scholarly journals Bacterial Toxins Are a Never-Ending Source of Surprises: From Natural Born Killers to Negotiators

Toxins ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 426
Author(s):  
Maria Lopez Chiloeches ◽  
Anna Bergonzini ◽  
Teresa Frisan

The idea that bacterial toxins are not only killers but also execute more sophisticated roles during bacteria–host interactions by acting as negotiators has been highlighted in the past decades. Depending on the toxin, its cellular target and mode of action, the final regulatory outcome can be different. In this review, we have focused on two families of bacterial toxins: genotoxins and pore-forming toxins, which have different modes of action but share the ability to modulate the host’s immune responses, independently of their capacity to directly kill immune cells. We have addressed their immuno-suppressive effects with the perspective that these may help bacteria to avoid clearance by the host’s immune response and, concomitantly, limit detrimental immunopathology. These are optimal conditions for the establishment of a persistent infection, eventually promoting asymptomatic carriers. This immunomodulatory effect can be achieved with different strategies such as suppression of pro-inflammatory cytokines, re-polarization of the immune response from a pro-inflammatory to a tolerogenic state, and bacterial fitness modulation to favour tissue colonization while preventing bacteraemia. An imbalance in each of those effects can lead to disease due to either uncontrolled bacterial proliferation/invasion, immunopathology, or both.

2020 ◽  
Vol 9 (1) ◽  
pp. 58-66
Author(s):  
Martina Kurnia Rohmah ◽  
Arif Rahman Nurdianto

COVID-19 is a type of Pneumonia caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). When COVID-19 arise in Wuhan China and rapidly spread throughout to the World, we need to learn how pathogenesis and immune responses occur in the bodies in more detail. COVID-19 is the third Severe Respiratory Disease outbreak caused by the Coronavirus in the past two decades after Severe Acute Respiratory Syndrome (SARS) in the 2002 and Middle East Respiratory Syndrome (MERS) in 2012. The Articles from PUBMED and Research Gate were searched for studies on the immune response of COVID-19 infection by SARS-CoV-2. SARS-CoV-2 increases the number of neutrophils, suppresses IFN, increases the activity of Th1/Th17, B cells, CD8+ and CD4+, and causes cytokine storms especially pro-inflammatory cytokines which can increase respiration disorders and multi-organ damage. This review tries to explain about pathogenesis and immune responses of COVID-19 to provide a reference in designing the appropriate immune intervention for treatment and therapeutic such as drug or vaccine based on the recent research progress SARS-CoV-2 and previous studies about SARS CoV and MERS CoV.


Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 113 ◽  
Author(s):  
Stephanie Maia Acuña ◽  
Lucile Maria Floeter-Winter ◽  
Sandra Marcia Muxel

An inflammatory response is essential for combating invading pathogens. Several effector components, as well as immune cell populations, are involved in mounting an immune response, thereby destroying pathogenic organisms such as bacteria, fungi, viruses, and parasites. In the past decade, microRNAs (miRNAs), a group of noncoding small RNAs, have emerged as functionally significant regulatory molecules with the significant capability of fine-tuning biological processes. The important role of miRNAs in inflammation and immune responses is highlighted by studies in which the regulation of miRNAs in the host was shown to be related to infectious diseases and associated with the eradication or susceptibility of the infection. Here, we review the biological aspects of microRNAs, focusing on their roles as regulators of gene expression during pathogen–host interactions and their implications in the immune response against Leishmania, Trypanosoma, Toxoplasma, and Plasmodium infectious diseases.


2020 ◽  
Vol 3 (2) ◽  
pp. 165-176
Author(s):  
Cássio Santana Meira ◽  
Vinícius Pinto Costa Rocha ◽  
Iasmim Diniz Orge ◽  
Danielle Devequi Gomes Nunes ◽  
Emanuelle de Souza Santos ◽  
...  

