scholarly journals Chagas Disease: Still Many Unsolved Issues

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
José M. Álvarez ◽  
Raissa Fonseca ◽  
Henrique Borges da Silva ◽  
Cláudio R. F. Marinho ◽  
Karina R. Bortoluci ◽  
...  
Keyword(s):  
Heart Disease ◽  
Immune System ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Innate Immune System ◽  
Innate Immune ◽  
Host Immune System ◽  
Immune Effector ◽  
The Past ◽  
Chronic Heart Disease

Over the past 20 years, the immune effector mechanisms involved in the control ofTrypanosoma cruzi, as well as the receptors participating in parasite recognition by cells of the innate immune system, have been largely described. However, the main questions on the physiopathology of Chagas disease remain unanswered: “Why does the host immune system fail to provide sterile immunity?” and “Why do only a proportion of infected individuals develop chronic pathology?” In this review, we describe the mechanisms proposed to explain the inability of the immune system to eradicate the parasite and the elements that allow the development of chronic heart disease. Moreover, we discuss the possibility that the inability of infected cardiomyocytes to sense intracellularT. cruzicontributes to parasite persistence in the heart and the development of chronic pathology.

scholarly journals Peptidoglycan O-Acetylation as a Virulence Factor: Its Effect on Lysozyme in the Innate Immune System

Antibiotics ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 94 ◽  
Author(s):  
Ashley S. Brott ◽  
Anthony J. Clarke
Keyword(s):  
Immune System ◽  
Virulence Factor ◽  
Innate Immune System ◽  
Innate Immune ◽  
Host Immune System ◽  
Gram Negative Bacteria ◽  
First Line ◽  
Structural Support ◽  
Important Virulence Factor ◽  
Novel Target

The peptidoglycan sacculus of both Gram-positive and Gram-negative bacteria acts as a protective mesh and provides structural support around the entirety of the cell. The integrity of this structure is of utmost importance for cell viability and so naturally is the first target for attack by the host immune system during bacterial infection. Lysozyme, a muramidase and the first line of defense of the innate immune system, targets the peptidoglycan sacculus hydrolyzing the β-(1→4) linkage between repeating glycan units, causing lysis and the death of the invading bacterium. The O-acetylation of N-acetylmuramoyl residues within peptidoglycan precludes the productive binding of lysozyme, and in doing so renders it inactive. This modification has been shown to be an important virulence factor in pathogens such as Staphylococcus aureus and Neisseria gonorrhoeae and is currently being investigated as a novel target for anti-virulence therapies. This article reviews interactions made between peptidoglycan and the host immune system, specifically with respect to lysozyme, and how the O-acetylation of the peptidoglycan interrupts these interactions, leading to increased pathogenicity.

scholarly journals Insights into the cardioprotective properties of n-3 PUFAs against ischemic heart disease via modulation of the innate immune system

2019 ◽  
Vol 308 ◽  
pp. 20-44 ◽  
Author(s):  
Ahmed M. Darwesh ◽  
Deanna K. Sosnowski ◽  
Tim YT. Lee ◽  
Hedieh Keshavarz-Bahaghighat ◽  
John M. Seubert
Keyword(s):  
Heart Disease ◽  
Immune System ◽  
Ischemic Heart Disease ◽  
Innate Immune System ◽  
Innate Immune ◽  
Ischemic Heart

scholarly journals Viral Modulation of TLRs and Cytokines and the Related Immunotherapies for HPV-Associated Cancers

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Marconi Rego Barros ◽  
Talita Helena Araújo de Oliveira ◽  
Cristiane Moutinho Lagos de Melo ◽  
Aldo Venuti ◽  
Antonio Carlos de Freitas
Keyword(s):  
Immune Response ◽  
Human Papillomavirus ◽  
Immune System ◽  
Immune Evasion ◽  
Innate Immune System ◽  
Innate Immune ◽  
Cell Maturation ◽  
Host Immune System ◽  
Key Factor ◽  
Infected Cells

The modulation of the host innate immune system is a well-established carcinogenesis feature of several tumors, including human papillomavirus- (HPV-) related cancers. This virus is able to interrupt the initial events of the immune response, including the expression of Toll-like receptors (TLRs), cytokines, and inflammation. Both TLRs and cytokines play a central role in HPV recognition, cell maturation and differentiation as well as immune signalling. Therefore, the imbalance of this sensitive control of the immune response is a key factor for developing immunotherapies, which strengthen the host immune system to accomplish an efficient defence against HPV and HPV-infected cells. Based on this, the review is aimed at exposing the HPV immune evasion mechanisms involving TLRs and cytokines and at discussing existing and potential immunotherapeutic TLR- and cytokine-related tools.

