The Life Cycle and Ultrastructure of the Host Response of the Smut Pathogen, Anthracocystis destruens, on Broomcorn Millet

2021 ◽  
Author(s):  
Enguo Wu ◽  
Long Liu ◽  
Mingqi Zhu ◽  
Huiqin Wu ◽  
Qinghua Yang ◽  
...  
Keyword(s):  
Life Cycle ◽  
Host Defense ◽  
Ultrastructural Study ◽  
Host Response ◽  
Defense Responses ◽  
Symptom Development ◽  
Active Defense ◽  
Pathogen Invasion ◽  
Broomcorn Millet ◽  
Dense Deposits

Broomcorn millet smut caused by the fungus Anthracocystis destruens is one of the most destructive diseases in broomcorn millet production. The life cycle of A. destruens and host defense responses against A. destruens remain elusive. Here we investigated the disease symptom development and the parasitic process of A. destruens as well as the ultrastructure of the host-pathogen interface. The results showed that there are four typical symptoms of broomcorn millet smut, which are blackfly, cluster leaves, hedgehog head and incomplete fruiting. A. destruens colonizes all tissues of broomcorn millet but only produces teliospores in the inflorescence. After infection, A. destruens proliferates in the host likely in a systemic manner. Ultrastructural study of the infected inflorescence showed that the pathogen grows intercellularly and intracellular within the host. The host active defense response against pathogen invasion, includes host secrets callose analogs and highly electron-dense deposits to prevent pathogen infection.

scholarly journals Paracoccidioides spp. catalases and their role in antioxidant defense against host defense responses

2017 ◽  
Vol 100 ◽  
pp. 22-32 ◽  
Author(s):  
Diana Tamayo ◽  
José F. Muñoz ◽  
Agostinho J. Almeida ◽  
Juan D. Puerta ◽  
Ángela Restrepo ◽  
...  
Keyword(s):  
Host Defense ◽  
Antioxidant Defense ◽  
Defense Responses ◽  
Paracoccidioides Spp

scholarly journals Mitochondrial fusion mediated by mitofusin 1 regulates macrophage mycobactericidal activity by enhancing autophagy

2021 ◽  
Author(s):  
Yuping Ning ◽  
Yi Cai ◽  
Youchao Dai ◽  
Fuxiang Li ◽  
Siwei Mo ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Life Cycle ◽  
Atp Synthase ◽  
Host Defense ◽  
Mitochondrial Dynamics ◽  
Critical Role ◽  
Mitochondrial Fusion ◽  
Atp Production ◽  
Metabolism Pathway ◽  
Mitofusin 1

Mitochondria as a highly dynamic organelle continuously changes morphology and position during its life cycle. Mitochondrial dynamics including fission and fusion play a critical role in maintaining functional mitochondria for ATP production, which is directly linked to host defense against Mtb infection. However, how macrophages regulate mitochondrial dynamics during Mycobacterium tuberculosis (Mtb) infection remains elusive. In this study, we found that Mtb infection induced mitochondrial fusion through enhancing the expression of mitofusin 1 ( MFN1 ), which resulted in increased ATP production. Silencing MFN1 inhibited mitochondrial fusion and subsequently reduced ATP production, which, in turn, severely impaired macrophages mycobactericidal activity by inhibiting autophagy. Impairment of mycobactericidal activity and autophagy was replicated using oligomycin, an inhibitor of ATP synthase. In summary, our study revealed MFN1-mediated mitochondrial fusion is essential for macrophages mycobactericidal activity through the regulation of ATP dependent autophagy. MFN1-mediated metabolism pathway might be targets for development of host direct therapy (HDT) strategy against TB.

Histopathology of Botryosphaeria ribis in Melaleuca quinquenervia: Pathogen Invasion and Host Response

1996 ◽  
Vol 157 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Min B. Rayachhetry ◽  
George M. Blakeslee ◽  
Thomas Miller
Keyword(s):  
Host Response ◽  
Melaleuca Quinquenervia ◽  
Pathogen Invasion

scholarly journals STING signaling and host defense against microbial infection

2019 ◽  
Vol 51 (12) ◽  
pp. 1-10 ◽  
Author(s):  
Jeonghyun Ahn ◽  
Glen N. Barber
Keyword(s):  
Host Defense ◽  
Innate Immune ◽  
Type I Interferons ◽  
Type I ◽  
Microbial Infection ◽  
Immune Signaling ◽  
Pathogen Invasion ◽  
Innate Immune Signaling ◽  
Specific Pathogen ◽  
Microbial Dna

