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Microbe–Host Interactions: From Infection to Innate Immunity Aspects

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

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 50973

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Dr. Ilias Kounatidis

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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

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Keywords

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

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Published Papers (10 papers)

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Research

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11 pages, 1837 KiB

Open AccessCommunication

Activation of the JNK/MAPK Signaling Pathway by TGF-β1 Enhances Neonatal Fc Receptor Expression and IgG Transcytosis

by Shaoju Qian, Chenxi Li, Xi Liu, Xiangchao Jia, Yuncai Xiao and Zili Li

Microorganisms 2021, 9(4), 879; https://doi.org/10.3390/microorganisms9040879 - 20 Apr 2021

Cited by 10 | Viewed by 2589

Abstract

The neonatal Fc receptor (FcRn) transports maternal immunoglobulin G (IgG) to the foetus or newborn and protects the IgG from degradation. FcRn is expressed in several porcine tissues and cell types and its expression levels are regulated by immune and inflammatory events. IPEC-J2 cells are porcine intestinal columnar epithelial cells that were isolated from neonatal piglet mid-jejunum. We hypothesized that transforming growth factor β1 (TGF-β1) upregulated pFcRn expression in IPEC-J2 cells. To test this hypothesis, we treated IPEC-J2 cells with TGF-β1 and demonstrated that porcine FcRn (pFcRn) expression was significantly increased. SP600125, a specific mitogen-activated protein kinase (MAPK) inhibitor, reduced TGF-β1-induced pFcRn expression in IPEC-J2 cells. We performed luciferase reporter assays and showed that the c-JUN sensitive region of the pFcRn promoter gene was located between positions −1215 and −140. The c-JUN sequence, in combination with the pFcRn promoter, regulated luciferase reporter activity in response to TGF-β1 stimulation. Chromatin immunoprecipitation confirmed that there were three c-JUN binding sites in the pFcRn promoter. Furthermore, in addition to increased pFcRn expression, TGF-β1 also enhanced IgG transcytosis in IPEC-J2 cells. In summary, our data showed that the modulation of JNK/MAPK signaling by TGF-β1 was sufficient to upregulate pFcRn expression. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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22 pages, 6413 KiB

Open AccessArticle

Chlamydia Uses K⁺ Electrical Signalling to Orchestrate Host Sensing, Inter-Bacterial Communication and Differentiation

by Susan C. Andrew, Maud Dumoux and Richard D. Hayward

Microorganisms 2021, 9(1), 173; https://doi.org/10.3390/microorganisms9010173 - 15 Jan 2021

Cited by 2 | Viewed by 2768

Abstract

Prokaryotic communities coordinate quorum behaviour in response to external stimuli to control fundamental processes including inter-bacterial communication. The obligate intracellular bacterial pathogen Chlamydia adopts two developmental forms, invasive elementary bodies (EBs) and replicative reticulate bodies (RBs), which reside within a specialised membrane-bound compartment within the host cell termed an inclusion. The mechanisms by which this bacterial community orchestrates different stages of development from within the inclusion in coordination with the host remain elusive. Both prokaryotic and eukaryotic kingdoms exploit ion-based electrical signalling for fast intercellular communication. Here we demonstrate that RBs specifically accumulate potassium (K⁺) ions, generating a gradient. Disruption of this gradient using ionophores or an ion-channel inhibitor stalls the Chlamydia lifecycle, inducing persistence. Using photobleaching approaches, we establish that the RB is the master regulator of this [K⁺] differential and observe a fast K⁺ exchange between RBs revealing a role for this ion in inter-bacterial communication. Finally, we demonstrate spatio-temporal regulation of bacterial membrane potential during RB to EB differentiation within the inclusion. Together, our data reveal that Chlamydia harnesses K⁺ to orchestrate host sensing, inter-bacteria communication and pathogen differentiation. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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21 pages, 15616 KiB