Sepsis begins at the interface of pathogen and host

2001 ◽  
Vol 29 (6) ◽  
pp. 853-859 ◽  
Author(s):  
B. Beutler
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Tissue Injury ◽  
Living Organism ◽  
Life Forms ◽  
Innate Immune ◽  
Host Immune System ◽  
Toxic Substances ◽  
Septic Syndrome ◽  
Modern Mind

To the modern mind, the term ‘sepsis’ conjures up images of microbes. It is easy to forget that the word predates any understanding of the microbial origins of infectious disease. Derived from the Greek ‘sepsios’ (rotten), sepsis denotes decay: a phenomenon that humans once regarded as a mysterious though inevitable natural process. A living organism does not accept decay passively. Virtually all multicellular life forms are capable of resisting infection through the generation of a vigorous immune response. In mammals, the response is so stereotypic that it has come to define sepsis itself: it is often called the ‘septic syndrome’. Our current understanding of the innate immune system is deeply rooted in the study of sepsis. The chain of events linking infection to tissue injury and cardiovascular collapse is not obvious, and affirmation of the concept required three major discoveries. First, the septic syndrome was found to be caused by toxic products of microbes. Secondly, these toxic substances were found to be toxic because of their propensity to activate cells of the innate immune system, prompting cytokine production. Thirdly, the activating events initiated by microbial toxins were traced to members of an ancient family of defensive molecules, versions of which operate in virtually all multicellular life forms. In mammals, proteins of this family are now known as Toll-like receptors. They represent a point of direct contact, and first contact, between a pathogen and the host immune system.

Chagas' disease: Trypanosoma cruzi vs. the host immune system

1991 ◽  
Vol 142 (2) ◽  
pp. 125-126 ◽  
Author(s):  
M. Hontebeyrie-Joskowicz ◽  
P. Minoprio
Keyword(s):  
Immune System ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Host Immune System

scholarly journals TRINITY OF SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS-2: ORIGIN, GENOTYPE, PHENOTYPE, AND IMMUNE RESPONSE IN CORONAVIRUS DISEASE-2019

2021 ◽  
pp. 28-36
Author(s):  
MURUGAN NANDAGOPAL ◽  
ARULMOZHI BALAKRISHNAN ◽  
CHIRAYU PADHIAR
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Severe Acute Respiratory Syndrome ◽  
Innate Immune System ◽  
Clinical Symptoms ◽  
Innate Immune ◽  
Host Immune System ◽  
Wide Range ◽  
Novel Coronavirus ◽  
Classification Structure

The coronavirus disease-2019 (COVID-19) outbreak by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) or a novel coronavirus (2019-CoV) has prompted global health concerns. A pandemic resulted from the disease’s transmission through many routes. In this pandemic, the interaction between coronavirus and the host immune system, particularly the innate immune system, is becoming more prominent. Against viruses and pathogens, innate immunity serves as a first line of defense. Our understanding of pathogenesis will benefit from a better grasp of the mechanisms of immune evasion techniques. The origin, classification, structure, and method of transmission of SARS-CoV-2 were summarized in this paper. We have discussed the importance of important communications. In this review, we have discussed the function of important components of the innate immune system in COVID-19 infection, as well as how the virus evades innate immunity through multiple tactics and contributes to a wide range of clinical symptoms and outcomes.

scholarly journals Synergistic elimination of bacteria by phage and the innate immune system

2016 ◽  
Author(s):  
Chung Yin (Joey) Leung ◽  
Joshua S. Weitz
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Numerical Simulations ◽  
Innate Immune System ◽  
Bacterial Infections ◽  
Phage Therapy ◽  
Innate Immune ◽  
Host Immune System ◽  
Burn Wound

