Infectious Diseases Immunology 2.0

A special issue of Vaccines (ISSN 2076-393X).

Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 16779

Special Issue Editor


E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, Institute of Microbiology, Università degli Studi di Brescia, 25123 Brescia, Italy
Interests: antibiotic resistance; antiviral resistance; molecular epidemiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The development of an infectious disease is the result of complex interactions between pathogens and host immune system. It exists a dynamic equilibrium between immune system which elaborates mechanisms to eradicate infections and the evolution of different microbial strategies to overcome immune defences such as antigenic variation, resistance to phagocytic or complement killing and the production of enzymes inactivating some host cellular proteins.

Our immune system is able to enhance protective immunity against an almost unlimited number of pathogens comprising bacteria, viruses, fungi and parasites. Immunity enhancing is traditionally obtained by using vaccines, even if other modalities of immune modulation are currently under investigation. Likewise, besides this friendly aspect (Mr. Hyde) of host immune system, there is a contradictory aspect (Mr. Jeckyll) where the immune system itself is responsible of disease and tissue damage because some microorganisms have evolved ingenious tools to subvert host’s immune responses for their own survival.

In this special issues, all papers, reviews, diagnostic methodologies able to shed new light both on the mechanisms able to enhance immunity or to elucidate the strategies adopted by pathogens to establish immune interference and induce persistent infections are welcome. Also all studies able to clarify the interrelationship between microorganisms and host immune responses are included.

Prof. Maria Antonia De Francesco
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. Vaccines 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.

Published Papers (4 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review, Other

19 pages, 6088 KiB  
Article
Characterization of Membrane-Associated Progesterone Receptor Component-2 (MAPRC2) from Trichinella spiralis and Its Interaction with Progesterone and Mifepristone
by Muhammad Tahir Aleem, Jiawen Shi, Zhengqing Yu, Zhaohai Wen, Yang Zhang, Meng Liang, Shakeel Ahmed Lakho, Muhammad Haseeb, Haider Ali, Muhammad Waqas Hassan, Xiaokai Song, Xiangrui Li, Lixin Xu and Ruofeng Yan
Vaccines 2021, 9(8), 934; https://doi.org/10.3390/vaccines9080934 - 23 Aug 2021
Cited by 4 | Viewed by 2285
Abstract
Trichinellosis is a foodborne zoonotic disease caused by Trichinella spp., including Trichinella spiralis. In the present study, T. spiralis membrane-associated progesterone receptor component-2 (Ts-MAPRC2) gene was cloned and characterized using protein sequencing analysis. Furthermore, the expression, purification, immunoblot assay, binding [...] Read more.
Trichinellosis is a foodborne zoonotic disease caused by Trichinella spp., including Trichinella spiralis. In the present study, T. spiralis membrane-associated progesterone receptor component-2 (Ts-MAPRC2) gene was cloned and characterized using protein sequencing analysis. Furthermore, the expression, purification, immunoblot assay, binding ability with progesterone antibody, and immunofluorescence assay were performed. A direct effect of progesterone (P4) and mifepristone (RU486) on the Ts-MAPRC2 gene was determined using in vitro cell culture that showed different expression levels at all developmental stages (muscle larvae (ML), female adult worm (F-AL), male adult worm (M-AL), and newborn larvae (NBL)). Subsequently, the in vitro phenotypic effects of P4, RU486, and rTs-MAPRC2-Ab on F-AL and ML stages were measured. Later, the in vivo phenotypic effect and relative mRNA expression of mifepristone on the F-AL stage were studied. Our results revealed that the Ts-MAPRC2 gene is critical to maintaining pregnancy in the female adult worm (F-AL) of T. spiralis. The 300 ng/mL of P4 and 100 ng/mL of RU486 showed downregulation of the Ts-MAPRC2 gene in F-AL (p ≤ 0.05). This plays an important role in abortion and possibly decreases the worm burden of T. spiralis in the host. Only 30 ng/mL P4 showed significant upregulation in F-AL (p ≤ 0.05). The current study provides new insights regarding the antihormone (P4 and RU486) drug design and vaccine therapy of recombinant (rTs-MAPRC2) protein as well as their combined effects to control T. spiralis infection. Full article
(This article belongs to the Special Issue Infectious Diseases Immunology 2.0)
Show Figures