Open AccessArticle

Microbiota Modulates the Immunomodulatory Effects of Filifolinone on Atlantic Salmon

by Mick Parra, Daniela Espinoza, Natalia Valdes, Rodrigo Vargas, Alex Gonzalez, Brenda Modak and Mario Tello

Microorganisms 2020, 8(9), 1320; https://doi.org/10.3390/microorganisms8091320 - 30 Aug 2020

Cited by 10 | Viewed by 2862

Abstract

Filifolinone is an aromatic geranyl derivative, a natural compound isolated from Heliotropum sclerocarpum, which has immunomodulatory effects on Atlantic salmon, upregulating cytokines involved in Th1-type responses through a mechanism that remains unknown. In this work, we determined whether the immunomodulatory effects of filifolinone depend on the host microbiotic composition. We evaluated the effect of filifolinone on immune genes and intestinal microbiotic composition of normal fish and fish previously treated with bacitracin/neomycin. Filifolinone induced the early expression of IFN-α1 and TGF-β, followed by the induction of TNF-α, IL-1β, and IFN-γ. A pre-treatment with antibiotics modified this effect, mainly changing the expression of IL-1β and IFN-γ. The evaluation of microbial diversity shows that filifolinone modifies the composition of intestinal microbiota, increasing the abundance of immunostimulating organisms like yeast and firmicutes. We identified 69 operational taxonomic units (OTUs) associated with filifolinone-induced IFN-γ. Our results indicate that filifolinone stimulates the immune system in two ways, one dependent on fish microbiota and the other not. To our knowledge, this is the first report of microbiota-dependent immunostimulation in Salmonids. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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13 pages, 2428 KiB

Open AccessArticle

The Drosophila melanogaster Metabolic Response against Parasitic Nematode Infection Is Mediated by TGF-β Signaling

by Yaprak Ozakman, Trishya Pagadala, Dhaivat Raval and Ioannis Eleftherianos

Microorganisms 2020, 8(7), 971; https://doi.org/10.3390/microorganisms8070971 - 29 Jun 2020

Cited by 4 | Viewed by 2985

Abstract

The nematode Heterorhabditis bacteriophora, its mutualistic bacterium Photorhabdus luminescens, and the fruit fly Drosophila melanogaster establish a unique system to study the basis of infection in relation to host metabolism. Our previous results indicate that the Transforming Growth Factor β (TGF-β) signaling pathway participates in the D. melanogaster metabolic response against nematode parasitism. However, our understanding of whether the presence of Photorhabdus bacteria in Heterorhabditis nematodes affects the metabolic state of D. melanogaster during infection is limited. Here, we investigated the involvement of TGF-β signaling branches, Activin and Bone Morphogenetic Protein (BMP), in the D. melanogaster metabolic response against axenic (lacking bacteria) or symbiotic (containing bacteria) H. bacteriophora infection. We show that BMP signaling mediates lipid metabolism against axenic or symbiotic H. bacteriophora and alters the size of fat body lipid droplets against symbiotic nematode infection. Also, following symbiotic H. bacteriophora infection, Activin signaling modulates sugar metabolism. Our results indicate that Activin and BMP signaling interact with the D. melanogaster metabolic response to H. bacteriophora infection regardless of the presence or absence of Photorhabdus. These findings provide evidence for the role of TGF-β signaling in host metabolism, which could lead to the development of novel treatments for parasitic diseases. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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13 pages, 1670 KiB

Open AccessArticle

Lipocalin2 Induced by Bacterial Flagellin Protects Mice against Cyclophosphamide Mediated Neutropenic Sepsis

by Daejin Lim, Hee Kyung Kim, Jae-Ho Jeong, Yoon Seok Jung, Shee Eun Lee, Hee-Chang Jang, Sook-In Jung, Hueng-Sik Choi, Joon Haeng Rhee, Sung-Gwon Lee, Chungoo Park, Miryoung Song and Hyon E. Choy

Microorganisms 2020, 8(5), 646; https://doi.org/10.3390/microorganisms8050646 - 29 Apr 2020