AbstractPhage therapy has been viewed as a potential treatment for bacterial infections for over a century. Yet, the year 2016 marks the first phase I/II human trial of a phage therapeutic - to treat burn wound patients in Europe. The slow progress in realizing clinical therapeutics is matched by a similar dearth in principled understanding of phage therapy. Theoretical models and in vitro experiments find that combining phage and bacteria often leads to coexistence of both phage and bacteria or phage elimination altogether. Both outcomes stand in contrast to the stated goals of phage therapy. A potential resolution to the gap between models, experiments, and therapeutic use of phage is the hypothesis that the combined effect of phage and host immune system can synergistically eliminate bacterial pathogens. Here, we propose a phage therapy model that considers the nonlinear dynamics arising from interactions between bacteria, phage and the host innate immune system. The model builds upon earlier efforts by incorporating a maximum capacity of the immune response and density-dependent immune evasion by bacteria. We analytically identify a synergistic regime in this model in which phage and the innate immune response jointly contribute to the elimination of the target bacteria. Crucially, we find that in this synergistic regime, neither phage alone nor the innate immune system alone can eliminate the bacteria. We confirm these findings using numerical simulations in biologically plausible scenarios. We utilize our numerical simulations to explore the synergistic effect and its significance for guiding the use of phage therapy in clinically relevant applications.

scholarly journals Cryptococcus neoformans Cells in Biofilms Are Less Susceptible than Planktonic Cells to Antimicrobial Molecules Produced by the Innate Immune System

2006 ◽  
Vol 74 (11) ◽  
pp. 6118-6123 ◽  
Author(s):  
Luis R. Martinez ◽  
Arturo Casadevall
Keyword(s):  
Immune System ◽  
Antimicrobial Peptides ◽  
Cryptococcus Neoformans ◽  
Innate Immune System ◽  
Capsular Polysaccharide ◽  
Pathogenic Fungus ◽  
Innate Immune ◽  
Planktonic Cells ◽  
Phagocytic Cells ◽  
Immune Effector

ABSTRACT The human pathogenic fungus Cryptococcus neoformans can form biofilms on polystyrene plates and medical devices in a process that requires capsular polysaccharide release. Although biofilms are known to be less susceptible to antimicrobial drugs, little is known about their susceptibility to antimicrobial molecules produced by the innate immune system. In this study, we investigated the susceptibility of C. neoformans cells in biofilm and planktonic states to oxidative and nonoxidative antimicrobial molecules produced by phagocytic cells. The effects of various immune effector molecules on the fungal mass, metabolic activity, and architecture of C. neoformans biofilms were measured by colony counts, 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino) carbonyl]-2H-tetrazolium hydroxide reduction, and confocal microscopy, respectively. Biofilms were more resistant than planktonic cells to oxidative stress but remained vulnerable to cationic antimicrobial peptides. However, melanized biofilms were significantly less susceptible to antimicrobial peptides than nonmelanized biofilms. These results suggest that the biofilm phenotype increases resistance against host immune mechanisms, a phenomenon that could contribute to the ability of biofilm-forming microbes to establish persistent infections.

scholarly journals Bacterial autolysins trim cell surface peptidoglycan to prevent detection by the Drosophila innate immune system

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Magda Luciana Atilano ◽  
Pedro Matos Pereira ◽  
Filipa Vaz ◽  
Maria João Catalão ◽  
Patricia Reed ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Pathogenic Bacteria ◽  
Bacterial Virulence ◽  
Innate Immune ◽  
Molecular Signature ◽  
Host Immune System ◽  
Bacterial Proteins ◽  
Successful Infection ◽  
Bacterial Surfaces

Bacteria have to avoid recognition by the host immune system in order to establish a successful infection. Peptidoglycan, the principal constituent of virtually all bacterial surfaces, is a specific molecular signature recognized by dedicated host receptors, present in animals and plants, which trigger an immune response. Here we report that autolysins from Gram-positive pathogenic bacteria, enzymes capable of hydrolyzing peptidoglycan, have a major role in concealing this inflammatory molecule from Drosophila peptidoglycan recognition proteins (PGRPs). We show that autolysins trim the outermost peptidoglycan fragments and that in their absence bacterial virulence is impaired, as PGRPs can directly recognize leftover peptidoglycan extending beyond the external layers of bacterial proteins and polysaccharides. The activity of autolysins is not restricted to the producer cells but can also alter the surface of neighboring bacteria, facilitating the survival of the entire population in the infected host.

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