scholarly journals Host-Microbial Relationship: Immune Response to Microbial Infections with or without Medication

2021 ◽  
Author(s):  
Faustina Pappoe ◽  
Samuel Victor Nuvor
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Drug Treatment ◽  
Host Immune System ◽  
Infectious Agents ◽  
Microbial Infection ◽  
Disease Condition ◽  
Microbial Infections ◽  
The Relationship

Immune responses of the host to any infectious agents vary in controlling the pathogens. The process begins by the entry of microorganisms into the host to initiate host immune response to understand the type of microorganisms and react accordingly for possible elimination of the organisms. In some cases the host co-exists with the pathogens or unable to effectively deal with them leading to disease condition. Thus, the pathogens establish, multiply and cause disease. The review considered the mode of acquisition of infection, pathogenesis and immune responses to microbial infection. Other areas included the enhancement of immune responses to control infection, immune responses of the host under drug treatment and the control of microbial infection. The understanding of the relationship between infectious microbes and the host immune system leading to protective immunity or disease state will give much information about treatment and controlling of microbial infection in our environment.

scholarly journals Review on the Relationship between Human Polyomaviruses-Associated Tumors and Host Immune System

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Serena Delbue ◽  
Manola Comar ◽  
Pasquale Ferrante
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Human Population ◽  
Host Immune System ◽  
Dna Viruses ◽  
Human Host ◽  
Immunosuppressed Patients ◽  
The Relationship ◽  
Associated Tumors ◽  
Human Polyomaviruses

The polyomaviruses are small DNA viruses that can establish latency in the human host. The name polyomavirus is derived from the Greek rootspoly-, which means “many,” and -oma, which means “tumours.” These viruses were originally isolated in mouse (mPyV) and in monkey (SV40). In 1971, the first human polyomaviruses BK and JC were isolated and subsequently demonstrated to be ubiquitous in the human population. To date, at least nine members of thePolyomaviridaefamily have been identified, some of them playing an etiological role in malignancies in immunosuppressed patients. Here, we describe the biology of human polyomaviruses, their nonmalignant and malignant potentials ability, and their relationship with the host immune response.

scholarly journals Inflammasome Activation in Bovine Peripheral Blood-Derived Macrophages Is Associated with Actin Rearrangement

Animals ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 655
Author(s):  
Amin Tahoun ◽  
Kirsty Jensen ◽  
Hanem El-Sharkawy ◽  
David Gally ◽  
Amira M. Rizk ◽  
...  
Keyword(s):  
Cell Death ◽  
Immune System ◽  
Immune Responses ◽  
Defense Mechanism ◽  
Inflammasome Activation ◽  
Host Immune System ◽  
Bovine Macrophage ◽  
The Relationship ◽  
Actin Localization ◽  
Actin Rearrangement

Inflammation is critical for infection control and acts as an arsenal defense mechanism against invading microbes through activation of the host immune system. It works via its inflammasome components to sense the dangerous invading microorganism and send messages to the immune system to destroy them. To date, the function of bovine macrophage inflammasome and its relationship with actin has not been identified. This study aimed to investigate the activation of bovine inflammasome by phase one flagellin from Salmonella typhimurium and its interaction with actin. Bovine monocyte-derived macrophages were prepared and challenged with S. typhimurium SL1344 phase one flagellin. The results demonstrated the relationship between the flagellin-based activation of inflammasome and actin rearrangement. The flagellin-based activation of inflammasome promoted the activation and co-localization of F-actin and the inflammasome complex. Actin was remodeled to different degrees according to the stage of inflammasome activation. The actin redistribution varied from polymerization to filopodia, while at the stage of pyroptotic cell death, actin was broken down and interacted with activated inflammasome complexes. In conclusion, flagellin-dependent inflammasome activation and actin localization to the inflammasome at the stage of pyroptotic cell death may be of importance for appropriate immune responses, pending further studies to explore the exact cross-linking between the inflammasome complex and actin.

scholarly journals Immunity against Helminths: Interactions with the Host and the Intercurrent Infections

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Emmanuelle Moreau ◽  
Alain Chauvin
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Chronic Infection ◽  
Inflammatory Diseases ◽  
Economic Importance ◽  
Host Immune System ◽  
Helminth Parasites ◽  
Strong Immune Response ◽  
Helminth Infections

