Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
6.4
4.5
Journals
Microorganisms
Special Issues
Parasitic Infection and Host Immunity 2.0
share announcement

Parasitic Infection and Host Immunity 2.0

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Parasitology".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 10189

Special Issue Editor

Dr. Célio Geraldo Freire-de-Lima

E-Mail Website
Guest Editor
Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, Brazil
Interests: glycobiology of fungi
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to this Special Issue entitled “Parasitic Infection and Host Immunity 2.0”. Infectious diseases are diseases caused by microorganisms such as viruses, bacteria, protozoa, or fungi, which can be present in the body without causing any damage to the body. However, when there is some change in the host immune system and other clinical conditions, these microorganisms can proliferate, causing disease and facilitating the entry of other microorganisms.

Infectious and contagious diseases can be caused by viruses, fungi, bacteria, or parasites and, depending on the infectious agent, can cause diseases with specific symptoms. Among the main infectious diseases, the following can be mentioned:

1) Infectious diseases caused by viruses; 2) Infectious diseases caused by bacteria; 3) Infectious diseases caused by fungi; 4) Infectious diseases caused by protozoa; 5) Infectious diseases caused by helminths.

Depending on the microorganism causing the disease, characteristic signs and symptoms of the disease may appear, the most common being headache, fever, nausea, weakness, and feeling unwell and tired, especially in the initial phase of the infectious process. However, depending on the disease, more serious symptoms may appear, such as an enlarged liver, stiff neck, convulsions, and coma, for example. Infectious diseases can be acquired through direct contact with the infectious agent or through exposure of the person to contaminated water or food as well as through respiratory, sexual, or animal injuries. These diseases can also often be transmitted from person to person, and are termed infectious diseases in these cases.

This Special Issue aims to review or describe the latest findings regarding the immunopathology, epidemiology, and diagnostic tools in parasitic infection of microorganisms and host immunity. The ultimate goal is to provide readers with new insights into the current and future state of the diagnosis and treatment procedures and pathologies for these diseases.

For this Special Issue, original research articles and reviews are welcome. Research areas of interest may include (but are not limited to) the following: epidemiology of human and animal infectious diseases, immunopathology of human and animal infectious diseases, and clinical treatment and diagnosis of humans. We look forward to receiving your contributions.

Dr. Célio Geraldo Freire-de-Lima
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • infectious diseases
  • parasite infection
  • host-parasite interaction
  • immunomodulation
  • immunopathology
  • epidemiology

Published Papers (6 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Other

19 pages, 2890 KiB  
Article
A Comparative Analysis of Innate Immune Responses and the Structural Characterization of Spike from SARS-CoV-2 Gamma Variants and Subvariants
by Aline Miranda Scovino, Elizabeth Chen Dahab, Israel Diniz-Lima, Etiele de Senna Silveira, Shana Priscila Coutinho Barroso, Karina Martins Cardoso, Dirlei Nico, Gustavo José Makhoul, Elias Barbosa da Silva-Junior, Celio Geraldo Freire-de-Lima, Leonardo Freire-de-Lima, Leonardo Marques da Fonseca, Natalia Valente, Valeria Nacife, Ana Machado, Mia Araújo, Gustavo Fioravanti Vieira, Alex Pauvolid-Corrêa, Marilda Siqueira and Alexandre Morrot
Microorganisms 2024, 12(4), 720; https://doi.org/10.3390/microorganisms12040720 - 02 Apr 2024
Viewed by 916
Abstract
The SARS-CoV-2 P.1 variant, responsible for an outbreak in Manaus, Brazil, is distinguished by 12 amino acid differences in the S protein, potentially increasing its ACE-2 affinity and immune evasion capability. We investigated the innate immune response of this variant compared to the [...] Read more.
The SARS-CoV-2 P.1 variant, responsible for an outbreak in Manaus, Brazil, is distinguished by 12 amino acid differences in the S protein, potentially increasing its ACE-2 affinity and immune evasion capability. We investigated the innate immune response of this variant compared to the original B.1 strain, particularly concerning cytokine production. Blood samples from three severe COVID-19 patients were analyzed post-infection with both strains. Results showed no significant difference in cytokine production of mononuclear cells and neutrophils for either variant. While B.1 had higher cytopathogenicity, neither showed viral replication in mononuclear cells. Structural analyses of the S protein highlighted physicochemical variations, which might be linked to the differences in infectivity between the strains. Our studies point to the increased infectivity of P.1 could stem from altered immunogenicity and receptor-binding affinity. Full article
(This article belongs to the Special Issue Parasitic Infection and Host Immunity 2.0)
►▼ Show Figures

