) ◽  
pp. 636-638 ◽  
Author(s):  
Petra C. Boevink ◽  
Hazel McLellan ◽  
Eleanor M. Gilroy ◽  
Shaista Naqvi ◽  
Qin He ◽  
...  
Keyword(s):  
Phytophthora Infestans ◽  
Host Susceptibility ◽  
Susceptibility Factors

scholarly journals Multiple Sclerosis and Obesity: Possible Roles of Adipokines

2016 ◽  
Vol 2016 ◽  
pp. 1-24 ◽  
Author(s):  
José de Jesús Guerrero-García ◽  
Lucrecia Carrera-Quintanar ◽  
Rocío Ivette López-Roa ◽  
Ana Laura Márquez-Aguirre ◽  
Argelia Esperanza Rojas-Mayorquín ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Early Life ◽  
Neural Tissue ◽  
Autoimmune Disorder ◽  
Susceptibility Factor ◽  
Related Risk ◽  
Inflammatory State ◽  
The Central Nervous System ◽  
Ms Pathogenesis

Multiple Sclerosis (MS) is an autoimmune disorder of the Central Nervous System that has been associated with several environmental factors, such as diet and obesity. The possible link between MS and obesity has become more interesting in recent years since the discovery of the remarkable properties of adipose tissue. Once MS is initiated, obesity can contribute to increased disease severity by negatively influencing disease progress and treatment response, but, also, obesity in early life is highly relevant as a susceptibility factor and causally related risk for late MS development. The aim of this review was to discuss recent evidence about the link between obesity, as a chronic inflammatory state, and the pathogenesis of MS as a chronic autoimmune and inflammatory disease. First, we describe the main cells involved in MS pathogenesis, both from neural tissue and from the immune system, and including a new participant, the adipocyte, focusing on their roles in MS. Second, we concentrate on the role of several adipokines that are able to participate in the mediation of the immune response in MS and on the possible cross talk between the latter. Finally, we explore recent therapy that involves the transplantation of adipocyte precursor cells for the treatment of MS.

scholarly journals Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70

2018 ◽  
Vol 115 (33) ◽  
pp. E7834-E7843 ◽  
Author(s):  
Qin He ◽  
Shaista Naqvi ◽  
Hazel McLellan ◽  
Petra C. Boevink ◽  
Nicolas Champouret ◽  
...  
Keyword(s):  
Late Blight ◽  
Plant Pathogens ◽  
Dominant Negative ◽  
Host Protein ◽  
Host Susceptibility ◽  
Dominant Negative Mutant ◽  
Virus Induced Gene Silencing ◽  
Pathogen Effector ◽  
Late Blight Disease ◽  
Blight Disease

Plant pathogens deliver effectors into plant cells to suppress immunity. Whereas many effectors inactivate positive immune regulators, other effectors associate with negative regulators of immunity: so-called susceptibility (S) factors. Little is known about how pathogens exploit S factors to suppress immunity. Phytophthora infestans RXLR effector Pi02860 interacts with host protein NRL1, which is an S factor whose activity suppresses INF1-triggered cell death (ICD) and is required for late blight disease. We show that NRL1 interacts in yeast and in planta with a guanine nucleotide exchange factor called SWAP70. SWAP70 associates with endosomes and is a positive regulator of immunity. Virus-induced gene silencing of SWAP70 in Nicotiana benthamiana enhances P. infestans colonization and compromises ICD. In contrast, transient overexpression of SWAP70 reduces P. infestans infection and accelerates ICD. Expression of Pi02860 and NRL1, singly or in combination, results in proteasome-mediated degradation of SWAP70. Degradation of SWAP70 is prevented by silencing NRL1, or by mutation of Pi02860 to abolish its interaction with NRL1. NRL1 is a BTB-domain protein predicted to form the substrate adaptor component of a CULLIN3 ubiquitin E3 ligase. A dimerization-deficient mutant, NRL1NQ, fails to interact with SWAP70 but maintains its interaction with Pi02860. NRL1NQ acts as a dominant-negative mutant, preventing SWAP70 degradation in the presence of effector Pi02860, and reducing P. infestans infection. Critically, Pi02860 enhances the association between NRL1 and SWAP70 to promote proteasome-mediated degradation of the latter and, thus, suppress immunity. Preventing degradation of SWAP70 represents a strategy to combat late blight disease.

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