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.

scholarly journals Role of Alternative Splicing in Regulating Host Response to Viral Infection

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1720
Author(s):  
Kuo-Chieh Liao ◽  
Mariano A. Garcia-Blanco
Keyword(s):  
Innate Immunity ◽  
Alternative Splicing ◽  
Immune Responses ◽  
Viral Infection ◽  
Rna Splicing ◽  
Type I ◽  
Host Immune Responses ◽  
Transcriptional Regulatory Mechanisms ◽  
Host Virus Interactions

The importance of transcriptional regulation of host genes in innate immunity against viral infection has been widely recognized. More recently, post-transcriptional regulatory mechanisms have gained appreciation as an additional and important layer of regulation to fine-tune host immune responses. Here, we review the functional significance of alternative splicing in innate immune responses to viral infection. We describe how several central components of the Type I and III interferon pathways encode spliced isoforms to regulate IFN activation and function. Additionally, the functional roles of splicing factors and modulators in antiviral immunity are discussed. Lastly, we discuss how cell death pathways are regulated by alternative splicing as well as the potential role of this regulation on host immunity and viral infection. Altogether, these studies highlight the importance of RNA splicing in regulating host–virus interactions and suggest a role in downregulating antiviral innate immunity; this may be critical to prevent pathological inflammation.

scholarly journals Protective and Pathogenic Immune Responses to Cutaneous Leishmaniasis

2021 ◽  
Author(s):  
Elina Panahi ◽  
Danielle I. Stanisic ◽  
Christopher S. Peacock ◽  
Lara J. Herrero
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Cutaneous Leishmaniasis ◽  
Adaptive Immune Response ◽  
Leishmania Parasite ◽  
Host Immune System ◽  
Phagocytic Cells ◽  
Host Immune Responses ◽  
Outcome Severity ◽  
Common Clinical Presentation

Leishmania (Kinetoplastida: Trypanosomatidae) parasites are known to cause a broad spectrum of clinical diseases in humans, collectively known as the leishmaniases. Cutaneous leishmaniasis is the most common clinical presentation with varying degrees of severity largely driven by host immune responses, specifically the interplay between innate and adaptive immune response. The establishment of a T lymphocyte driven cell-mediated immune response, leading to activated phagocytic cells, leading to Leishmania parasite killing and control of infection. Alternatively, the Leishmania parasite manipulates the host immune system, enabling parasite proliferation and clinical disease. Here we review how the cumulative interactions of different aspects of the host immune response determines disease outcome, severity, and immunity to re-infection.

An appraisal of survival strategies

Parasitology ◽  
1984 ◽  
Vol 88 (4) ◽  
pp. 575-577 ◽  
Author(s):  
N. A. Mitchison
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Survival Strategies ◽  
Host Immune System ◽  
Cellular Immunology ◽  
Host Immune Responses ◽  
Host Defence System ◽  
Bio Engineering

Only a few years ago parasite immunology looked an unattractive subject better left to the dogged specialists. Parasites and hosts had been playing chess together for a million years, and there seemed little prospect of perturbing matters in favour of the host immune system. All that has changed, for three reasons. Firstly, we have learned how to grow at least some parasites in vitro, and prospects of doing so with others are encouraging. Secondly, progress in cellular immunology has revealed the sort of loopholes in the host defence system which parasites are likely to exploit: we are learning the questions which matter about parasites as antigens. Thirdly, and most importantly, molecular genetics is being brought to bear on parasites: we can now see a real, though long-term, prospect of manufacturing practicable vaccines through bio-engineering, and more immediately it gives us the tools needed to probe the host immune responses in the form of cloned antigens.

Leishmanial selenoproteins and the host immune system: towards new therapeutic strategies?

2020 ◽  
Vol 114 (7) ◽  
pp. 541-544
Author(s):  
Sajad Rashidi ◽  
Kurosh Kalantar ◽  
Paul Nguewa ◽  
Gholamreza Hatam
Keyword(s):  
Immune System ◽  
Adverse Effects ◽  
Immune Responses ◽  
Immune Cells ◽  
Therapeutic Strategies ◽  
Host Immune System ◽  
Host Immune Responses ◽  
Leishmania Parasites

Abstract Optimum levels of selenoproteins are essential for starting and managing the host immune responses against pathogens. According to the expression of selenoproteins in Leishmania parasites, and since high levels of selenoproteins lead to adverse effects on immune cells and their functions, Leishmania parasites might then express selenoproteins such as selenomethionine in their structure and/or secretions able to challenge the host immune system. Finally, this adaptation may lead to evasion of the parasite from the host immune system. The expression of selenoproteins in Leishmania parasites might then induce the development of infection. We therefore suggest these molecules as new therapeutic candidates for the treatment of leishmaniasis.