AbstractThe first line of host defense against infectious agents involves activation of innate immune signaling pathways that recognize specific pathogen-associated molecular patterns (PAMPs). Key triggers of innate immune signaling are now known to include microbial-specific nucleic acid, which is rapidly detected in the cytosol of the cell. For example, RIG-I-like receptors (RLRs) have evolved to detect viral RNA species and to activate the production of host defense molecules and cytokines that stimulate adaptive immune responses. In addition, host defense countermeasures, including the production of type I interferons (IFNs), can also be triggered by microbial DNA from bacteria, viruses and perhaps parasites and are regulated by the cytosolic sensor, stimulator of interferon genes (STING). STING-dependent signaling is initiated by cyclic dinucleotides (CDNs) generated by intracellular bacteria following infection. CDNs can also be synthesized by a cellular synthase, cGAS, following interaction with invasive cytosolic self-DNA or microbial DNA species. The importance of STING signaling in host defense is evident since numerous pathogens have developed strategies to prevent STING function. Here, we review the relevance of STING-controlled innate immune signaling in host defense against pathogen invasion, including microbial endeavors to subvert this critical process.

scholarly journals Comparative phosphoproteomic analysis of blast resistant and susceptible rice cultivars in response to salicylic acid

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ranran Sun ◽  
Shiwen Qin ◽  
Tong Zhang ◽  
Zhenzhong Wang ◽  
Huaping Li ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Molecular Mechanisms ◽  
Defense Responses ◽  
Differentially Expressed ◽  
Phosphoglycerate Mutase ◽  
Regulatory Function ◽  
Rice Cultivars ◽  
Resistance Response ◽  
Basal Resistance ◽  
Pathogen Invasion

Abstract Background Salicylic acid (SA) is a significant signaling molecule that induces rice resistance against pathogen invasion. Protein phosphorylation carries out an important regulatory function in plant defense responses, while the global phosphoproteome changes in rice response to SA-mediated defense response has not been reported. In this study, a comparative phosphoproteomic profiling was conducted by two-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS) analysis, with two near-isogenic rice cultivars after SA treatment. Results Thirty-seven phosphoprotein spots were differentially expressed after SA treatment, twenty-nine of which were identified by MALDI-TOF/TOF MS, belonging to nine functional categories. Phosphoproteins involved in photosynthesis, antioxidative enzymes, molecular chaperones were similarly expressed in the two cultivars, suggesting SA might alleviate decreases in plant photosynthesis, regulate the antioxidant defense activities, thus improving basal resistance response in both cultivars. Meanwhile, phosphoproteins related to defense, carbohydrate metabolism, protein synthesis and degradation were differentially expressed, suggesting phosphorylation regulation mediated by SA may coordinate complex cellular activities in the two cultivars. Furthermore, the phosphorylation sites of four identified phosphoproteins were verified by NanoLC-MS/MS, and phosphorylated regulation of three enzymes (cinnamoyl-CoA reductase, phosphoglycerate mutase and ascorbate peroxidase) was validated by activity determination. Conclusions Our study suggested that phosphorylation regulation mediated by SA may contribute to the different resistance response of the two cultivars. To our knowledge, this is the first report to measure rice phosphoproteomic changes in response to SA, which provides new insights into molecular mechanisms of SA-induced rice defense.

Staphylococcal enterotoxin B induces fever, brain c-Fos expression, and serum corticosterone in rats

2001 ◽  
Vol 280 (5) ◽  
pp. R1434-R1439 ◽  
Author(s):  
Lisa E. Goehler ◽  
Ron P. A. Gaykema ◽  
Michael K. Hansen ◽  
Jayme L. Kleiner ◽  
Steven F. Maier ◽  
...  
Keyword(s):  
T Cell ◽  
Host Defense ◽  
Intraperitoneal Injection ◽  
Defense Responses ◽  
Plasma Corticosterone ◽  
Significant Rise ◽  
Staphylococcal Enterotoxin ◽  
Staphylococcal Enterotoxin B ◽  
Enterotoxin B ◽  
Fos Expression

