Special Issue "Microbe–Host Interactions: From Infection to Innate Immunity Aspects"

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

Deadline for manuscript submissions: 29 February 2020.

Special Issue Editor

Dr. Ilias Kounatidis
E-Mail Website
Guest Editor
1. Cell Biology, Development, and Genetics Laboratory, Department of Biochemistry, University of Oxford, South Park Road, Oxford OX1 3QU, UK
2. Life Sciences Department, Diamond Light Source, Harwell Science and Innovation Campus, Didcot, Oxfordshire, OX11 0DE, UK
Interests: cryo X-ray tomography; microbiology; innate immunity; bacteria phagocytocis; fungal pathogenesis; host-pathogen interactions

Special Issue Information

Dear Colleagues,

Microbe–host interactions are defined as the mechanisms employed by microbes to sustain themselves within hosts in the presence of the host immune responses. The outcome of the above interplay can be as diverse as the organisms involved, including obligatory or accidental interactions which result into various states like symbiosis, commensalism or disease. The initial host–microbe interaction involves the recognition of conserved microbial components known as the pathogen-associated molecular patterns (PAMPs) by the host pattern recognition receptors (PRRs). Following PAM–PRR binding, signal transduction initiates a complex cascade of cellular reactions, leading to an early host response that not only contributes to microbial elimination but also provides an essential stimulus to the adaptive immune response.

This Special Issue will focus on the innate immune signaling pathways within in vivo and ex vivo research models, such as cell lines, invertebrates and rodent models, which define the interaction frame between the host and pathogenic or non-pathogenic microbial strains including bacteria, fungi or viruses. Contributions will range from the molecular and cellular level, studying the infection routes employed by microbes to invade the host, to the organismal and population level, investigating pathogen persistence and colonization and host homeostatic imbalance factors.

Recent advances and modern tools, such as next-generation sequencing, metagenomics and advanced microscopy methods like super-resolution microscopy, have provided a glimpse into intimate details of the functional and molecular interface between microbial strains and their hosts.

Dr. Ilias Kounatidis
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 papers will be 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 1200 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.


  • Host–microbe interaction
  • Colonization
  • Fungal pathogenesis
  • Innate immunity
  • Immune signaling pathways
  • Next-generation sequencing
  • Metagenomics
  • Super-resolution microscopy

Published Papers (1 paper)

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Open AccessArticle
HP1717 Contributes to Streptococcus suis Virulence by Inducing an Excessive Inflammatory Response and Influencing the Biosynthesis of the Capsule
Microorganisms 2019, 7(11), 522; https://doi.org/10.3390/microorganisms7110522 - 03 Nov 2019
Streptococcus suis 2 (SS2) is an important zoonotic pathogen that substantially harms the swine industry and poses threats to human health. Excessive inflammation is considered to be a hallmark of SS2 infection because it is responsible for most clinical signs of SS2, especially [...] Read more.
Streptococcus suis 2 (SS2) is an important zoonotic pathogen that substantially harms the swine industry and poses threats to human health. Excessive inflammation is considered to be a hallmark of SS2 infection because it is responsible for most clinical signs of SS2, especially streptococcal toxic shock-like syndrome. However, the current knowledge of SS2-induced excessive inflammation remains limited. In this study, we identified HP1717 as a novel extracellular pro-inflammatory protein in SS2 that can induce robust expression of inflammatory cytokines in RAW264.7 macrophages. Notably, the pro-inflammatory ability of HP1717 was dose-dependent and heat-sensitive, and it required the recognition of Toll-like receptor 2 (TLR2) and the phosphorylation of both extracellular signal-regulated kinases 1/2 (ERK1/2) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). Further, by constructing a deletion mutant, we demonstrated that HP1717 significantly influenced the biosynthesis of the bacterial capsule, which plays a critical role in the virulence of SS2 by interfering with the ability of host immune cells to phagocytize and kill the pathogen. Indeed, the mutant strain displayed reduced resistance to whole-blood killing compared with the wild strain. Finally, murine experiments indicated that the deletion of hp1717 in SS2 reduced the lethality, pro-inflammatory activity, and bacterial loads in mice. Collectively, our data reveal HP1717 as a novel virulence-related factor of SS2 that can induce an excessive inflammatory response and significantly affect the bacterial capsule, thus expanding our understanding of the pathogenesis of S. suis. Full article
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