Figure 1

14 pages, 3444 KiB  
Article
Transcriptome Analysis Identifies the Crosstalk between Dendritic and Natural Killer Cells in Human Cutaneous Leishmaniasis
by Sara Nunes, Rafael Tibúrcio, Icaro Bonyek-Silva, Pablo Rafael Oliveira, Ricardo Khouri, Viviane Boaventura, Aldina Barral, Cláudia Brodskyn and Natalia Machado Tavares
Microorganisms 2023, 11(8), 1937; https://doi.org/10.3390/microorganisms11081937 - 29 Jul 2023
Viewed by 1071
Abstract
Skin ulcers of cutaneous leishmaniasis (CL) are characterized by a localized inflammatory response mediated by innate and adaptive immune cells, including dendritic cells (DC) and natural killer (NK) cells. Bidirectional interactions between DCs and NK cells contribute to tailor leishmaniasis outcome. Despite advances [...] Read more.
Skin ulcers of cutaneous leishmaniasis (CL) are characterized by a localized inflammatory response mediated by innate and adaptive immune cells, including dendritic cells (DC) and natural killer (NK) cells. Bidirectional interactions between DCs and NK cells contribute to tailor leishmaniasis outcome. Despite advances in the Leishmania biology field in recent decades, the mechanisms involved in DC/NK-mediated control of Leishmania sp. pathogenesis as well as the cellular and molecular players involved in such interaction remain unclear. The present study sought to investigate canonical pathways associated with CL arising from Leishmania braziliensis infection. Initially, two publicly available microarray datasets of skin biopsies from active CL lesions were analyzed, and five pathways were identified using differentially expressed genes. The “Crosstalk between DCs and NK cells” pathway was notable due to a high number of modulated genes. The molecules significantly involved in this pathway were identified, and our findings were validated in newly obtained CL biopsies. We found increased expression of TLR4, TNFRSF1B, IL-15, IL-6, CD40, CCR7, TNF and IFNG, confirming the analysis of publicly available datasets. These findings reveal the “crosstalk between DCs and NK cells” as a potential pathway to be further explored in the pathogenesis of CL, especially the expression of CCR7, which is correlated with lesion development. Full article
(This article belongs to the Special Issue Parasitic Infection and Host Immunity 2.0)
►▼ Show Figures

Graphical abstract

21 pages, 5670 KiB  
Article
Cytokine Responses during Mycobacterium tuberculosis H37Rv and Ascaris lumbricoides Costimulation Using Human THP-1 and Jurkat Cells, and a Pilot Human Tuberculosis and Helminth Coinfection Study
by Khethiwe N. Bhengu, Ravesh Singh, Pragalathan Naidoo, Miranda N. Mpaka-Mbatha, Nomzamo Nembe-Mafa and Zilungile L. Mkhize-Kwitshana
Microorganisms 2023, 11(7), 1846; https://doi.org/10.3390/microorganisms11071846 - 21 Jul 2023
Viewed by 1324
Abstract
Background: Helminth infections are widespread in tuberculosis-endemic areas and are associated with an increased risk of active tuberculosis. In contrast to the pro-inflammatory Th1 responses elicited by Mycobacterium tuberculosis (Mtb) infection, helminth infections induce anti-inflammatory Th2/Treg responses. A robust Th2 response has been [...] Read more.
Background: Helminth infections are widespread in tuberculosis-endemic areas and are associated with an increased risk of active tuberculosis. In contrast to the pro-inflammatory Th1 responses elicited by Mycobacterium tuberculosis (Mtb) infection, helminth infections induce anti-inflammatory Th2/Treg responses. A robust Th2 response has been linked to reduced tuberculosis protection. Several studies show the effect of helminth infection on BCG vaccination and TB, but the mechanisms remain unclear. Aim: To determine the cytokine response profiles during tuberculosis and intestinal helminth coinfection. Methods: For the in vitro study, lymphocytic Jurkat and monocytic THP-1 cell lines were stimulated with Mtb H37Rv and Ascaris lumbricoides (A. lumbricoides) excretory-secretory protein extracts for 24 and 48 h. The pilot human ex vivo study consisted of participants infected with Mtb, helminths, or coinfected with both Mtb and helminths. Thereafter, the gene transcription levels of IFN-γ, TNF-α, granzyme B, perforin, IL-2, IL-17, NFATC2, Eomesodermin, IL-4, IL-5, IL-10, TGF-β and FoxP3 in the unstimulated/uninfected controls, singly stimulated/infected and costimulated/coinfected groups were determined using RT-qPCR. Results: TB-stimulated Jurkat cells had significantly higher levels of IFN-γ, TNF-α, granzyme B, and perforin compared to unstimulated controls, LPS- and A. lumbricoides-stimulated cells, and A. lumbricoides plus TB-costimulated cells (p < 0.0001). IL-2, IL-17, Eomes, and NFATC2 levels were also higher in TB-stimulated Jurkat cells (p < 0.0001). Jurkat and THP-1 cells singly stimulated with TB had lower IL-5 and IL-4 levels compared to those singly stimulated with A. lumbricoides and those costimulated with TB plus A. lumbricoides (p < 0.0001). A. lumbricoides-singly stimulated cells had higher IL-4 levels compared to TB plus A. lumbricoides-costimulated Jurkat and THP-1 cells (p < 0.0001). TGF-β levels were also lower in TB-singly stimulated cells compared to TB plus A. lumbricoides-costimulated cells (p < 0.0001). IL-10 levels were lower in TB-stimulated Jurkat and THP-1 cells compared to TB plus A. lumbricoides-costimulated cells (p < 0.0001). Similar results were noted for the human ex vivo study, albeit with a smaller sample size. Conclusions: Data suggest that helminths induce a predominant Th2/Treg response which may downregulate critical Th1 responses that are crucial for tuberculosis protection. Full article
(This article belongs to the Special Issue Parasitic Infection and Host Immunity 2.0)
►▼ Show Figures