Cited by 6 | Viewed by 3593

Abstract

Neutropenic sepsis is a fatal consequence of chemotherapy, and septic complications are the principal cause of mortality. Chemotherapy-induced neutropenia leads to the formation of microscopic ulcers in the gastrointestinal epithelium that function as a portal of entry for intraluminal bacteria, which translocate across the intestinal mucosal barrier and gain access to systemic sites, causing septicemia. A cyclophosphamide-induced mouse model was developed to mimic the pathophysiologic sequence of events that occurs in patients with neutropenic sepsis. The TLR5 agonist bacterial flagellin derived from Vibrio vulnificus extended the survival of cyclophosphamide-treated mice by reducing the bacterial load in internal organs. The protective effect of flagellin was mediated by the antimicrobial protein lipocalin 2 (Lcn2), which is induced by TLR5-NF-κB activation in hepatocytes. Lcn2 sequestered iron from infecting bacteria, particularly siderophore enterobactin-dependent members of the Enterobacteriaceae family, thereby limiting their proliferation. Lcn2 should be considered for the treatment of neutropenic sepsis and gastrointestinal damage during chemotherapy to prevent or minimize the adverse effects of cancer chemotherapy. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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18 pages, 4820 KiB

Open AccessArticle

Staphylococcus aureus Lung Infection Results in Down-Regulation of Surfactant Protein-A Mainly Caused by Pro-Inflammatory Macrophages

by Elisabeth Schicke, Zoltán Cseresnyés, Knut Rennert, Vanessa Vau, Karoline Frieda Haupt, Franziska Hornung, Sandor Nietzsche, Fatina Swiczak, Michaela Schmidtke, Brigitte Glück, Mirijam Koch, Michael Schacke, Regine Heller, Alexander S. Mosig, Marc Thilo Figge, Christina Ehrhardt, Bettina Löffler and Stefanie Deinhardt-Emmer

Microorganisms 2020, 8(4), 577; https://doi.org/10.3390/microorganisms8040577 - 16 Apr 2020

Cited by 18 | Viewed by 4857

Abstract

Pneumonia is the leading cause of hospitalization worldwide. Besides viruses, bacterial co-infections dramatically exacerbate infection. In general, surfactant protein-A (SP-A) represents a first line of immune defense. In this study, we analyzed whether influenza A virus (IAV) and/or Staphylococcus aureus (S. aureus) infections affect SP-A expression. To closely reflect the situation in the lung, we used a human alveolus-on-a-chip model and a murine pneumonia model. Our results show that S. aureus can reduce extracellular levels of SP-A, most likely attributed to bacterial proteases. Mono-epithelial cell culture experiments reveal that the expression of SP-A is not directly affected by IAV or S. aureus. Yet, the mRNA expression of SP-A is strongly down-regulated by TNF-α, which is highly produced by professional phagocytes in response to bacterial infection. By using the human alveolus-on-a-chip model, we show that the down-regulation of SP-A is strongly dependent on macrophages. In a murine model of pneumonia, we can confirm that S. aureus decreases SP-A levels in vivo. These findings indicate that (I) complex interactions of epithelial and immune cells induce down-regulation of SP-A expression and (II) bacterial mono- and super-infections reduce SP-A expression in the lung, which might contribute to a severe outcome of bacterial pneumonia. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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18 pages, 7446 KiB

Open AccessArticle

HP1717 Contributes to Streptococcus suis Virulence by Inducing an Excessive Inflammatory Response and Influencing the Biosynthesis of the Capsule

by Liang Liu, Qiang Zhang, Zhongmin Xu, Jingjing Huang, Weifeng Zhu, Anding Zhang, Xiaomei Sun and Meilin Jin

Microorganisms 2019, 7(11), 522; https://doi.org/10.3390/microorganisms7110522 - 3 Nov 2019

Cited by 2 | Viewed by 2644

Abstract

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

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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Review

