scholarly journals Ubiquitination-Mediated Inflammasome Activation during Bacterial Infection

2019 ◽  
Vol 20 (9) ◽  
pp. 2110 ◽  
Author(s):  
Tao Xu ◽  
Yu Guo ◽  
Xiaopeng Qi
Keyword(s):  
Immune Responses ◽  
Bacterial Infection ◽  
Pathogenic Bacteria ◽  
Inflammasome Activation ◽  
Post Translational Modification ◽  
Therapeutic Approaches ◽  
Host Immune Responses ◽  
Ubiquitination Machinery ◽  
Major Target ◽  
Pathogenic Infection

Inflammasome activation is essential for host immune responses during pathogenic infection and sterile signals insult, whereas excessive activation is injurious. Thus, inflammasome activation is tightly regulated at multiple layers. Ubiquitination is an important post-translational modification for orchestrating inflammatory immune responses during pathogenic infection, and a major target hijacked by pathogenic bacteria for promoting their survival and proliferation. This review summarizes recent insights into distinct mechanisms of the inflammasome activation and ubiquitination process triggered by bacterial infection. We discuss the complex regulatory of inflammasome activation mediated by ubiquitination machinery during bacterial infection, and provide therapeutic approaches for specifically targeting aberrant inflammasome activation.

scholarly journals Inflammasomes inMycobacterium tuberculosis-Driven Immunity

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Sebastian Wawrocki ◽  
Magdalena Druszczynska
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Inflammatory Response ◽  
Immune Responses ◽  
Proinflammatory Cytokines ◽  
Immune Cells ◽  
Protein Complexes ◽  
Inflammasome Activation ◽  
Host Immune Responses ◽  
Multimeric Protein

The development of effective innate and subsequent adaptive host immune responses is highly dependent on the production of proinflammatory cytokines that increase the activity of immune cells. The key role in this process is played by inflammasomes, multimeric protein complexes serving as a platform for caspase-1, an enzyme responsible for proteolytic cleavage of IL-1βand IL-18 precursors. Inflammasome activation, which triggers the multifaceted activity of these two proinflammatory cytokines, is a prerequisite for developing an efficient inflammatory response against pathogenicMycobacterium tuberculosis(M.tb). This review focuses on the role of NLRP3 and AIM2 inflammasomes inM.tb-driven immunity.

Activation of the NLRP3 and AIM2 inflammasomes in a mouse model of Schistosoma mansoni infection

2019 ◽  
Vol 94 ◽  
Author(s):  
T.T.W. Chen ◽  
P.C. Cheng ◽  
K.C. Chang ◽  
J.P. Cao ◽  
J.L. Feng ◽  
...  
Keyword(s):  
Immune Responses ◽  
Schistosoma Mansoni ◽  
Infected Mouse ◽  
Mitochondrial Damage ◽  
Carcinoma Cells ◽  
Inflammasome Activation ◽  
Host Immune Responses ◽  
Significant Release ◽  
The Relationship ◽  
Egg Antigen

Abstract Schistosomiasis is an inflammatory disease that occurs when schistosome species eggs are deposited in the liver, resulting in fibrosis and portal hypertension. Schistosomes can interact with host inflammasomes to elicit host immune responses, leading to mitochondrial damage, generation of high levels of reactive oxygen species (ROS) and activation of apoptosis during inflammation. This study aims to examine whether ROS and NF-κB (p65) expression elicited other types of inflammasome activation in Schistosoma mansoni-infected mouse livers. We examine the relationship between inflammasome activation, mitochondrial damage and ROS production in mouse livers infected with S. mansoni. We demonstrate a significant release of ROS and superoxides and increased NF-κB (p65) in S. mansoni-infected mouse livers. Moreover, activation of the NLRP3 and AIM2 inflammasomes was triggered by S. mansoni infection. Stimulation of HuH-7 hepatocellular carcinoma cells with soluble egg antigen induced activation of the AIM2 inflammasome pathway. In this study, we demonstrate that S. mansoni infection promotes both NLRP3 and AIM2 inflammasome activation.

