Innate Immunity against Pathogens

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 3492

Special Issue Editors


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Guest Editor
1. Institute for Molecular Bioscience, University of Queensland, Brisbane 4072, Australia
2. A*STAR ID Labs, Agency for Science, Technology and Research (A*STAR), Singapore 138648, Singapore
Interests: innate immunity; inflammation; cell biology

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Guest Editor
Institute for Molecular Bioscience, The University of Queesland, Brisbane, QLD 4072, Australia
Interests: innate immunity; immunometabolism; GPCR signaling; cardiovascular development; stem cells

E-Mail Website
Guest Editor
Institute for Molecular Bioscience, The University of Queesland, Brisbane, QLD 4072, Australia
Interests: innate immunity; inflammation; immunometabolism; host–pathogen interaction; macrophages

Special Issue Information

Dear Colleagues,

The innate immune system is an evolutionary oldest form of defense system and is found in all species. Although it is ancient, the innate immune system is highly complex and is the body’s first line of defense and generates a rapid inflammatory response against invading pathogens such as viruses, bacteria, and parasites. It consists of physical barriers, antimicrobial peptides, and humoral and cellular components that prevent or slow down the establishment of pathogens’ invasion, clear both host and microbial debris, and modulate stress response for the maintenance of tissue or whole-body homeostasis. While some innate responses are antigen non-specific, others depend on soluble molecules and pattern-recognition receptors to mark or recognize conserved molecular patterns found in many microorganisms. In addition, the innate immunity helps to shape both the extent and the type of adaptive immune response to a given pathogen by releasing cytokines, chemokines, and signaling molecules that are critical in lymphocyte recruitment, activation, and differentiation.

Our understanding of the innate immune system is rapidly evolving with newly discovered cell types and molecular pathways, with paradigms changing continuously. Innate and adaptive immune responses are traditionally viewed as separate from each other, but emerging evidence suggests that they overlap and mutually interact. Recently discovered cell types, particularly innate lymphoid cells and myeloid-derived suppressor cells, are gaining increasing attention. More importantly,  defective  innate immunity is often associated with invasive and life-threatening diseases.

In this Special Issue on “Innate Immunity against Pathogens”, we will cover recent research topics and current review articles in the field of host innate responses against pathogen invasion and its role in diseases.

Dr. Zhixuan Loh
Dr. Yuanzhao Cao
Dr. Kaustav Das Gupta
Guest Editors

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. Pathogens 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

  • innate immunity
  • barriers to infection
  • inflammasome
  • complement system
  • immune cells
  • receptor signaling
  • ER stress
  • defensins
  • public health impact
  • prevention and treatment
  • pathogenicity

Published Papers (1 paper)

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Research

17 pages, 2640 KiB  
Article
Diverse Cell Death Mechanisms Are Simultaneously Activated in Macrophages Infected by Virulent Mycobacterium tuberculosis
by Lucero A. Ramon-Luing, Yessica Olvera, Julio Flores-Gonzalez, Yadira Palacios, Claudia Carranza, Yerany Aguilar-Duran, Marco Antonio Vargas, Neptali Gutierrez, Karen Medina-Quero and Leslie Chavez-Galan
Pathogens 2022, 11(5), 492; https://doi.org/10.3390/pathogens11050492 - 21 Apr 2022
Cited by 8 | Viewed by 2836
Abstract
Macrophages are necessary to eliminate pathogens. However, some pathogens have developed mechanisms to avoid the immune response. One of them is modulating the cell death mechanism to favor pathogen survival. In this study, we evaluated if virulent Mycobacterium tuberculosis (M. tb) [...] Read more.
Macrophages are necessary to eliminate pathogens. However, some pathogens have developed mechanisms to avoid the immune response. One of them is modulating the cell death mechanism to favor pathogen survival. In this study, we evaluated if virulent Mycobacterium tuberculosis (M. tb) can simultaneously activate more than one cell death mechanism. We infected human monocyte-derived macrophages (MDM) in vitro with avirulent (H37Ra) and virulent (H37Rv) strains, and then we measured molecules involved in apoptosis, necroptosis, and pyroptosis. Our data showed that H37Rv infection increased the BCL-2 transcript and protein, decreased the BAX transcript, and increased phosphorylated BCL-2 at the protein level. Moreover, H37Rv infection increased the expression of the molecules involved in the necroptotic pathway, such as ASK1, p-38, RIPK1, RIPK3, and caspase-8, while H37Ra increased caspase-8 and decreased RIPK3 at the transcriptional level. In addition, NLRP3 and CASP1 expression was increased at low MOI in both strains, while IL-1β was independent of virulence but dependent on infection MOI, suggesting the activation of pyroptosis. These findings suggest that virulent M. tb inhibits the apoptosis mediated by BCL-2 family molecules but, at the same time, increases the expression of molecules involved in apoptosis, necroptosis, and pyroptosis at the transcriptional and protein levels, probably as a mechanism to avoid the immune response and guarantee its survival. Full article
(This article belongs to the Special Issue Innate Immunity against Pathogens)
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