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 Immune Responses in Hookworm Infections

2001 ◽  
Vol 14 (4) ◽  
pp. 689-703 ◽  
Author(s):  
Alex Loukas ◽  
Paul Prociv
Keyword(s):  
Immune Responses ◽  
Immunoglobulin E ◽  
Age Groups ◽  
Immunomodulatory Activity ◽  
Type I ◽  
Host Immune Responses ◽  
Tropical Conditions ◽  
Ancylostoma Duodenale ◽  
Key Aspects ◽  
Hookworm Infections

SUMMARY Hookworms infect perhaps one-fifth of the entire human population, yet little is known about their interaction with our immune system. The two major species are Necator americanus, which is adapted to tropical conditions, and Ancylostoma duodenale, which predominates in more temperate zones. While having many common features, they also differ in several key aspects of their biology. Host immune responses are triggered by larval invasion of the skin, larval migration through the circulation and lungs, and worm establishment in the intestine, where adult worms feed on blood and mucosa while injecting various molecules that facilitate feeding and modulate host protective responses. Despite repeated exposure, protective immunity does not seem to develop in humans, so that infections occur in all age groups (depending on exposure patterns) and tend to be prolonged. Responses to both larval and adult worms have a characteristic T-helper type 2 profile, with activated mast cells in the gut mucosa, elevated levels of circulating immunoglobulin E, and eosinoophilia in the peripheral blood and local tissues, features also characteristic of type I hypersensitivity reactions. The longevity of adult hookworms is determined probably more by parasite genetics than by host immunity. However, many of the proteins released by the parasites seem to have immunomodulatory activity, presumably for self-protection. Advances in molecular biotechnology enable the identification and characterization of increasing numbers of these parasite molecules and should enhance our detailed understanding of the protective and pathogenetic mechanisms in hookworm infections.

scholarly journals Evolution of animal immunity in the light of beneficial symbioses

2020 ◽  
Vol 375 (1808) ◽  
pp. 20190601 ◽  
Author(s):  
Nicole M. Gerardo ◽  
Kim L. Hoang ◽  
Kayla S. Stoy
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Host Immune System ◽  
System Evolution ◽  
Symbiotic Associations ◽  
Host Immune Responses ◽  
Immune System Evolution ◽  
System Maintenance ◽  
Key Aspects ◽  
Host Evolution

Immune system processes serve as the backbone of animal defences against pathogens and thus have evolved under strong selection and coevolutionary dynamics. Most microorganisms that animals encounter, however, are not harmful, and many are actually beneficial. Selection should act on hosts to maintain these associations while preventing exploitation of within-host resources. Here, we consider how several key aspects of beneficial symbiotic associations may shape host immune system evolution. When host immunity is used to regulate symbiont populations, there should be selection to evolve and maintain targeted immune responses that recognize symbionts and suppress but not eliminate symbiont populations. Associating with protective symbionts could relax selection on the maintenance of redundant host-derived immune responses. Alternatively, symbionts could facilitate the evolution of host immune responses if symbiont-conferred protection allows for persistence of host populations that can then adapt. The trajectory of immune system evolution will likely differ based on the type of immunity involved, the symbiont transmission mode and the costs and benefits of immune system function. Overall, the expected influence of beneficial symbiosis on immunity evolution depends on how the host immune system interacts with symbionts, with some interactions leading to constraints while others possibly relax selection on immune system maintenance. This article is part of the theme issue ‘The role of the microbiome in host evolution’.

scholarly journals Plasmodium yoelii Erythrocyte-Binding-like Protein Modulates Host Cell Membrane Structure, Immunity, and Disease Severity

mBio ◽  
2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yu-chih Peng ◽  
Yanwei Qi ◽  
Cui Zhang ◽  
Xiangyu Yao ◽  
Jian Wu ◽  
...  
Keyword(s):  
Immune Responses ◽  
Disease Severity ◽  
Type I Interferon ◽  
Control Strategies ◽  
Plasmodium Yoelii ◽  
Type I ◽  
Parasite Invasion ◽  
Content Type ◽  
Host Immune Responses ◽  
Erythrocyte Binding