Figure 1

21 pages, 3140 KiB  
Article
Is There Any Difference in the In Situ Immune Response in Active Localized Cutaneous Leishmaniasis That Respond Well or Poorly to Meglumine Antimoniate Treatment or Spontaneously Heal?
by Jéssica Leite-Silva, Carla Oliveira-Ribeiro, Fernanda Nazaré Morgado, Maria Inês Fernandes Pimentel, Marcelo Rosandiski Lyra, Aline Fagundes, Luciana Freitas Campos Miranda, Claudia Maria Valete-Rosalino, Armando Oliveira Schubach and Fátima Conceição-Silva
Microorganisms 2023, 11(7), 1631; https://doi.org/10.3390/microorganisms11071631 - 22 Jun 2023
Cited by 1 | Viewed by 931
Abstract
Localized cutaneous leishmaniasis caused by Leishmania braziliensis can either respond well or poorly to the treatment or heal spontaneously; It seems to be dependent on the parasite and/or host factors, but the mechanisms are not fully understood. We evaluated the in situ immune [...] Read more.
Localized cutaneous leishmaniasis caused by Leishmania braziliensis can either respond well or poorly to the treatment or heal spontaneously; It seems to be dependent on the parasite and/or host factors, but the mechanisms are not fully understood. We evaluated the in situ immune response in eighty-two active lesions from fifty-eight patients prior to treatment classified as early spontaneous regression (SRL-n = 14); treatment responders (GRL-n = 20); and non-responders (before first treatment/relapse, PRL1/PRL2-n = 24 each). Immunohistochemistry was used to identify cell/functional markers which were correlated with the clinical characteristics. PRL showed significant differences in lesion number/size, clinical evolution, and positive parasitological examinations when compared with the other groups. SRL presented a more efficient immune response than GRL and PRL, with higher IFN-γ/NOS2 and a lower percentage of macrophages, neutrophils, NK, B cells, and Ki-67+ cells. Compared to SRL, PRL had fewer CD4+ Tcells and more CD163+ macrophages. PRL1 had more CD68+ macrophages and Ki-67+ cells but less IFN-γ than GRL. PRL present a less efficient immune profile, which could explain the poor treatment response, while SRL had a more balanced immune response profile for lesion healing. Altogether, these evaluations suggest a differentiated profile of the organization of the inflammatory process for lesions of different tegumentary leishmaniasis evolution. Full article
(This article belongs to the Special Issue Parasitic Infection and Host Immunity 2.0)
►▼ Show Figures

