scholarly journals Venom-Induced Immunosuppression: An Overview of Hemocyte-Mediated Responses

2011 ◽  
Vol 2011 ◽  
pp. 1-14 ◽  
Author(s):  
Aylin Er ◽  
Olga Sak ◽  
Ekrem Ergin ◽  
Fevzi Uçkan ◽  
David B. Rivers

Parasitic wasps are important natural enemies of several insect pests. They use a variety of methods to modulate their insect host for their progeny to develop. For example, the female wasp needs to avoid or suppress the host immune responses by introducing venom with or without virus like particles and/or polydnaviruses. The aim of this paper is to provide a synthesis of current knowledge regarding the immunosuppression of host immunity with venom in parasitoids that are devoid of symbiotic viruses. Special emphasis is given through disabling host hemocytes by venom of the endoparasitoidPimpla turionellae(Hymenoptera: Ichneumonidae) with comparisons of venoms from other parasitoid species.

2022 ◽  
Vol 23 (1) ◽  
pp. 525
Author(s):  
Tarina Sharma ◽  
Anwar Alam ◽  
Aquib Ehtram ◽  
Anshu Rani ◽  
Sonam Grover ◽  
...  

Mycobacterium tuberculosis (M.tb) is a successful pathogen that can reside within the alveolar macrophages of the host and can survive in a latent stage. The pathogen has evolved and developed multiple strategies to resist the host immune responses. M.tb escapes from host macrophage through evasion or subversion of immune effector functions. M.tb genome codes for PE/PPE/PE_PGRS proteins, which are intrinsically disordered, redundant and antigenic in nature. These proteins perform multiple functions that intensify the virulence competence of M.tb majorly by modulating immune responses, thereby affecting immune mediated clearance of the pathogen. The highly repetitive, redundant and antigenic nature of PE/PPE/PE_PGRS proteins provide a critical edge over other M.tb proteins in terms of imparting a higher level of virulence and also as a decoy molecule that masks the effect of effector molecules, thereby modulating immuno-surveillance. An understanding of how these proteins subvert the host immunological machinery may add to the current knowledge about M.tb virulence and pathogenesis. This can help in redirecting our strategies for tackling M.tb infections.


2021 ◽  
Vol 59 (1) ◽  
pp. 423-445
Author(s):  
Pradeep Kachroo ◽  
Tessa M. Burch-Smith ◽  
Murray Grant

Chloroplasts are key players in plant immune signaling, contributing to not only de novo synthesis of defensive phytohormones but also the generation of reactive oxygen and nitrogen species following activation of pattern recognition receptors or resistance (R) proteins. The local hypersensitive response (HR) elicited by R proteins is underpinned by chloroplast-generated reactive oxygen species. HR-induced lipid peroxidation generates important chloroplast-derived signaling lipids essential to the establishment of systemic immunity. As a consequence of this pivotal role in immunity, pathogens deploy effector complements that directly or indirectly target chloroplasts to attenuate chloroplast immunity (CI). Our review summarizes the current knowledge of CI signaling and highlights common pathogen chloroplast targets and virulence strategies. We address emerging insights into chloroplast retrograde signaling in immune responses and gaps in our knowledge, including the importance of understanding chloroplast heterogeneity and chloroplast involvement in intraorganellular interactions in host immunity.


2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Lifang Zhao ◽  
Zhaoying Fu

The pathogenesis of viral myocarditis includes both the direct damage mediated by viral infection and the indirect lesion resulted from host immune responses. Myocarditis can progress into dilated cardiomyopathy that is also associated with immunopathogenesis. T cell-mediated autoimmunity, antibody-mediated autoimmunity (autoantibodies), and innate immunity, working together, contribute to the development of myocarditis and dilated cardiomyopathy.


2021 ◽  
Vol 48 (3) ◽  
pp. 77-82
Author(s):  
R. Cherneva ◽  
Z. Cherneva

Abstract The COVID-19 pandemic caused by the SARS-CoV-2 has increased the burden on healthcare system. Despite some progress in its diagnostics has been made, effective prevention and treatment are still insufficient. Since SARS-CoV-2 infections often cause systemic inflammation and multiple organ failure, the therapeutic options aimed at modulating the host immune responses to prevent subsequent systemic complications are demanding. The review provides a summary of the SARS-CoV-2 virus infection and underlines the current perception of pulmonary host’s immune response and its contributions to disease severity and systemic inflammation. Signaling pathways which have the potential to manipulate host immunity and improve clinical outcomes are also presented.


Author(s):  
Ashlesh Patil ◽  
Jaya Prasad Tripathy ◽  
Vishwajit Deshmukh ◽  
Bharat Sontakke ◽  
Satyendra C. Tripathi

Novel coronavirus disease (COVID-19) has affected nearly 7 million individuals and claimed more than 0.4 million lives to date. There are several reports of gender differences related to infection and death due to COVID-19. This raises important questions such as “Whether there are differences based on gender in risk and severity of infection or mortality rate?” and “What are the biological explanation and mechanisms underlying these differences?” Emerging evidence has proposed sex-based immunological, genetic, and hormonal differences to explain this ambiguity. Besides biological differences, women have also faced social inequities and economic hardships due to this pandemic. Several recent studies have shown that independent of age males are at higher risk for severity and mortality in COVID-19 patients. Although susceptibility to SARS-CoV-2 was found to be similar across both genders in several disease cohorts, a disproportionate death ratio in men can be partly explained by the higher burden of pre-existing diseases and occupational exposures among men. From an immunological point of view, females can engage a more active immune response, which may protect them and counter infectious diseases as compared to men. This attribute of better immune responses towards pathogens is thought to be due to high estrogen levels in females. Here we review the current knowledge about sex differences in susceptibility, the severity of infection and mortality, host immune responses, and the role of sex hormones in COVID-19 disease.


