scholarly journals Solution of the Marchuk model of infectious disease and immune response

1986 ◽  
Vol 7 (5-8) ◽  
pp. 803-807
Author(s):  
G. Adomian ◽  
G.E. Adomian
Keyword(s):  
Infectious Disease ◽  
Immune Response

scholarly journals Expression of IL-1 Family Cytokines in Patients Before and After Cutaneous Leishmaniasis Cure

2021 ◽  
Author(s):  
Ester Amorim ◽  
Marton Kaique Andrade Cavalcante ◽  
Ailton Alvaro Silva ◽  
Vanessa Lucília Silveira Medeiros ◽  
Maria Edileuza Felinto Brito ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Cutaneous Leishmaniasis ◽  
Mechanisms Of Resistance ◽  
Marked Inhibition ◽  
Gene And Protein Expression ◽  
Th2 Responses ◽  
Before And After ◽  
Response Profiles ◽  
Effector Immune Response

Abstract Cutaneous leishmaniasis is an infectious disease that presents an immune response marked by the activation of lymphocytes and production of cytokines, including those of the IL-1 family, which act as an important trigger for the activation of an effector immune response. Despite this, inflammation exacerbation is sometimes also attributed to IL-1 cytokines, although some others down-regulate inflammation or produce Th2 responses, which need to be further clarified in the CL. Assessing the gene and protein expression of IL-1 cytokines associated with different immune response profiles in PBMCs from patients with active and healed lesions, this study demonstrated that stimulation by L. braziliensis positively regulates inflammatory and anti-inflammatory IL-1 cytokines, as IL-1α/β and IL-37, while there was a marked inhibition of IL-1Ra and IL-18 genes in patients treated with antimony, which perhaps contributes to the mechanisms of resistance that control Leishmania infection.

scholarly journals Molecular and Immunological Mechanisms of Miana Leaf (Coleus Scutellariodes [L] Benth) in Infectious Diseases

2020 ◽  
Vol 13 (4) ◽  
pp. 1607-1618
Author(s):  
Theo Audi Yanto ◽  
Mochammad Hatta ◽  
Agussalim Bukhari ◽  
Rosdiana Natzir
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Premature Mortality ◽  
Antimicrobial Effect ◽  
Immunological Mechanism ◽  
Mortality And Morbidity ◽  
Immunological Mechanisms ◽  
To Come ◽  
Antibiotic Efficacy ◽  
Anti Inflammation

Infectious disease is still a massive world burden of disease. It causes premature mortality and morbidity. Regardless of antibiotic therapy, the increased numbers of antibiotic resistance bring emerging problems in infectious disease. Several pathogens have unique roles to deactivate host immune response causing difficulty to treat the infection. Alack of antibiotic efficacy is crucial to modulate the immune response as a brilliant strategy to face infectious disease in years to come. Various herbal medicine has been known to have a pivotal role in enhancing immune response at the molecular level. Miana leaves extract (MLE) has a potential role in regulating the immune response to the infection. Besides its antimicrobial effect, MLE has other properties such as anti-inflammation, antioxidant. Several studies have revealedthe molecular mechanism of MLE in immune response, such as enhancing IL 37, IL 10, regulating TLR 4, and IFN-g. The objectives of this article are to review the molecular and immunological mechanism of Miana in treating various infective diseases comprehensively.

Adaptive immunity

2010 ◽  
pp. 224-234
Author(s):  
Paul Klenerman
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Pattern Recognition ◽  
Adaptive Immunity ◽  
Adaptive Response ◽  
Critical Role ◽  
Adaptive Immune Response ◽  
Structural Features ◽  
Adaptive Immune ◽  
Single Organism

Following the innate immune response, which acts very rapidly, the adaptive immune response plays a critical role in host defence against infectious disease. Unlike the innate response, which is triggered by pattern recognition of pathogens, i.e. features that are common to many bacteria or viruses, the adaptive response is triggered by structural features—known as antigens or epitopes—that are typically unique to a single organism....