Figure 1

14 pages, 3074 KiB  
Article
Gene Signatures of Symptomatic and Asymptomatic Clinical-Immunological Profiles of Human Infection by Leishmania (L.) chagasi in Amazonian Brazil
by Vania Lucia R. da Matta, André N. Gonçalves, Cláudia Maria C. Gomes, Islam H. Chouman, Frederico M. Ferreira, Marliane B. Campos, Luciana V. Lima, Thiago Vasconcelos dos Santos, Patrícia Karla Ramos, Rodrigo R. Furtado, Marcia D. Laurenti, Carlos Eduardo P. Corbett, Helder I. Nakaya and Fernando T. Silveira
Microorganisms 2023, 11(3), 653; https://doi.org/10.3390/microorganisms11030653 - 03 Mar 2023
Cited by 1 | Viewed by 1553
Abstract
Individuals infected with Leishmania (L.) chagasi may present different asymptomatic and symptomatic stages of infection, which vary in the clinical–immunological profiles that can be classified as asymptomatic infection (AI), subclinical resistant infection (SRI), indeterminate initial infection (III), subclinical oligosymptomatic infection (SOI), [...] Read more.
Individuals infected with Leishmania (L.) chagasi may present different asymptomatic and symptomatic stages of infection, which vary in the clinical–immunological profiles that can be classified as asymptomatic infection (AI), subclinical resistant infection (SRI), indeterminate initial infection (III), subclinical oligosymptomatic infection (SOI), and symptomatic infection (SI) (=American visceral leishmaniasis, AVL). However, little is known about the molecular differences between individuals having each profile. Here, we performed whole-blood transcriptomic analyses of 56 infected individuals from Pará State (Brazilian Amazon), covering all five profiles. We then identified the gene signatures of each profile by comparing their transcriptome with those of 11 healthy individuals from the same area. Symptomatic individuals with SI (=AVL) and SOI profiles showed higher transcriptome perturbation when compared to those asymptomatic III, AI and SRI profiles, suggesting that disease severity may be associated with greater transcriptomic changes. Although the expression of many genes was altered on each profile, very few genes were shared among the profiles. This indicated that each profile has a unique gene signature. The innate immune system pathway was strongly activated only in asymptomatic AI and SRI profiles, suggesting the control of infection. In turn, pathways such as MHC Class II antigen presentation and NF-kB activation in B cells seemed to be specifically induced in symptomatic SI (=AVL) and SOI profiles. Moreover, cellular response to starvation was down-regulated in those symptomatic profiles. Overall, this study revealed five distinct transcriptional patterns associated to the clinical–immunological (symptomatic and asymptomatic) profiles of human L. (L.) chagasi-infection in the Brazilian Amazon. Full article
(This article belongs to the Special Issue Parasitic Infection and Host Immunity 2.0)
►▼ Show Figures

Figure 1

Other

Jump to: Research

13 pages, 1761 KiB  
Perspective
Visiting Molecular Mimicry Once More: Pathogenicity, Virulence, and Autoimmunity
by Yuri Chaves Martins, Arnon Dias Jurberg and Cláudio Tadeu Daniel-Ribeiro
Microorganisms 2023, 11(6), 1472; https://doi.org/10.3390/microorganisms11061472 - 01 Jun 2023
Cited by 3 | Viewed by 3462
Abstract
The concept of molecular mimicry describes situations in which antigen sharing between parasites and hosts could benefit pathogen evasion from host immune responses. However, antigen sharing can generate host responses to parasite-derived self-like peptides, triggering autoimmunity. Since its conception, molecular mimicry and the [...] Read more.
The concept of molecular mimicry describes situations in which antigen sharing between parasites and hosts could benefit pathogen evasion from host immune responses. However, antigen sharing can generate host responses to parasite-derived self-like peptides, triggering autoimmunity. Since its conception, molecular mimicry and the consequent potential cross-reactivity following infections have been repeatedly described in humans, raising increasing interest among immunologists. Here, we reviewed this concept focusing on the challenge of maintaining host immune tolerance to self-components in parasitic diseases. We focused on the studies that used genomics and bioinformatics to estimate the extent of antigen sharing between proteomes of different organisms. In addition, we comparatively analyzed human and murine proteomes for peptide sharing with proteomes of pathogenic and non-pathogenic organisms. We conclude that, although the amount of antigenic sharing between hosts and both pathogenic and non-pathogenic parasites and bacteria is massive, the degree of this antigen sharing is not related to pathogenicity or virulence. In addition, because the development of autoimmunity in response to infections by microorganisms endowed with cross-reacting antigens is rare, we conclude that molecular mimicry by itself is not a sufficient factor to disrupt intact self-tolerance mechanisms. Full article
(This article belongs to the Special Issue Parasitic Infection and Host Immunity 2.0)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-6
Back to TopTop