Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Inflammation Cell Signaling and Infectious Diseases

Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (20 May 2023) | Viewed by 10195

Share This Special Issue

Special Issue Editor

Prof. Dr. Imad Kansau

E-Mail Website
Guest Editor

1. Faculté de Pharmacie, Université Paris-Saclay, 91400 Orsay, France
2. Hopital Antoine Beclere (APHP), 92140 Clamart, France
Interests: infectious diseases; microbiology; host-response; clostridioides difficile; inflammation cell signaling; flagella; TLR5 signaling; miRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammation is the typical response of the immune system to external (infection, allergy, trauma, burn, etc.) or internal (cancer) aggression aimed at suppressing the source of aggression and repairing tissues. This ubiquitous process involves all tissues and engages both innate and adaptive immune responses. Chronic inflammatory processes can be triggered in response to numerous environmental stimuli, including infectious ones, particularly those linked to alterations in the human microbiota and exposure to xenobiotics, including pollutants. Faced with these major challenges, it is important to fully understand the complex mechanisms of inflammation, as well as the specific cell signaling pathways finely regulated by closely interwoven cellular mechanisms. This Special Issue will be devoted to the mechanisms of inflammation in the pathophysiology of infections in humans. All scientific studies that contribute to enriching our knowledge of the signaling pathways involved in inflammation, as well as the intimate mechanisms of the regulation of these pathways in different pathophysiological situations during infection, are welcome.

Prof. Dr. Imad Kansau
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

human microbiota
cell signaling
immune response
innate immune response
TLR signaling pathways
NOD signaling pathways
inflammasome signaling pathways
adaptive immune response
regulation of gene expression

Published Papers (4 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

17 pages, 2888 KiB

Open AccessArticle

Characterization of Systemic Disease Development and Paw Inflammation in a Susceptible Mouse Model of Mayaro Virus Infection and Validation Using X-ray Synchrotron Microtomography

by Ana Carolina de Carvalho, Carlos Sato B. Dias, Laís D. Coimbra, Rebeca P. F. Rocha, Alexandre Borin, Marina A. Fontoura, Murilo Carvalho, Paul Proost, Maurício L. Nogueira, Sílvio R. Consonni, Renata Sesti-Costa and Rafael Elias Marques

Int. J. Mol. Sci. 2023, 24(5), 4799; https://doi.org/10.3390/ijms24054799 - 2 Mar 2023

Cited by 2 | Viewed by 2161

Abstract

Mayaro virus (MAYV) is an emerging arthropod-borne virus endemic in Latin America and the causative agent of arthritogenic febrile disease. Mayaro fever is poorly understood; thus, we established an in vivo model of infection in susceptible type-I interferon receptor-deficient mice (IFNAR−/−) to characterize the disease. MAYV inoculations in the hind paws of IFNAR−/− mice result in visible paw inflammation, evolve into a disseminated infection and involve the activation of immune responses and inflammation. The histological analysis of inflamed paws indicated edema at the dermis and between muscle fibers and ligaments. Paw edema affected multiple tissues and was associated with MAYV replication, the local production of CXCL1 and the recruitment of granulocytes and mononuclear leukocytes to muscle. We developed a semi-automated X-ray microtomography method to visualize both soft tissue and bone, allowing for the quantification of MAYV-induced paw edema in 3D with a voxel size of 69 µm³. The results confirmed early edema onset and spreading through multiple tissues in inoculated paws. In conclusion, we detailed features of MAYV-induced systemic disease and the manifestation of paw edema in a mouse model extensively used to study infection with alphaviruses. The participation of lymphocytes and neutrophils and expression of CXCL1 are key features in both systemic and local manifestations of MAYV disease. Full article

(This article belongs to the Special Issue Inflammation Cell Signaling and Infectious Diseases)

► Show Figures

Figure 1

20 pages, 4737 KiB

Open AccessArticle

Coordinated Loss and Acquisition of NK Cell Surface Markers Accompanied by Generalized Cytokine Dysregulation in COVID-19

by Maria O. Ustiuzhanina, Julia D. Vavilova, Anna A. Boyko, Maria A. Streltsova, Sofya A. Kust, Leonid M. Kanevskiy, Alexander M. Sapozhnikov, Rustam N. Iskhakov, Ekaterina O. Gubernatorova, Marina S. Drutskaya, Mikhail V. Bychinin, Oksana A. Zhukova, Oksana N. Novikova, Anna G. Sotnikova, Gaukhar M. Yusubalieva, Vladimir P. Baklaushev and Elena I. Kovalenko

Int. J. Mol. Sci. 2023, 24(3), 1996; https://doi.org/10.3390/ijms24031996 - 19 Jan 2023

