Streptococcus suis (S. suis) is a family of pathogenic gram-positive bacterial strains that represents a primary health problem in the swine industry worldwide. S. suis is also an emerging zoonotic pathogen that causes severe human infections clinically featuring with varied diseases/syndromes (such as meningitis, septicemia, and arthritis). Over the past few decades, continued efforts have made significant progress toward better understanding this zoonotic infectious entity, contributing in part to the elucidation of the molecular mechanism underlying its high pathogenicity. This review is aimed at presenting an updated overview of this pathogen from the perspective of molecular epidemiology, clinical diagnosis and typing, virulence mechanism, and protective antigens contributing to its zoonosis.

https://www.tandfonline.com/doi/pdf/10.4161/viru.28595

Streptococcus suis infection: An emerging/reemerging challenge of bacterial infectious diseases?

Recent data suggest that NETosis plays a crucial role in the innate immune response and disturbs the homeostasis of the immune system. NETosis is a form of neutrophil-specific cell death characterized by the release of large web-like structures referred to as neutrophil extracellular traps (NETs). NETs are composed of DNA strands associated with histones and decorated with about 20 different proteins including neutrophil elastase (NE), myeloperoxidase (MPO), cathepsin G, proteinase 3 (PR3), high mobility group protein B1 (HMGB1), and LL37. Reportedly, NETosis can be induced by several microbes, and particulate matter including sterile stimuli, via distinct cellular mechanisms. Meanwhile, suicidal NETosis and vital NETosis are controversial. As we enter the second decade of research on NETosis, we have partly understood NETs as double-edged swords of innate immunity. In this review we will discuss the mechanisms of NETosis, its antimicrobial action and role in autoimmune diseases, as well as the relatively new field of NET-associated mitochondrial DNA.

/pdf/new-insights-into-neutrophil-extracellular-traps-mechanisms-5a8d3swsyt.pdf

New Insights into Neutrophil Extracellular Traps: Mechanisms of Formation and Role in Inflammation

Tissue macrophages are derived from either circulating blood monocytes that originate in the bone marrow, or embryonic precursors that establish residence in tissues and are maintained independent of bone marrow progenitors. Macrophages perform diverse functions including tissue repair, the maintenance of homeostasis, and immune regulation. Recent studies have demonstrated that macrophages produce extracellular traps (ETs). ETs are an immune response by which a cell undergoes “ETosis” to release net-like material, with strands composed of cellular DNA that is studded with histones and cellular proteins. ETs are thought to immobilize and kill microorganisms, but also been implicated in disease pathology including aseptic inflammation and autoimmune disease. We conducted a scoping review to define what is known from the existing literature about the ETs produced by monocytes or macrophages. The results suggest that macrophage ETs (METs) are produced in response to various microorganisms and have similar features to neutrophil ETs (NETs), in that METs are produced by a unique cell death program (METosis), which results in release of fibers composed of DNA and studded with cellular proteins. METs function to immobilize and kill some microorganisms, but may also play a role in disease pathology.

/pdf/macrophage-extracellular-traps-a-scoping-review-37m3sdwbsc.pdf

Macrophage Extracellular Traps: A Scoping Review.

Bacterial meningitis is a devastating disease occurring worldwide with up to half of the survivors left with permanent neurological sequelae. Due to intrinsic properties of the meningeal pathogens and the host responses they induce, infection can cause relatively specific lesions and clinical syndromes that result from interference with the function of the affected nervous system tissue. Pathogenesis is based on complex host–pathogen interactions, some of which are specific for certain bacteria, whereas others are shared among different pathogens. In this review, we summarize the recent progress made in understanding the molecular and cellular events involved in these interactions. We focus on selected major pathogens, Streptococcus pneumonia, S. agalactiae (Group B Streptococcus), Neisseria meningitidis, and Escherichia coli K1, and also include a neglected zoonotic pathogen, Streptococcus suis. These neuroinvasive pathogens represent common themes of host–pathogen interactions, such as colonization and invasion of mucosal barriers, survival in the blood stream, entry into the central nervous system by translocation of the blood–brain and blood–cerebrospinal fluid barrier, and induction of meningeal inflammation, affecting pia mater, the arachnoid and subarachnoid spaces.

/pdf/host-pathogen-interactions-in-bacterial-meningitis-1o7z41glud.pdf

Host-pathogen interactions in bacterial meningitis.

The differentiation and effector functions of both the innate and adaptive immune system are inextricably linked to cellular metabolism. The features of metabolism which affect both arms of the immune system include metabolic substrate availability, expression of enzymes, transport proteins, and transcription factors which control catabolism of these substrates, and the ability to perform anabolic metabolism. The control of lipid metabolism is central to the appropriate differentiation and functions of T lymphocytes, and ultimately to the maintenance of immune tolerance. This review will focus on the role of fatty acid (FA) metabolism in T cell differentiation, effector function, and survival. FAs are important sources of cellular energy, stored as triglycerides. They are also used as precursors to produce complex lipids such as cholesterol and membrane phospholipids. FA residues also become incorporated into hormones and signaling moieties. FAs signal via nuclear receptors and their channeling, between storage as triacyl glycerides or oxidation as fuel, may play a role in survival or death of the cell. In recent years, progress in the field of immunometabolism has highlighted diverse roles for FA metabolism in CD4 and CD8 T cell differentiation and function. This review will firstly describe the sensing and modulation of the environmental FAs and lipid intracellular signaling and will then explore the key role of lipid metabolism in regulating the balance between potentially damaging pro-inflammatory and anti-inflammatory regulatory responses. Finally the complex role of extracellular FAs in determining cell survival will be discussed.