Figure 1

Review

Jump to: Research, Other

12 pages, 524 KiB  
Review
The Gut Microbiome in Psoriasis and Crohn’s Disease: Is Its Perturbation a Common Denominator for Their Pathogenesis?
by Maria Antonia De Francesco and Arnaldo Caruso
Vaccines 2022, 10(2), 244; https://doi.org/10.3390/vaccines10020244 - 5 Feb 2022
Cited by 13 | Viewed by 3607
Abstract
Psoriasis and inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), are interlinked. In fact, the prevalence of IBD is higher in patients with psoriasis, with a risk of ulcerative colitis of 1.6-times higher than in the general population. Analogously, [...] Read more.
Psoriasis and inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), are interlinked. In fact, the prevalence of IBD is higher in patients with psoriasis, with a risk of ulcerative colitis of 1.6-times higher than in the general population. Analogously, patients with psoriasis have a greater risk of developing IBD. Furthermore, they share some clinical features and pathogenic mechanisms. Both are chronic inflammatory diseases with a relapsing-remitting condition that persists for the patient’s whole life and exhibit increased permeability of the mucosal barrier of skin and gut, allowing an increased interaction of pathogens with inflammatory receptors of the immune cells. A key element in the pathogenesis of these diseases is represented by the microbiota; in particular, the gut microbiota is an important driver of CD pathogenesis, while in psoriasis changes in gut and skin microbiota have been described without a defined pathogenic function. Furthermore, genetic predispositions or environmental factors contribute to disease manifestation, with a central role attributed to the immune responses and, in particular, to a dysregulated role played by T helper 17 cells both in psoriasis and IBD. The purpose of this review was to summarize present information about the links between psoriasis, inflammatory bowel disease, in particular Crohn’s disease, and changes in gut and/or skin microbiome. Full article
(This article belongs to the Special Issue Infectious Diseases Immunology 2.0)
Show Figures

Figure 1

14 pages, 311 KiB  
Review
Antibody Responses to Natural SARS-CoV-2 Infection or after COVID-19 Vaccination
by Haya Altawalah
Vaccines 2021, 9(8), 910; https://doi.org/10.3390/vaccines9080910 - 16 Aug 2021
Cited by 46 | Viewed by 7548
Abstract
The novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is the causative agent of the ongoing pandemic of coronavirus disease 2019 (COVID-19). The clinical severity of COVID-19 ranges from asymptomatic to critical disease and, eventually, death in smaller subsets of patients. The [...] Read more.
The novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is the causative agent of the ongoing pandemic of coronavirus disease 2019 (COVID-19). The clinical severity of COVID-19 ranges from asymptomatic to critical disease and, eventually, death in smaller subsets of patients. The first case of COVID-19 was declared at the end of 2019 and it has since spread worldwide and remained a challenge in 2021, with the emergence of variants of concern. In fact, new concerns were the still unclear situation of SARS-CoV-2 immunity during the ongoing pandemic and progress with vaccination. If maintained at sufficiently high levels, the immune response could effectively block reinfection, which might confer long-lived protection. Understanding the protective capacity and the duration of humoral immunity during SARS-CoV-2 infection or after vaccination is critical for managing the pandemic and would also provide more evidence about the efficacy of SARS-CoV-2 vaccines. However, the exact features of antibody responses that govern SARS-CoV-2 infection or after vaccination remain unclear. This review summarizes the main knowledge that we have about the humoral immune response during COVID-19 disease or after vaccination. Such knowledge should help to optimize vaccination strategies and public health decisions. Full article
(This article belongs to the Special Issue Infectious Diseases Immunology 2.0)

Other

Jump to: Research, Review

9 pages, 1439 KiB  
Brief Report
Management of Invasive Infections due to a Rare Arthroconidial Yeast, Saprochaete capitata, in Two Patients with Acute Hematological Malignancies
by Francesca Gurrieri, Silvia Corbellini, Giorgio Piccinelli, Alessandro Turra, Enrico Morello, Michele Malagola, Domenico Russo, Arnaldo Caruso and Maria Antonia De Francesco
Vaccines 2021, 9(11), 1289; https://doi.org/10.3390/vaccines9111289 - 6 Nov 2021
Cited by 3 | Viewed by 2366
Abstract
Saprochaete capitata is an arthroconidial yeast, found principally in the environment, even if it belongs also to the normal microbial flora that colonize human subjects. This yeast is increasingly associated with invasive infections in hematological patients, in particular in those affected by acute [...] Read more.
Saprochaete capitata is an arthroconidial yeast, found principally in the environment, even if it belongs also to the normal microbial flora that colonize human subjects. This yeast is increasingly associated with invasive infections in hematological patients, in particular in those affected by acute leukemia. An important risk factor that predisposes to this infection is the profound neutropenia present in such immunocompromised patients. Saprochaete spp. were found resistant to both echinocandins and fluconazole so the treatment is often difficult. Here, we report two cases of sepsis in two patients with acute leukemia. All of them had fatal events, due to the worsening of their clinical condition. An early diagnosis and appropriate management of these pathogens is important in consideration of the poor prognosis associated to these fungal invasive infections. Full article
(This article belongs to the Special Issue Infectious Diseases Immunology 2.0)
Show Figures

Figure 1

Back to TopTop