Helminth parasites are of considerable medical and economic importance. Studies of the immune response against helminths are of great interest in understanding interactions between the host immune system and parasites. Effector immune mechanisms against tissue-dwelling helminths and helminths localized in the lumen of organs, and their regulation, are reviewed. Helminth infections are characterized by an association of Th2-like and Treg responses. Worms are able to persist in the host and are mainly responsible for chronic infection despite a strong immune response developed by the parasitized host. Two types of protection against the parasite, namely, premune and partial immunities, have been described. Immune responses against helminths can also participate in pathogenesis. Th2/Treg-like immunomodulation allows the survival of both host and parasite by controlling immunopathologic disorders and parasite persistence. Consequences of the modified Th2-like responses on co-infection, vaccination, and inflammatory diseases are discussed.

scholarly journals Chronic microbial infections: Manipulation of host immunity as interventional approach

1970 ◽  
Vol 1 (1) ◽  
pp. 13-19
Author(s):  
Sheikh Mohammad Fazle Akbar ◽  
Md Sakirul Islam Khan ◽  
Shunji Mishiro
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Viral Infections ◽  
Inflammatory Diseases ◽  
Acute Infection ◽  
Immune Surveillance ◽  
Host Immune System ◽  
Related Factors ◽  
Chronic Viral Infections ◽  
Microbial Infections

Chronic viral infections represent major challenges in contemporary medicine, virology and pharmacology. The virus-bearing hosts are commonly found in every parts of the world and it is extremely difficult to manage these patients. In addition, considerable numbers of these patients develop progressive diseases and severe complications. Finally, most of these patients act as permanent reservoirs of virus. Understandings of viral life cycle during the last decade of 20th century and the first decade of 21st century have allowed development of hundreds of antiviral agents for different diseases. But, the clinical efficacy of these drugs is not yet satisfactory. In addition, virologists have provided conclusive evidences suggesting that eradication of most chronic virus from infected hosts may an unachievable goal. In this context, it is essential to develop alternative, novel, and evidence-based therapeutic maneuver for these patients. Manipulation of host immune system may be one of these approaches. We would discuss about scopes, limitations, and strategies for manipulation for controlling of chronic viral infections. The primary function of the host's immune system is to mount responses that protect the individual from various microbial infections including viruses. Host's immune responses also control the spread and virulence of the viruses [1]. This is applicable to viruses that cause acute infection. After entering the hosts, these viruses are localized in host's tissues, proliferate and induce antiviral immunity. These cellular events may cause damage and destruction of tissues and the host exhibit features of acute inflammatory diseases. However, the viruses are either almost completely eliminated from the hosts or adequately controlled in situ by host's immune systems. However, chronic infection is established by many viruses because the hosts induce improper and uncoordinated immune responses against these viruses. Most viruses cause persistent infection by evading the host immune surveillance mechanism. Both virus-related factors and host-dependent factors are primarily responsible for viral persistency in subjects with chronic viral infections.    doi: 10.3329/blj.v1i1.2620 Bangladesh Liver Journal Vol.1(1) 2009 p.13-19 

scholarly journals Diversity of vaccination-induced immune responses can prevent the spread of vaccine escape mutants

2021 ◽  
Author(s):  
Judith Aveline Bouman ◽  
Céline Capelli ◽  
Roland Regoes
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Drug Treatment ◽  
Critical Levels ◽  
Response Diversity ◽  
Escape Depth ◽  
The Face ◽  
Escape Mutants ◽  
The Cost

Pathogens that are resistant against drug treatment are widely observed. In contrast, pathogens that escape the immune response elicited upon vaccination are rare. Previous studies showed that the prophylactic character of vaccines, the multiplicity of epitopes to which the immune system responds within a host, and their diversity between hosts delay the evolution and emergence of escape mutants in a vaccinated population. By extending previous mathematical models, we find that, depending on the cost of the escape mutations, there even exist critical levels of immune response diversity that completely prevent vaccine escape. Furthermore, to quantify the potential for vaccine escape below these critical levels, we propose a concept of escape depth which measures the fraction of escape mutants that can spread in a vaccinated population. Determining this escape depth for a vaccine could help to predict its sustainability in the face of pathogen evolution.