scholarly journals Glycopeptides and -Mimetics to Detect, Monitor and Inhibit Bacterial and Viral Infections: Recent Advances and Perspectives

Molecules ◽  
2019 ◽  
Vol 24 (6) ◽  
pp. 1004 ◽  
Author(s):  
Sandra Behren ◽  
Ulrika Westerlind
Keyword(s):  
Cell Surface ◽  
Immune Responses ◽  
Viral Infections ◽  
Host Cells ◽  
Initial Contact ◽  
Host Immune Responses ◽  
Recent Advances ◽  
Multivalent Display ◽  
Important Objective ◽  
Pathogenic Infection

The initial contact of pathogens with host cells is usually mediated by their adhesion to glycan structures present on the cell surface in order to enable infection. Furthermore, glycans play important roles in the modulation of the host immune responses to infection. Understanding the carbohydrate-pathogen interactions are of importance for the development of novel and efficient strategies to either prevent, or interfere with pathogenic infection. Synthetic glycopeptides and mimetics thereof are capable of imitating the multivalent display of carbohydrates at the cell surface, which have become an important objective of research over the last decade. Glycopeptide based constructs may function as vaccines or anti-adhesive agents that interfere with the ability of pathogens to adhere to the host cell glycans and thus possess the potential to improve or replace treatments that suffer from resistance. Additionally, synthetic glycopeptides are used as tools for epitope mapping of antibodies directed against structures present on various pathogens and have become important to improve serodiagnostic methods and to develop novel epitope-based vaccines. This review will provide an overview of the most recent advances in the synthesis and application of glycopeptides and glycopeptide mimetics exhibiting a peptide-like backbone in glycobiology.

scholarly journals Myeloid Cell Sirtuin-1 Expression Does Not Alter Host Immune Responses to Gram-Negative Endotoxemia or Gram-Positive Bacterial Infection

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e84481 ◽  
Author(s):  
Laura E. Crotty Alexander ◽  
Brenda J. Marsh ◽  
Anjuli M. Timmer ◽  
Ann E. Lin ◽  
Kayvan Zainabadi ◽  
...  
Keyword(s):  
Immune Responses ◽  
Bacterial Infection ◽  
Myeloid Cell ◽  
Sirtuin 1 ◽  
Gram Positive ◽  
Gram Negative ◽  
Host Immune Responses

scholarly journals MicroRNA-30e-5p Regulates SOCS1 and SOCS3 During Bacterial Infection

2021 ◽  
Vol 10 ◽  
Author(s):  
Richa Mishra ◽  
Pandikannan Krishnamoorthy ◽  
Himanshu Kumar
Keyword(s):  
Innate Immunity ◽  
Immune Responses ◽  
Bacterial Infection ◽  
Messenger Rna ◽  
Bacterial Infections ◽  
Pathogenic Bacteria ◽  
Innate Immune ◽  
Host Cells ◽  
Microbial Infection ◽  
Major Player

Host innate immunity is the major player against continuous microbial infection. Various pathogenic bacteria adopt the strategies to evade the immunity and show resistance toward the various established therapies. Despite the advent of many antibiotics for bacterial infections, there is a substantial need for the host-directed therapies (HDTs) to combat the infection. HDTs are recently being adopted to be useful in eradicating intracellular bacterial infection. Changing the innate immune responses of the host cells alters pathogen’s ability to reside inside the cell. MicroRNAs are the small non-coding endogenous molecules and post-transcriptional regulators to target the 3’UTR of the messenger RNA. They are reported to modulate the host’s immune responses during bacterial infections. Exploiting microRNAs as a therapeutic candidate in HDTs upon bacterial infection is still in its infancy. Here, initially, we re-analyzed the publicly available transcriptomic dataset of macrophages, infected with different pathogenic bacteria and identified significant genes and microRNAs common to the differential infections. We thus identified and miR-30e-5p, to be upregulated in different bacterial infections which enhances innate immunity to combat bacterial replication by targeting key negative regulators such as SOCS1 and SOCS3 of innate immune signaling pathways. Therefore, we propose miR-30e-5p as one of the potential candidates to be considered for additional clinical validation toward HDTs.