/pdf/the-role-of-lipid-metabolism-in-t-lymphocyte-differentiation-11ymelf32g.pdf

The Role of Lipid Metabolism in T Lymphocyte Differentiation and Survival.

Lipid alterations in human blood-derived neutrophils lead to formation of neutrophil extracellular traps

Several antibiotics are known for their ability to accumulate in neutrophils and thereby modulate the antimicrobial functions of those cells. This study demonstrates for the first time that an antibiotic, namely the fluoroquinolone enrofloxacin, enhances the formation of bovine neutrophil extracellular traps (NETs). Pharmacologically inactivated NADPH oxidase or peptidyl-arginine deiminase-4 distinctly reduced enrofloxacin-induced NET formation. Additionally, when cells were treated with cytochalasin D or nocodazole, the enrofloxacin-mediated NET induction was abolished, indicating that besides oxidative burst and histone citrullination also actin and microtubule polymerization are involved in this process.

/pdf/enrofloxacin-enhances-the-formation-of-neutrophil-57z08w6i5y.pdf

Enrofloxacin enhances the formation of neutrophil extracellular traps in bovine granulocytes

Guarea kunthiana is used in folk remedies for the treatment of several diseases including microbial infections. The mechanism behind this phenomenon still needs to be elucidated. Here, we investigated the effect of G. kunthiana bark extract on antimicrobial functions of human and bovine neutrophils as the first line of defense against infections. For this aim, neutrophils were isolated from either human or bovine blood and treated with G. kunthiana bark extract. The antimicrobial activity of the neutrophils against Staphylococcus (S.) aureus and Escherichia (E.) coli was tested in a bacterial survival assay and a fluorescence-based phagocytosis assay. Furthermore, the formation of neutrophil extracellular traps (NETs) was visualized by immunofluorescence microscopy. We show that neutrophils treated with G. kunthiana extract distinctly increased phagocytosis of S. aureus or E. coli. Interestingly, we demonstrate that G. kunthiana bark extract induces the formation of NETs in both cell types. This effect was abolished when treating the cells with diphenyleniodonium chloride (DPI) pointing to a direct implication of the NADPH oxidase-dependent formation of reactive oxygen species in this process. In summary, our data strongly suggest that G. kunthiana bark extract boosts the antimicrobial activities of neutrophils as the first line of defense against invading pathogens.

https://journals.sagepub.com/doi/pdf/10.1177/1934578X1601100617

Guarea kunthiana Bark Extract Enhances the Antimicrobial Activities of Human and Bovine Neutrophils.

Streptococcus suis is an important cause of different pathologies in pigs and humans, most importantly fibrinosuppurative meningitis. Tissue infected with this pathogen is substantially infiltrated with neutrophils, but the function of neutrophil extracellular traps (NETs) - a more recently discovered antimicrobial strategy of neutrophils - in host defence against Strep. suis has not been investigated. The objective of this work was to investigate the interaction of Strep. suis with NETs in vitro. Strep. suis induced NET formation in porcine neutrophils and was entrapped but not killed by those NETs. As the amount of NETs decreased over time, we hypothesized that a known extracellular DNase of Strep. suis degrades NETs. Though this nuclease was originally designated Strep. suis-secreted nuclease A (SsnA), this work demonstrated surface association in accordance with an LPXTG cell wall anchor motif and partial release into the supernatant. Confirming our hypothesis, an isogenic ssnA mutant was significantly attenuated in NET degradation and in protection against the antimicrobial activity of NETs as determined in assays with phorbol myristate acetate (PMA)-stimulated human neutrophils. Though assays with PMA-stimulated porcine neutrophils suggested that SsnA also degrades porcine NETs, phenotypic differences between wt and the isogenic ssnA mutant were less distinct. As SsnA expression was crucial for neither growth in vitro nor for survival in porcine or human blood, the results indicated that SsnA is the first specific NET evasion factor to be identified in Strep. suis.

Streptococcus suis DNase SsnA contributes to degradation of neutrophil extracellular traps (NETs) and evasion of NET-mediated antimicrobial activity

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Lipid alterations in human blood-derived neutrophils lead to formation of neutrophil extracellular traps

Enrofloxacin enhances the formation of neutrophil extracellular traps in bovine granulocytes

Guarea kunthiana Bark Extract Enhances the Antimicrobial Activities of Human and Bovine Neutrophils.

Streptococcus suis DNase SsnA contributes to degradation of neutrophil extracellular traps (NETs) and evasion of NET-mediated antimicrobial activity