scholarly journals Cryptococcus neoformans Rim101 Is Associated with Cell Wall Remodeling and Evasion of the Host Immune Responses

mBio ◽  
2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Teresa R. O'Meara ◽  
Stephanie M. Holmer ◽  
Kyla Selvig ◽  
Fred Dietrich ◽  
J. Andrew Alspaugh
Keyword(s):  
Immune Response ◽  
Cell Wall ◽  
Transcription Factor ◽  
Immune System ◽  
Immune Responses ◽  
Cryptococcus Neoformans ◽  
Host Immune Response ◽  
Host Immune System ◽  
Content Type ◽  
Host Pathogen

ABSTRACTInfectious microorganisms often play a role in modulating the immune responses of their infected hosts. We demonstrate thatCryptococcus neoformanssignals through the Rim101 transcription factor to regulate cell wall composition and the host-pathogen interface. In the absence of Rim101,C. neoformansexhibits an altered cell surface in response to host signals, generating an excessive and ineffective immune response that results in accelerated host death. This host immune response to therim101Δ mutant strain is characterized by increased neutrophil influx into the infected lungs and an altered pattern of host cytokine expression compared to the response to wild-type cryptococcal infection. To identify genes associated with the observed phenotypes, we performed whole-genome RNA sequencing experiments under capsule-inducing conditions. We defined the downstream regulon of the Rim101 transcription factor and determined potential cell wall processes involved in the capsule attachment defects and altered mechanisms of virulence in therim101Δ mutant. The cell wall generates structural stability for the cell and allows the attachment of surface molecules such as capsule polysaccharides. In turn, the capsule provides an effective mask for the immunogenic cell wall, shielding it from recognition by the host immune system.IMPORTANCECryptococcus neoformansis an opportunistic human pathogen that is a significant cause of death in immunocompromised individuals. There are two major causes of death due to this pathogen: meningitis due to uncontrolled fungal proliferation in the brain in the face of a weakened immune system and immune reconstitution inflammatory syndrome characterized by an overactive immune response to subclinical levels of the pathogen. In this study, we examined howC. neoformansuses the conserved Rim101 transcription factor to specifically remodel the host-pathogen interface, thus regulating the host immune response. These studies explored the complex ways in which successful microbial pathogens induce phenotypes that ensure their own survival while simultaneously controlling the nature and degree of the associated host response.

scholarly journals Impact of Zinc, Glutathione, and Polyphenols as Antioxidants in the Immune Response against SARS-CoV-2

Processes ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 506
Author(s):  
José Manuel Pérez de la Lastra ◽  
Celia Andrés-Juan ◽  
Francisco J. Plou ◽  
Eduardo Pérez-Lebeña
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Rational Design ◽  
Global Scale ◽  
Key Factors ◽  
Central Function ◽  
Antiviral Immune Response ◽  
The Relationship

SARS-CoV-2, the coronavirus triggering the disease COVID-19, has a catastrophic health and socioeconomic impact at a global scale. Three key factors contribute to the pathogenesis of COVID-19: excessive inflammation, immune system depression/inhibition, and a set of proinflammatory cytokines. Common to these factors, a central function of oxidative stress has been highlighted. A diversity of clinical trials focused predominantly on antioxidants are being implemented as potential therapies for COVID-19. In this study, we look at the role of zinc, glutathione, and polyphenols, as key antioxidants of possible medicinal or nutritional significance, and examine their role in the antiviral immune response induced by SARS-Cov-2. An unresolved question is why some people experience chronic COVID and others do not. Understanding the relationship between SARS-CoV-2 and the immune system, as well as the role of defective immune responses to disease development, would be essential to recognize the pathogenesis of COVID-19, the risk factors that affect the harmful consequences of the disease, and the rational design of successful therapies and vaccinations. We expect that our research will provide a novel perspective that contributes to the design of clinical or nutritional targets for the prevention of this pandemic.