Coronavirus disease 2019 (COVID-19) emerged in Wuhan, China, in December 2019 and quickly spread worldwide becoming a global health problem unprecedented. The infection is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that is characterized as a RNA virus with an envelope derived from host cell with glycoprotein spikes, appearing like a crown-like external structure under electron microscope. Due to the aggressive spread profile of SARS-CoV-2, the scientific community is under pressure to generate knowledge about the morphology of the virus and the immune response against SARS-CoV-2, in order to generate useful information for the development of vaccines and methods of immunological diagnosis. Previous knowledge about other coronaviruses, such as SARS-CoV-1 and MERS-CoV, were the pillars for understanding the immune response of SARS-CoV-2. Until now, we know that the anti-SARS-CoV-2 immune response in the host involves mechanisms related to innate immunity, activation of CD4+ and CD8+ T cells and production of antibodies (IgA, IgG and IgM) against the virus. In spite of being a new pathogen, the literature on SARS-CoV-2 has increased dramatically in the past few months, especially in the immunology field. Here, we review the literature on SARS-CoV-2 immunology, focusing on the innate and adaptative immune responses.  


2008 ◽  
Vol 3 (4) ◽  
pp. 254-265 ◽  
Author(s):  
P. A. McCombe ◽  
S. J. Read

Inflammatory and immune responses play important roles following ischaemic stroke. Inflammatory responses contribute to damage and also contribute to repair. Injury to tissue triggers an immune response. This is initiated through activation of the innate immune system. In stroke there is microglial activation. This is followed by an influx of lymphocytes and macrophages into the brain, triggered by production of pro-inflammatory cytokines. This inflammatory response contributes to further tissue injury. There is also a systemic immune response to stroke, and there is a degree of immunosuppression that may contribute to the stroke patient's risk of infection. This immunosuppressive response may also be protective, with regulatory lymphocytes producing cytokines and growth factors that are neuroprotective. The specific targets of the immune response after stroke are not known, and the details of the immune and inflammatory responses are only partly understood. The role of inflammation and immune responses after stroke is twofold. The immune system may contribute to damage after stroke, but may also contribute to repair processes. The possibility that some of the immune response after stroke may be neuroprotective is exciting and suggests that deliberate enhancement of these responses may be a therapeutic option.


2018 ◽  
Vol 8 (1) ◽  
pp. 194-201
Author(s):  
KM. Terlikowska ◽  
MA. Strzyż-Skalij ◽  
K. Kryński ◽  
M. Osmólska ◽  
Z. Łada ◽  
...  

Ovarian cancer is the most threatening cause of death among gynecologic malignancies and represents the fifth leading cause of death from all cancers for women. Research reveals that ovarian cancer patients exhibit significant immune responses against the tumor. In this review of the current literature chiefly the interaction of ovarian cancer tumor cells and the immune system is discussed. There is increasingly growing evidence that pro-inflammatory cytokines are involved in intricate complex of mechanisms responsible for tumorigenesis, and delicate balance between pro- and anti-inflammatory cytokines is critical for the antitumor host immune response.


2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Mauricio M. Rodrigues ◽  
Ana Carolina Oliveira ◽  
Maria Bellio

In the past ten years, studies have shown the recognition ofTrypanosoma cruzi-associated molecular patterns by members of the Toll-like receptor (TLR) family and demonstrated the crucial participation of different TLRs during the experimental infection with this parasite. In the present review, we will focus on the role of TLR-activated pathways in the modulation of both innate and acquired immune responses toT. cruziinfection, as well as discuss the state of the art of vaccine research and development against the causative agent of Chagas disease (or American trypanosomiasis).


2020 ◽  
Author(s):  
PT Dhanagovind ◽  
Prabeer K. Kujur ◽  
Rajeeb K. Swain ◽  
Sanjita Banerjee

AbstractHost immune responses to Staphylococcus epidermidis, a frequent cause of nosocomial infections, are not well understood. We have established a novel bath immersion model of this infection in zebrafish larvae. S.epidermidis infection activates Tlr-2 signalling pathway by upregulation of tlr-2. Macrophages play a primary role in the host immune response and are involved in clearance of infection in the larvae. There is marked inflammation characterised by heightened NF-κB signalling and elevation of several pro-inflammatory cytokines. Infected larvae show rapid upregulation of il-1b and tnf-a transcripts and relatively slower elevation of il-6 transcription. The IL-6 signalling pathway is additionally subject to amplification by elevation of IL-6 signal transducer (il-6st) levels, which negatively correlates with miRNA dre-miR-142-5p expression. Enhanced IL-6 signalling is protective to the host in this model as inhibition of the signalling pathway resulted in increased mortality upon S.epidermidis infection. Our study describes the host immune responses to S.epidermidis infection, identifies a likely role for miR-142-5p – il-6st interaction in modulating this response and establishes the importance of IL-6 signalling in this infection model.