ENTOMON ◽  
2021 ◽  
Vol 46 (2) ◽  
pp. 113-120
Author(s):  
S.J. Reuolin ◽  
N. Muthukrishnan ◽  
M. Paramasivam ◽  
K.S. Subramanian ◽  
N. Maragatham

A total of 43 insect parasitoid species belonging to fourteen families (Aphelinidae, Braconidae, Ceraphronidae, Diapriidae, Encyrtidae, Eulophidae, Eurytomidae, Ichneumonidae, Megaspilidae, Mymaridae, Platygasteridae, Proctotrupidae, Pteromalidae, Trichogrammatidae) has been documented in the rice ecosystem using yellow pan trap. The observations were made at four important stages of rice crop like early tillering, active tillering, booting and panicle development. The parasitoids were also compared with the occurrence of sixteen insect pests that were recorded simultaneously in each stage of the crop. The result revealed that, there is a significant difference in the occurrence of parasitoids according to the stage of the crop and insect host availability. This understanding help in the introduction of specific parasitoids at respective stages for effective biocontrol.


2020 ◽  
Vol 8 (11) ◽  
pp. 1840
Author(s):  
Souvik Ghosh ◽  
Yashpal S. Malik

The COVID-19 pandemic, caused by a novel zoonotic coronavirus (CoV), SARS-CoV-2, has infected 46,182 million people, resulting in 1,197,026 deaths (as of 1 November 2020), with devastating and far-reaching impacts on economies and societies worldwide. The complex origin, extended human-to-human transmission, pathogenesis, host immune responses, and various clinical presentations of SARS-CoV-2 have presented serious challenges in understanding and combating the pandemic situation. Human CoVs gained attention only after the SARS-CoV outbreak of 2002–2003. On the other hand, animal CoVs have been studied extensively for many decades, providing a plethora of important information on their genetic diversity, transmission, tissue tropism and pathology, host immunity, and therapeutic and prophylactic strategies, some of which have striking resemblance to those seen with SARS-CoV-2. Moreover, the evolution of human CoVs, including SARS-CoV-2, is intermingled with those of animal CoVs. In this comprehensive review, attempts have been made to compare the current knowledge on evolution, transmission, pathogenesis, immunopathology, therapeutics, and prophylaxis of SARS-CoV-2 with those of various animal CoVs. Information on animal CoVs might enhance our understanding of SARS-CoV-2, and accordingly, benefit the development of effective control and prevention strategies against COVID-19.


2021 ◽  
Vol SP (2) ◽  
Author(s):  
Uzma A. Jilani ◽  
Zulhabri Othman ◽  
Syed A. Jilani

The coronavirus disease 2019 (COVID‐19) has created a worldwide crisis, raising fears and concerns regarding clinical outcomes in patients with comorbidities. Some of the highly prevalent communicable and non-communicable diseases worldwide are cardiovascular diseases, diabetes, HIV/AIDS, and hepatitis B and C, which reduce the host immune responses to concurrent acute infections. Despite over 170 million confirmed cases of COVID‐19 worldwide as of 24 June 2021, insufficient data is reporting the prognosis of HIV and SARS-CoV-2 co‐infection. This narrative review aims to present current knowledge on the impact of SARS-CoV-2 on people living with HIV/AIDS, in terms of immunological responses and clinical outcome. Although some studies have been performed and are in progress to determine the impact of SARS-CoV-2 infection on patients living with HIV/AIDS, controversies still exist whether COVID-19 severity and mortality are higher among this special subgroup or similar to the general population.


Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 765
Author(s):  
Huibin Yu ◽  
Ryan C. Bruneau ◽  
Greg Brennan ◽  
Stefan Rothenburg

Host pattern recognition receptors (PRRs) sense pathogen-associated molecular patterns (PAMPs), which are molecular signatures shared by different pathogens. Recognition of PAMPs by PRRs initiate innate immune responses via diverse signaling pathways. Over recent decades, advances in our knowledge of innate immune sensing have enhanced our understanding of the host immune response to poxviruses. Multiple PRR families have been implicated in poxvirus detection, mediating the initiation of signaling cascades, activation of transcription factors, and, ultimately, the expression of antiviral effectors. To counteract the host immune defense, poxviruses have evolved a variety of immunomodulators that have diverse strategies to disrupt or circumvent host antiviral responses triggered by PRRs. These interactions influence the outcomes of poxvirus infections. This review focuses on our current knowledge of the roles of PRRs in the recognition of poxviruses, their elicited antiviral effector functions, and how poxviral immunomodulators antagonize PRR-mediated host immune responses.


Dermatology ◽  
2019 ◽  
Vol 235 (4) ◽  
pp. 295-305 ◽  
Author(s):  
Danuta Nowicka ◽  
Ewelina Grywalska

Staphylococcus aureus is one of the severest and most persistent bacterial pathogens. The most frequent S. aureus infections include impetigo, folliculitis, furuncles, furunculosis, abscesses, hidradenitis suppurativa, and mastitis. S. aureus produces a great variety of cellular and extracellular factors responsible for its invasiveness and ability to cause pathological lesions. Their expression depends on the growth phase, environmental factors, and location of the infection. Susceptibility to staphylococcal infections is rooted in multiple mechanisms of host immune responses and reactions to bacterial colonization. Immunological and inflammatory processes of chronic furunculosis are based on the pathogenicity of S. aureus as well as innate and acquired immunity. In-depth knowledge about them may help to discover the whole pathomechanism of the disease and to develop effective therapeutic options. In this review, we focus on the S. aureus-host immune interactions in the pathogenesis of recurrent furunculosis according to the most recent experimental and clinical findings.


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