scholarly journals Concomitant infections, parasites and immune responses

Parasitology ◽  
2001 ◽  
Vol 122 (S1) ◽  
pp. S23-S38 ◽  
Author(s):  
F. E. G. COX
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
The Other ◽  
Clinical Disease ◽  
Mixed Infections ◽  
Infectious Agents ◽  
Cytokine Network ◽  
Immune Effector ◽  
Effector Molecules

Concomitant infections are common in nature and often involve parasites. A number of examples of the interactions between protozoa and viruses, protozoa and bacteria, protozoa and other protozoa, protozoa and helminths, helminths and viruses, helminths and bacteria, and helminths and other helminths are described. In mixed infections the burden of one or both the infectious agents may be increased, one or both may be suppressed or one may be increased and the other suppressed. It is now possible to explain many of these interactions in terms of the effects parasites have on the immune system, particularly parasite-induced immunodepression, and the effects of cytokines controlling polarization to the Th1or Th2arms of the immune response. In addition, parasites may be affected, directly or indirectly, by cytokines and other immune effector molecules and parasites may themselves produce factors that affect the cells of the immune system. Parasites are, therefore, affected when they themselves, or other organisms, interact with the immune response and, in particular, the cytokine network. The importance of such interactions is discussed in relation to clinical disease and the development and use of vaccines.

scholarly journals Crosstalk between gut microbiota and intestinal mucosal immunity in the development of ulcerative colitis

2021 ◽  
Author(s):  
Junfeng Zou ◽  
Chen Liu ◽  
Shu Jiang ◽  
Dawei Qian ◽  
Jinao Duan
Keyword(s):  
Ulcerative Colitis ◽  
Immune System ◽  
Immune Responses ◽  
Mucosal Immunity ◽  
Mucosal Damage ◽  
Host Immune System ◽  
Microbiota Composition ◽  
Intestinal Immunity ◽  
Microbial Dysbiosis ◽  
The Relationship

Ulcerative colitis (UC), a nonspecific inflammatory disease, is characterized by inflammation and mucosal damage in the colon, and its prevalence in the worldwide is increasing. Nevertheless, the exact pathogenesis of UC is still unclear. Accumulating data have suggested that its pathogenesis is multifactorial, involving genetic predisposition, environmental factors, microbial dysbiosis and dysregulated immune responses. Generally, UC is aroused by inappropriate immune activation based on the interaction of host and intestinal microbiota. The relationship between microbiota and host immune system in the pathogenesis of UC is complicated. However, increasing evidence indicates that the shift of microbiota composition can substantially influence intestinal immunity. In this review, we primarily focus on the delicate balance between microbiota and gut mucosal immunity during UC progression.

scholarly journals How the insect immune system interacts with an obligate symbiotic bacterium

2010 ◽  
Vol 278 (1704) ◽  
pp. 333-338 ◽  
Author(s):  
A. E. Douglas ◽  
S. Bouvaine ◽  
R. R. Russell
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Acyrthosiphon Pisum ◽  
Gene Expression Pattern ◽  
Symbiotic Bacterium ◽  
Host Cells ◽  
Host Immune System ◽  
S2 Cells ◽  
Microbial Infection ◽  
Imd Pathway

The animal immune system provides defence against microbial infection, and the evolution of certain animal–microbial symbioses is predicted to involve adaptive changes in the host immune system to accommodate the microbial partner. For example, the reduced humoral immune system in the pea aphid Acyrthosiphon pisum , including an apparently non-functional immune deficiency (IMD) signalling pathway and absence of peptidoglycan recognition proteins (PGRPs), has been suggested to be an adaptation for the symbiosis with the bacterium Buchnera aphidicola . To investigate this hypothesis, the interaction between Buchnera and non-host cells, specifically cultured Drosophila S2 cells, was investigated. Microarray analysis of the gene expression pattern in S2 cells indicated that Buchnera triggered an immune response, including upregulated expression of genes for antimicrobial peptides via the IMD pathway with the PGRP-LC as receptor. Buchnera cells were readily taken up by S2 cells, but were subsequently eliminated over 1–2 days. These data suggest that Buchnera induces in non-host cells a defensive immune response that is deficient in its host. They support the proposed contribution of the Buchnera symbiosis to the evolution of the apparently reduced immune function in the aphid host.

Sign in / Sign up

Export Citation Format

Share Document