scholarly journals Infectious disease, the innate immune response, and fibrosis

2007 ◽  
Vol 117 (3) ◽  
pp. 530-538 ◽  
Author(s):  
Alessia Meneghin ◽  
Cory M. Hogaboam
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune

scholarly journals Exosomes Recovered From the Plasma of COVID-19 Patients Expose SARS-CoV-2 Spike-Derived Fragments and Contribute to the Adaptive Immune Response

2022 ◽  
Vol 12 ◽  
Author(s):  
Elisa Pesce ◽  
Nicola Manfrini ◽  
Chiara Cordiglieri ◽  
Spartaco Santi ◽  
Alessandra Bandera ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Mass Spectrometry ◽  
Immune Response ◽  
Immune System ◽  
Adaptive Immune Response ◽  
Active Role ◽  
Extracellular Vesicle ◽  
Pathological State ◽  
Cell Responses ◽  
Adaptive Immune

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by beta-coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that has rapidly spread across the globe starting from February 2020. It is well established that during viral infection, extracellular vesicles become delivery/presenting vectors of viral material. However, studies regarding extracellular vesicle function in COVID-19 pathology are still scanty. Here, we performed a comparative study on exosomes recovered from the plasma of either MILD or SEVERE COVID-19 patients. We show that although both types of vesicles efficiently display SARS-CoV-2 spike-derived peptides and carry immunomodulatory molecules, only those of MILD patients are capable of efficiently regulating antigen-specific CD4+ T-cell responses. Accordingly, by mass spectrometry, we show that the proteome of exosomes of MILD patients correlates with a proper functioning of the immune system, while that of SEVERE patients is associated with increased and chronic inflammation. Overall, we show that exosomes recovered from the plasma of COVID-19 patients possess SARS-CoV-2-derived protein material, have an active role in enhancing the immune response, and possess a cargo that reflects the pathological state of patients in the acute phase of the disease.

scholarly journals Exploring the Innate Immunological Response of an Alternative Nonhuman Primate Model of Infectious Disease; the Common Marmoset

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
M. Nelson ◽  
M. Loveday
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Nonhuman Primate ◽  
Immune Cell ◽  
Common Marmoset ◽  
Cell Types ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
The Common ◽  
Activation Status

The common marmoset (Callithrix jacchus) is increasingly being utilised as a nonhuman primate model for human disease, ranging from autoimmune to infectious disease. In order to fully exploit these models, meaningful comparison to the human host response is necessary. Commercially available reagents, primarily targeted to human cells, were utilised to assess the phenotype and activation status of key immune cell types and cytokines in naive and infected animals. Single cell suspensions of blood, spleen, and lung were examined. Generally, the phenotype of cells was comparable between humans and marmosets, with approximately 63% of all lymphocytes in the blood of marmosets being T cells, 25% B-cells, and 12% NK cells. The percentage of neutrophils in marmoset blood were more similar to human values than mouse values. Comparison of the activation status of cells following experimental systemic or inhalational infection exhibited different trends in different tissues, most obvious in cell types active in the innate immune response. This work significantly enhances the ability to understand the immune response in these animals and fortifies their use as models of infectious disease.

scholarly journals RIG-I-Like Receptor and Toll-Like Receptor Signaling Pathways Cause Aberrant Production of Inflammatory Cytokines/Chemokines in a Severe Fever with Thrombocytopenia Syndrome Virus Infection Mouse Model

2018 ◽  
Vol 92 (13) ◽  
pp. e02246-17 ◽  
Author(s):  
Shintaro Yamada ◽  
Masayuki Shimojima ◽  
Ryo Narita ◽  
Yuta Tsukamoto ◽  
Hiroki Kato ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Tlr Signaling ◽  
Cytokines And Chemokines ◽  
Severe Fever