scholarly journals Effectors from a Bacterial Vector-Borne Pathogen Exhibit Diverse Subcellular Localization, Expression Profiles and Manipulation of Plant Defense

2021 ◽  
Author(s):  
PA Reyes-Caldas ◽  
Jie Zhu ◽  
A Breakspear ◽  
SP Thapa ◽  
T Toruño ◽  
...  
Keyword(s):  
Immune Responses ◽  
Pathogenic Bacteria ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Bactericera Cockerelli ◽  
Host Immune Responses ◽  
Bacterial Vector ◽  
Citrus Huanglongbing ◽  
Liberibacter Asiaticus ◽  
Vector Borne

ABSTRACTClimate change is predicted to increase the prevalence of vector borne disease due to expansion of insect populations. Candidatus Liberibacter solanacearum (Lso) is a phloem-limited pathogen associated with multiple economically important diseases in Solanaceous crops. Little is known about the strategies and pathogenicity factors Lso uses to colonize vector and host. We determined the Lso effector repertoire by predicting SEC secreted proteins across four different Lso haplotypes. Compared with C. Liberibacter asiaticus, the causal agent of citrus Huanglongbing, Lso possess a more variable effector repertoire, with greater similarity between haplotypes infecting the same host. The localization of Lso effectors in Nicotiana revealed diverse subcellular targets. The majority of tested effectors were unable to suppress plant immune responses, indicating they possess unique activities. Expression profiling in tomato and the psyllid Bactericera cockerelli indicated Lso differentially interacts with its vector and host and can switch effector expression in response to the environment. This study reveals Lso effectors possess complex expression patterns, target diverse host organelles and the majority are unable to suppress host immune responses, unlike effectors from foliar plant pathogenic bacteria. A mechanistic understanding of Lso effector function will reveal novel targets and provide insight into phloem biology.

scholarly journals Chitin, Chitinase Responses, and Invasive Fungal Infections

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Karina Vega ◽  
Markus Kalkum
Keyword(s):  
Immune Responses ◽  
Fungal Infections ◽  
Pathogenic Fungi ◽  
Therapeutic Approaches ◽  
Human Immune System ◽  
Cell Wall Component ◽  
Diagnostic Assays ◽  
Host Immune Responses ◽  
Human Immune ◽  
Novel Therapeutic

The human immune system is capable of recognizing and degrading chitin, an important cell wall component of pathogenic fungi. In the context of host-immune responses to fungal infections, herein we review the particular contributions and interplay of fungus and chitin recognition, and chitin-degrading enzymes, known as chitinases. The mechanisms of host chitinase responses may have implications for diagnostic assays as well as novel therapeutic approaches for patients that are at risk of contracting fatal fungal infections.

scholarly journals Therapeutic Approaches for COVID-19 Based on the Interferon-mediated Immune Responses

2021 ◽  
Vol 16 ◽  
Author(s):  
Pouria Mosaddeghi ◽  
Farbod Shahabinezhad ◽  
Zahra Dehghani ◽  
Mitra Farahmandnejad ◽  
Mohammad Javad Taghipour ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Genetic Similarity ◽  
The Body ◽  
Therapeutic Approaches ◽  
Host Immune Responses ◽  
Antiviral Responses ◽  
Interferon Induction ◽  
Optimum Approach ◽  
Novel Virus