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21 pages, 797 KiB

Open AccessReview

The Impact of Age on Response to Infection in Drosophila

by Noah Sciambra and Stanislava Chtarbanova

Microorganisms 2021, 9(5), 958; https://doi.org/10.3390/microorganisms9050958 - 29 Apr 2021

Cited by 9 | Viewed by 5118

Abstract

This review outlines the known cellular pathways and mechanisms involved in Drosophila age-dependent immunity to pathogenic microorganisms such as bacteria and fungi. We discuss the implication of host signaling pathways such as the Toll, Immune Deficiency (IMD), Janus kinase signal transducer and activator of transcription (JAK/STAT), and Insulin/Insulin Growth Factor/Target of Rapamycin (IIS/TOR) on immune function with aging. Additionally, we review the effects that factors such as sexual dimorphism, environmental stress, and cellular physiology exert on age-dependent immunity in Drosophila. We discuss potential tradeoffs between heightened immune function and longevity in the absence of infection, and we provide detailed tables outlining the various assays and pathogens used in the cited studies, as well as the age, sex, and strains of Drosophila used. We also discuss the overlapping effects these pathways and mechanisms have on one another. We highlight the great utility of Drosophila as a model organism and the importance of a greater focus on age-dependent antiviral immunity for future studies. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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23 pages, 1616 KiB

Open AccessReview

An Overview of the Elusive Passenger in the Gastrointestinal Tract of Cattle: The Shiga Toxin Producing Escherichia coli

by Panagiotis Sapountzis, Audrey Segura, Mickaël Desvaux and Evelyne Forano

Microorganisms 2020, 8(6), 877; https://doi.org/10.3390/microorganisms8060877 - 10 Jun 2020

Cited by 38 | Viewed by 5201

Abstract

For approximately 10,000 years, cattle have been our major source of meat and dairy. However, cattle are also a major reservoir for dangerous foodborne pathogens that belong to the Shiga toxin-producing Escherichia coli (STEC) group. Even though STEC infections in humans are rare, they are often lethal, as treatment options are limited. In cattle, STEC infections are typically asymptomatic and STEC is able to survive and persist in the cattle GIT by escaping the immune defenses of the host. Interactions with members of the native gut microbiota can favor or inhibit its persistence in cattle, but research in this direction is still in its infancy. Diet, temperature and season but also industrialized animal husbandry practices have a profound effect on STEC prevalence and the native gut microbiota composition. Thus, exploring the native cattle gut microbiota in depth, its interactions with STEC and the factors that affect them could offer viable solutions against STEC carriage in cattle. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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25 pages, 1261 KiB

Open AccessReview

Salmonella Virulence and Immune Escape

by Mengyao Wang, Izhar Hyder Qazi, Linli Wang, Guangbin Zhou and Hongbing Han

Microorganisms 2020, 8(3), 407; https://doi.org/10.3390/microorganisms8030407 - 13 Mar 2020

Cited by 75 | Viewed by 17028

Abstract

Salmonella genus represents the most common foodborne pathogens causing morbidity, mortality, and burden of disease in all regions of the world. The introduction of antimicrobial agents and Salmonella-specific phages has been considered as an effective intervention strategy to reduce Salmonella contamination. However, data from the United States, European countries, and low- and middle-income countries indicate that Salmonella cases are still a commonly encountered cause of bacterial foodborne diseases globally. The control programs have not been successful and even led to the emergence of some multidrug-resistant Salmonella strains. It is known that the host immune system is able to effectively prevent microbial invasion and eliminate microorganisms. However, Salmonella has evolved mechanisms of resisting host physical barriers and inhibiting subsequent activation of immune response through their virulence factors. There has been a high interest in understanding how Salmonella interacts with the host. Therefore, in the present review, we characterize the functions of Salmonella virulence genes and particularly focus on the mechanisms of immune escape in light of evidence from the emerging mainstream literature. Full article

(This article belongs to the Special Issue Microbe–Host Interactions: From Infection to Innate Immunity Aspects)

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