ABSTRACT Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a tick-borne phlebovirus of the family Bunyaviridae, SFTS virus (SFTSV). Wild-type and type I interferon (IFN-I) receptor 1-deficient (IFNAR1−/−) mice have been established as nonlethal and lethal models of SFTSV infection, respectively. However, the mechanisms of IFN-I production in vivo and the factors causing the lethal disease are not well understood. Using bone marrow-chimeric mice, we found that IFN-I signaling in hematopoietic cells was essential for survival of lethal SFTSV infection. The disruption of IFN-I signaling in hematopoietic cells allowed an increase in viral loads in serum and produced an excess of multiple inflammatory cytokines and chemokines. The production of IFN-I and inflammatory cytokines was abolished by deletion of the signaling molecules IPS-1 and MyD88, essential for retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) and Toll-like receptor (TLR) signaling, respectively. However, IPS-1−/− MyD88−/− mice exhibited resistance to lethal SFTS with a moderate viral load in serum. Taken together, these results indicate that adequate activation of RLR and TLR signaling pathways under low to moderate levels of viremia contributed to survival through the IFN-I-dependent antiviral response during SFTSV infection, whereas overactivation of these signaling pathways under high levels of viremia resulted in abnormal induction of multiple inflammatory cytokines and chemokines, causing the lethal disease. IMPORTANCE SFTSV causes a severe infectious disease in humans, with a high fatality rate of 12 to 30%. To know the pathogenesis of the virus, we need to clarify the innate immune response as a front line of defense against viral infection. Here, we report that a lethal animal model showed abnormal induction of multiple inflammatory cytokines and chemokines by an uncontrolled innate immune response, which triggered the lethal SFTS. Our findings suggest a new strategy to target inflammatory humoral factors to treat patients with severe SFTS. Furthermore, this study may help the investigation of other tick-borne viruses.

scholarly journals Cell Surface Delivery of the Measles Virus Nucleoprotein: a Viral Strategy To Induce Immunosuppression

2004 ◽  
Vol 78 (21) ◽  
pp. 11952-11961 ◽  
Author(s):  
Julien C. Marie ◽  
Frédéric Saltel ◽  
Jean-Michel Escola ◽  
Pierre Jurdic ◽  
T. Fabian Wild ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Blood Cells ◽  
Measles Virus ◽  
Interleukin 12 ◽  
Fcγ Receptor ◽  
Extracellular Compartment ◽  
High Infant Mortality ◽  
Infected Cells ◽  
Novel Strategy

ABSTRACT Although only a few blood cells are infected during measles, this infectious disease is followed by acute immunosuppression, associated with high infant mortality. Measles virus nucleoprotein has been suggested to contribute to virus-induced inhibition of the immune response. However, it has been difficult to understand how this cytosolic viral protein could leave an infected cell and then perturb the immune response. Here we demonstrate that intracellularly synthesized nucleoprotein enters the late endocytic compartment, where it recruits its cellular ligand, the Fcγ receptor. Nucleoprotein is then expressed at the surfaces of infected leukocytes associated with the Fcγ receptor and is secreted into the extracellular compartment, allowing its interaction with uninfected cells. Finally, cell-derived nucleoprotein inhibits the secretion of interleukin-12 and the generation of the inflammatory reaction, both shown to be impaired during measles. These results reveal nucleoprotein egress from infected cells as a novel strategy in measles-induced immunosuppression.

scholarly journals Decomposing variation in immune response in a wild rodent population

2019 ◽  
Author(s):  
Klara M. Wanelik ◽  
Mike Begon ◽  
Elena Arriero ◽  
Janette E. Bradley ◽  
Ida M. Friberg ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Immune Response ◽  
Individual Variation ◽  
Natural Variation ◽  
Wild Population ◽  
Microtus Agrestis ◽  
Wild Rodent ◽  
Rodent Population ◽  
Immune Pathways ◽  
Underlying Processes

AbstractIndividuals vary in their immune response and, as a result, some are more susceptible to infectious disease than others. Little is known about which components of immune pathways are responsible for this variation, but understanding these underlying processes could allow us to predict the outcome of infection for an individual, and to manage their health more effectively. In this study, we describe transcriptome-wide variation in immune response (to a standardised challenge) in a wild population of field voles (Microtus agrestis). We find that this variation can be categorised into three main types. We also identify markers, across these three categories, which display particularly strong individual variation in response. This work shows how a simple standardised challenge performed on a natural population can reveal complex patterns of natural variation in immune response.

Sign in / Sign up

Export Citation Format

Share Document