ABSTRACT Erythrocyte-binding-like (EBL) proteins are known to play an important role in malaria parasite invasion of red blood cells (RBCs); however, any roles of EBL proteins in regulating host immune responses remain unknown. Here, we show that Plasmodium yoelii EBL (PyEBL) can shape disease severity by modulating the surface structure of infected RBCs (iRBCs) and host immune responses. We identified an amino acid substitution (a change of C to Y at position 741 [C741Y]) in the protein trafficking domain of PyEBL between isogenic P. yoellii nigeriensis strain N67 and N67C parasites that produce different disease phenotypes in C57BL/6 mice. Exchanges of the C741Y alleles altered parasite growth and host survival accordingly. The C741Y substitution also changed protein processing and trafficking in merozoites and in the cytoplasm of iRBCs, reduced PyEBL binding to band 3, increased phosphatidylserine (PS) surface exposure, and elevated the osmotic fragility of iRBCs, but it did not affect invasion of RBCs in vitro. The modified iRBC surface triggered PS-CD36-mediated phagocytosis of iRBCs, host type I interferon (IFN-I) signaling, and T cell differentiation, leading to improved host survival. This study reveals a previously unknown role of PyEBL in regulating host-pathogen interaction and innate immune responses, which may be explored for developing disease control strategies. IMPORTANCE Malaria is a deadly parasitic disease that continues to afflict hundreds of millions of people every year. Infections with malaria parasites can be asymptomatic, with mild symptoms, or fatal, depending on a delicate balance of host immune responses. Malaria parasites enter host red blood cells (RBCs) through interactions between parasite ligands and host receptors, such as erythrocyte-binding-like (EBL) proteins and host Duffy antigen receptor for chemokines (DARC). Plasmodium yoelii EBL (PyEBL) is known to play a role in parasite invasion of RBCs. Here, we show that PyEBL also affects disease severity through modulation of host immune responses, particularly type I interferon (IFN-I) signaling. This discovery assigns a new function to PyEBL and provides a mechanism for developing disease control strategies.

Here’s the TIP (Tri-Immuno – Phasic periodontal therapy) – A dive to thrive!

2021 ◽  
Vol 13 (4) ◽  
pp. 288-292
Author(s):  
Kahon Chakraborty ◽  
Sachin S Shivanaikar ◽  
Darsha Jain
Keyword(s):  
Immune Responses ◽  
Alveolar Bone ◽  
Periodontal Diseases ◽  
Chronic Inflammatory Disease ◽  
Host Immune System ◽  
Alternative Technique ◽  
Lifestyle Modifications ◽  
Host Immune Responses ◽  
Periodontal Tissues ◽  
The Past

Periodontitis is a multifactorial chronic inflammatory disease of the periodontium that destroys periodontium due to the exaggeration of the host immune responses to the disease-causing perio-pathogens, resulting in attachment loss and bone loss, eventually leading to loss of the tooth. Various advancements in modalities of treatment of periodontal disease have occurred in the past few years to overcome the disadvantages of traditional periodontal therapies as well as to improve the clinical outcomes. The Tri-Immuno – phasic periodontal (TIP) therapy is one such new technique developed by William Hoisington which is a minimally invasive, efficient, safe, and less traumatic alternative technique for treating periodontal diseases. TIP therapy is based on the fact that periodontal tissues heal in the same way as other parts of the human body. TIP therapy is an aerobic method of treating periodontal diseases that modulates various phases of the host immune system to eliminate the perio-pathogens and form a new attachment, and also attempts to regenerate the alveolar bone. The TIP therapy method includes - Bone One Session Treatment (BOST), controlling the occlusal forces, oral hygiene reinforcement with adjuvant modalities, lifestyle modifications, enhancing nutrition, and exercise.

scholarly journals Chlamydia and Its Many Ways of Escaping the Host Immune System

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Won Fen Wong ◽  
James P. Chambers ◽  
Rishein Gupta ◽  
Bernard P. Arulanandam
Keyword(s):  
Immune Responses ◽  
Host Cell ◽  
Acid Synthesis ◽  
Host Immune System ◽  
Amino Acid Synthesis ◽  
Future Studies ◽  
Host Immune Responses ◽  
Host Cell Apoptosis ◽  
Host Cell Death ◽  
Intracytoplasmic Inclusions

The increasing number of new cases of Chlamydia infection worldwide may be attributed to the pathogen’s ability to evade various host immune responses. Summarized here are means of evasion utilized by Chlamydia enabling survival in a hostile host environment. The pathogen's persistence involves a myriad of molecular interactions manifested in a variety of ways, e.g., formation of membranous intracytoplasmic inclusions and cytokine-induced amino acid synthesis, paralysis of phagocytic neutrophils, evasion of phagocytosis, inhibition of host cell apoptosis, suppression of antigen presentation, and induced expression of a check point inhibitor of programmed host cell death. Future studies could focus on the targeting of these molecules associated with immune evasion, thus limiting the spread and tissue damage caused by this pathogen.

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