Cited by 5 | Viewed by 2592

Abstract

Coronavirus disease 2019 (COVID-19), caused by the SARS-CoV-2 virus, is accompanied by a dysregulated immune response. In particular, NK cells, involved in the antiviral response, are affected by the infection. This study aimed to investigate circulating NK cells with a focus on their activation, depletion, changes in the surface expression of key receptors, and functional activity during COVID-19, among intensive care unit (ICU) patients, moderately ill patients, and convalescents (CCP). Our data confirmed that NK cell activation in patients with COVID-19 is accompanied by changes in circulating cytokines. The progression of COVID-19 was associated with a coordinated decrease in the proportion of NKG2D⁺ and CD16⁺ NK cells, and an increase in PD-1, which indicated their exhaustion. A higher content of NKG2D⁺ NK cells distinguished surviving patients from non-survivors in the ICU group. NK cell exhaustion in ICU patients was additionally confirmed by a strong negative correlation of PD-1 and natural cytotoxicity levels. In moderately ill patients and convalescents, correlations were found between the levels of CD57, NKG2C, and NKp30, which may indicate the formation of adaptive NK cells. A reduced NKp30 level was observed in patients with a lethal outcome. Altogether, the phenotypic changes in circulating NK cells of COVID-19 patients suggest that the intense activation of NK cells during SARS-CoV-2 infection, most likely induced by cytokines, is accompanied by NK cell exhaustion, the extent of which may be critical for the disease outcome. Full article

(This article belongs to the Special Issue Inflammation Cell Signaling and Infectious Diseases)

► Show Figures

Figure 1

27 pages, 6761 KiB

Open AccessArticle

siRNA-Mediated Timp1 Silencing Inhibited the Inflammatory Phenotype during Acute Lung Injury

by Ivan V. Chernikov, Yaroslav Yu. Staroseletz, Irina S. Tatarnikova, Aleksandra V. Sen’kova, Innokenty A. Savin, Andrey V. Markov, Evgeniya B. Logashenko, Elena L. Chernolovskaya, Marina A. Zenkova and Valentin V. Vlassov

Int. J. Mol. Sci. 2023, 24(2), 1641; https://doi.org/10.3390/ijms24021641 - 13 Jan 2023

Cited by 4 | Viewed by 2707

Abstract

Acute lung injury is a complex cascade process that develops in response to various damaging factors, which can lead to acute respiratory distress syndrome. Within this study, based on bioinformatics reanalysis of available full-transcriptome data of acute lung injury induced in mice and humans by various factors, we selected a set of genes that could serve as good targets for suppressing inflammation in the lung tissue, evaluated their expression in the cells of different origins during LPS-induced inflammation, and chose the tissue inhibitor of metalloproteinase Timp1 as a promising target for suppressing inflammation. We designed an effective chemically modified anti-TIMP1 siRNA and showed that Timp1 silencing correlates with a decrease in the pro-inflammatory cytokine IL6 secretion in cultured macrophage cells and reduces the severity of LPS-induced acute lung injury in a mouse model. Full article

(This article belongs to the Special Issue Inflammation Cell Signaling and Infectious Diseases)

► Show Figures

Figure 1

21 pages, 10811 KiB

Open AccessArticle

Autophagy Mediates Escherichia Coli-Induced Cellular Inflammatory Injury by Regulating Calcium Mobilization, Mitochondrial Dysfunction, and Endoplasmic Reticulum Stress

by Jianguo Liu, Rendong Qiu, Ran Liu, Pengjie Song, Pengfei Lin, Huatao Chen, Dong Zhou, Aihua Wang and Yaping Jin

Int. J. Mol. Sci. 2022, 23(22), 14174; https://doi.org/10.3390/ijms232214174 - 16 Nov 2022

Cited by 6 | Viewed by 1920

Abstract

Bovine endometritis is a reproductive disorder that is induced by mucus or purulent inflammation of the uterine mucosa. However, the intracellular control chain during inflammatory injury remains unclear. In the present study, we found that E. coli activated the inflammatory response through the assembly of the NLRP3 inflammasome and activation of the NF-κB p65 subunit in primary bovine endometrial epithelial cells (bEECs). Infection with E. coli also led to an abnormal increase in cytoplasmic calcium and mitochondrial dysfunction. Additionally, live-cell imaging of calcium reporters indicated that the increase in cytosolic calcium mainly was caused by the release of Ca²⁺ ions stored in the ER and mitochondria, which was independent of extracellular calcium. Cytoplasmic calcium regulates mitochondrial respiratory chain transmission, DNA replication, and biogenesis. Pretreatment with NAC, BAPTA-AM, or 2-APB reduced the expression of IL-1β and IL-18. Moreover, ERS was involved in the regulation of bovine endometritis and cytosolic calcium was an important factor for regulating ERS in E. coli-induced inflammation. Finally, activation of autophagy inhibited the release of IL-1β and IL-18, cytochrome c, ATP, ERS-related proteins, and cytoplasmic calcium. Collectively, our findings demonstrate that autophagy mediated E. coli-induced cellular inflammatory injury by regulating cytoplasmic calcium, mitochondrial dysfunction, and ERS. Full article

(This article belongs to the Special Issue Inflammation Cell Signaling and Infectious Diseases)

► Show Figures

Journal Menu

Journal Browser

Inflammation Cell Signaling and Infectious Diseases

Share This Special Issue

Special Issue Editor

Special Issue Information

Keywords

Published Papers (4 papers)

Research

Further Information

Guidelines

MDPI Initiatives

Follow MDPI