Background: As the outbreak of COVID-19 has accelerated, an urgent need for finding strategies to combat the virus is growing. Thus, gaining more knowledge on the pathogenicity mechanism of SARS-CoV-2, the causing agent of COVID-19, and its interaction with the immune system is of utmost importance. Although this novel virus is not well known yet, its structural and genetic similarity with SARS-CoV as well as the comparable pattern of age-mortality relations suggest that some previous findings on SARS could be applicable for COVID-19. Objective: The aim of this study was to investigate the most important signaling pathways activated by coronaviruses to better understand the viral pathogenesis and host immune responses. Method: Here, a systems biology study was conducted on a SARS database. It was followed by a literature review on the cognate subject. Results: It was proved that interferons may possess a crucial role in the defense against coronavirus diseases. The literature supported the validity of the employed approach and the notion that interferon induction could play a key role in the body defense against coronavirus infections. Conclusion: Altogether, administration of interferons or interferon-inducing agents in a prophylactic manner or at early stages of the disease, could mimic the effective antiviral responses against SARS-CoV-2 and reduce the disease severity. At later stages of the disease, however, the balance of the immune reactions would be disrupted and the responses would shift toward immunopathogenic over-reactions, which could be exacerbated by interferon usage. Moderating the activity of the immune system by anti-inflammatory agents, might be the optimum approach in such conditions.

scholarly journals YTHDF1 drives intestinal immune response against bacterial infection

2020 ◽  
Author(s):  
Xin Zong ◽  
Xiao Xiao ◽  
Bin Shen ◽  
Qin Jiang ◽  
Hong Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Bacterial Infection ◽  
Pathogenic Bacteria ◽  
Stop Codon ◽  
Tumor Necrosis Factor Receptor ◽  
Underlying Mechanism ◽  
Innate Immune Responses ◽  
Key Driver ◽  
Unique Mechanism

AbstractInvasion of pathogenic bacteria is a serious threat to intestinal health. Recent emerging evidence has demonstrated that N6-methyladenosine (m6A) is closely associated with innate immunity; however, the underlying mechanism remains unclear. Herein, we aim to explore the function and mechanism of m6A modification in the regulation of innate immune responses against bacterial pathogens in the intestine. Ribo-seq and m6A-seq data have demonstrated that YTHDF1, an m6A reader, directs the translation of tumor necrosis factor receptor-associated factor 6 (TRAF6) mRNA to regulate immune responses via modulation of m6A methylation near stop codon. Furthermore, we have identified a unique mechanism that the interaction between YTHDF1 and the host factor DDX60 are critical in regulating intestinal immune response against bacterial infection by recognizing TRAF6 target transcripts. Additionally, our results provide novel insights as to why YTHDF1 could recognize its unique targets using the same domain as other YTHDF proteins. This work identifies YTHDF1 as a key driver of intestinal immune responses and provides an avenue for development of novel strategies to modulate intestinal immune response against bacterial infection.

scholarly journals TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects

2017 ◽  
Vol 214 (5) ◽  
pp. 1297-1311 ◽  
Author(s):  
Min-Kyung Choo ◽  
Yasuyo Sano ◽  
Changhoon Kim ◽  
Kei Yasuda ◽  
Xiao-Dong Li ◽  
...  
Keyword(s):  
Immune Responses ◽  
Pathogenic Bacteria ◽  
Etiologic Agent ◽  
Bacterial Spore ◽  
Host Immune System ◽  
Type I ◽  
Immunostimulatory Activity ◽  
Host Immune Responses ◽  
Host Cell Response ◽  
Spore Forming Bacteria

The spores of pathogenic bacteria are involved in host entry and the initial encounter with the host immune system. How bacterial spores interact with host immunity, however, remains poorly understood. Here, we show that the spores of Bacillus anthracis (BA), the etiologic agent of anthrax, possess an intrinsic ability to induce host immune responses. This immunostimulatory activity is attributable to high amounts of RNA present in the spore surface layer. RNA-sensing TLRs, TLR7, and TLR13 in mice and their human counterparts, are responsible for detecting and triggering the host cell response to BA spores, whereas TLR2 mediates the sensing of vegetative BA. BA spores, but not vegetative BA, induce type I IFN (IFN-I) production. Although TLR signaling in itself affords protection against BA, spore RNA–induced IFN-I signaling is disruptive to BA clearance. Our study suggests a role for bacterial spore–associated RNA in microbial pathogenesis and illustrates a little known aspect of interactions between the host and spore-forming bacteria.

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