The paraventricular nucleus of the hypothalamus (PVH) occupies a pivotal point within the network of brain nuclei coordinating critical host-defense responses. In mice, T cell-dependent immune stimuli, including the bacterial superantigen staphylococcal enterotoxin B (SEB), can activate the PVH. To determine whether T cell-dependent immune stimuli activate the PVH in rats, we assessed plasma corticosterone (Cort) levels, fever responses, and c-Fos expression in the PVH in animals treated with intraperitoneal injections of SEB. In animals with previously implanted abdominal thermisters, intraperitoneal injection of 1 mg/kg SEB resulted in a significant rise in body temperature, with a latency of 3.5–4 h. In separate animals, intraperitoneal injection of 1 mg/kg SEB resulted in a significant elevation of plasma Cort and induced c-Fos expression in parvocellular neurons within the PVH. These results support the idea that T cell-dependent immune stimuli activate brain pathways mediating host-defense responses such as fever and neuroendocrine changes.

scholarly journals Immune Immunomodulation in Coronavirus Disease 2019 (COVID-19): Strategic Considerations for Personalized Therapeutic Intervention

2020 ◽  
Author(s):  
Mark W Hall ◽  
Ila Joshi ◽  
Luis Leal ◽  
Eng Eong Ooi
Keyword(s):  
Immune Response ◽  
Critical Illness ◽  
Severe Acute Respiratory Syndrome ◽  
Systemic Inflammation ◽  
Host Defense ◽  
Shortest Path ◽  
Immune Suppression ◽  
Host Response ◽  
Repair Mechanisms ◽  
Anticytokine Therapy

Abstract We are learning that the host response to severe acute respiratory syndrome coronavirus 2 ( SARS-CoV-2) infection is complex and highly dynamic. Effective initial host defense in the lung is associated with mild symptoms and disease resolution. Viral evasion of the immune response can lead to refractory alveolar damage, ineffective lung repair mechanisms, and systemic inflammation with associated organ dysfunction. The immune response in these patients is highly variable and can include moderate to severe systemic inflammation and/or marked systemic immune suppression. There is unlikely to be a “one size fits all” approach to immunomodulation in patients with coronavirus disease 2019 (COVID-19). We believe that a personalized, immunophenotype-driven approach to immunomodulation that may include anticytokine therapy in carefully selected patients and immunostimulatory therapies in others is the shortest path to success in the study and treatment of patients with critical illness due to COVID-19.

Unmasking cellular response of a bloom-forming alga to virus infection by resolving expression profiling at a single-cell level

2017 ◽  
Author(s):  
Shilo Rosenwasser ◽  
Miguel J. Frada ◽  
David Pilzer ◽  
Ron Rotkopf ◽  
Assaf Vardi
Keyword(s):  
Gene Expression ◽  
Viral Infection ◽  
Single Cell ◽  
Host Defense ◽  
Host Response ◽  
Expression Profiles ◽  
Life Cycles ◽  
Viral Gene ◽  
Single Cell Level ◽  
Cell Level

AbstractMarine viruses are major evolutionary and biogeochemical drivers of microbial life in the ocean. Host response to viral infection typically includes virus-induced rewiring of metabolic network to supply essential building blocks for viral assembly, as opposed to activation of anti-viral host defense. Nevertheless, there is a major bottleneck to accurately discern between viral hijacking strategies and host defense responses when averaging bulk population response. Here we use Emiliania huxleyi, a bloom-forming alga and its specific virus (EhV), as one of the most ecologically important host-virus model system in the ocean. Using automatic microfluidic setup to capture individual algal cells, we quantified host and virus gene expression on a single-cell resolution during the course of infection. We revealed high heterogeneity in viral gene expression among individual cells. Simultaneous measurements of expression profiles of host and virus genes at a single-cell level allowed mapping of infected cells into newly defined infection states and uncover a yet unrecognized early phase in host response that occurs prior to viral expression. Intriguingly, resistant cells emerged during viral infection, showed unique expression profiles of metabolic genes which can provide the basis for discerning between viral resistant and sensitive cells within heterogeneous populations in the marine environment. We propose that resolving host-virus arms race at a single-cell level will provide important mechanistic insights into viral life cycles and will uncover host defense strategies.

The host response to infection in the critically ill

2016 ◽  
Author(s):  
W. Joost Wiersinga ◽  
Tom van der Poll
Keyword(s):  
Critically Ill ◽  
Host Response ◽  
Inflammatory Responses ◽  
Coagulation Cascade ◽  
Microbial Infection ◽  
Pathogen Invasion ◽  
New Therapeutic Approaches ◽  
Microbial Invasion ◽  
Molecular Patterns

Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.

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