2021 ◽  
Vol 9 (6) ◽  
pp. 1317
Author(s):  
Matteo Bulati ◽  
Rosalia Busà ◽  
Claudia Carcione ◽  
Gioacchin Iannolo ◽  
Giuseppina Di Mento ◽  
...  

Currently, Klebsiella pneumoniae is a pathogen of clinical relevance due to its plastic ability of acquiring resistance genes to multiple antibiotics. During K. pneumoniae infections, lipopolysaccharides (LPS) play an ambiguous role as they both activate immune responses but can also play a role in immune evasion. The LPS O2a and LPS O2afg serotypes are prevalent in most multidrug resistant K. pneumoniae strains. Thus, we sought to understand if those two particular LPS serotypes were involved in a mechanism of immune evasion. We have extracted LPS (serotypes O1, O2a and O2afg) from K. pneumoniae strains and, using human monocytes ex vivo, we assessed the ability of those LPS antigens to induce the production of pro-inflammatory cytokines and chemokines. We observed that, when human monocytes are incubated with LPS serotypes O1, O2a or O2afg strains, O2afg and, to a lesser extent, O2a but not O1 failed to elicit the production of pro-inflammatory cytokines and chemokines, which suggests a role in immune evasion. Our preliminary data also shows that nuclear translocation of NF-κB, a process which regulates an immune response against infections, occurs in monocytes incubated with LPS O1 and, to a smaller extent, with LPS O2a, but not with the LPS serotype O2afg. Our results indicate that multidrug resistant K. pneumoniae expressing LPS O2afg serotypes avoid an initial inflammatory immune response and, consequently, are able to systematically spread inside the host unharmed, which results in the several pathologies associated with this bacterium.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Michael Lawrence Crichton ◽  
David Alexander Muller ◽  
Alexandra Christina Isabelle Depelsenaire ◽  
Frances Elizabeth Pearson ◽  
Jonathan Wei ◽  
...  

Abstract Micro-device use for vaccination has grown in the past decade, with the promise of ease-of-use, painless application, stable solid formulations and greater immune response generation. However, the designs of the highly immunogenic devices (e.g. the gene gun, Nanopatch or laser adjuvantation) require significant energy to enter the skin (30–90 mJ). Within this study, we explore a way to more effectively use energy for skin penetration and vaccination. These modifications change the Nanopatch projections from cylindrical/conical shapes with a density of 20,000 per cm2 to flat-shaped protrusions at 8,000 per cm2, whilst maintaining the surface area and volume that is placed within the skin. We show that this design results in more efficient surface crack initiations, allowing the energy to be more efficiently be deployed through the projections into the skin, with a significant overall increase in penetration depth (50%). Furthermore, we measured a significant increase in localized skin cell death (>2 fold), and resultant infiltrate of cells (monocytes and neutrophils). Using a commercial seasonal trivalent human influenza vaccine (Fluvax 2014), our new patch design resulted in an immune response equivalent to intramuscular injection with approximately 1000 fold less dose, while also being a practical device conceptually suited to widespread vaccination.


2006 ◽  
Vol 26 (1) ◽  
pp. 8-25 ◽  
Author(s):  
Michelle L. McCully ◽  
Joaquín Madrenas

During the past few years, there has been a substantial increase in the understanding of innate immunity. Dendritic cells are emerging as key players in the orchestration of this early phase of immune responses, with a role that will translate into the subsequent type of adaptive immune response against infection. Here we provide an overview of dendritic cell differentiation and function, with particular emphasis on those features unique to the immune defense of the peritoneal cavity and in the context of peritoneal dialysis-associated immune responses. The reader is referred to the primary references included in the accompanying list for specific details in this fascinating field.


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