scholarly journals Neutrophils in Streptococcus suis Infection: From Host Defense to Pathology

2021 ◽  
Vol 9 (11) ◽  
pp. 2392
Author(s):  
Marêva Bleuzé ◽  
Marcelo Gottschalk ◽  
Mariela Segura
Keyword(s):  
Host Defense ◽  
Immune Cells ◽  
Immune Surveillance ◽  
Clinical Manifestations ◽  
Streptococcus Suis ◽  
Cellular Level ◽  
Economic Losses ◽  
Cell Type ◽  
Swine Pathogen

Streptococcus suis is a swine pathogen and zoonotic agent responsible for economic losses to the porcine industry. Infected animals may develop meningitis, arthritis, endocarditis, sepsis and/or sudden death. The pathogenesis of the infection implies that bacteria breach mucosal host barriers and reach the bloodstream, where they escape immune-surveillance mechanisms and spread throughout the organism. The clinical manifestations are mainly the consequence of an exacerbated inflammation, defined by an exaggerated production of cytokines and recruitment of immune cells. Among them, neutrophils arrive first in contact with the pathogens to combat the infection. Neutrophils initiate and maintain inflammation, by producing cytokines and deploying their arsenal of antimicrobial mechanisms. Furthermore, neutrophilic leukocytosis characterizes S. suis infection, and lesions of infected subjects contain a large number of neutrophils. Therefore, this cell type may play a role in host defense and/or in the exacerbated inflammation. Nevertheless, a limited number of studies addressed the role or functions of neutrophils in the context of S. suis infection. In this review, we will explore the literature about S. suis and neutrophils, from their interaction at a cellular level, to the roles and behaviors of neutrophils in the infected host in vivo.

scholarly journals A cytokine network involving IL-36γ, IL-23, and IL-22 promotes antimicrobial defense and recovery from intestinal barrier damage

2018 ◽  
Vol 115 (22) ◽  
pp. E5076-E5085 ◽  
Author(s):  
Vu L. Ngo ◽  
Hirohito Abo ◽  
Estera Maxim ◽  
Akihito Harusato ◽  
Duke Geem ◽  
...  
Keyword(s):  
Host Defense ◽  
Immune Cells ◽  
Intracellular Signaling ◽  
Intestinal Barrier ◽  
Intestinal Damage ◽  
Cytokine Network ◽  
Potent Inducer ◽  
Intracellular Signaling Cascade

The gut epithelium acts to separate host immune cells from unrestricted interactions with the microbiota and other environmental stimuli. In response to epithelial damage or dysfunction, immune cells are activated to produce interleukin (IL)-22, which is involved in repair and protection of barrier surfaces. However, the specific pathways leading to IL-22 and associated antimicrobial peptide (AMP) production in response to intestinal tissue damage remain incompletely understood. Here, we define a critical IL-36/IL-23/IL-22 cytokine network that is instrumental for AMP production and host defense. Using a murine model of intestinal damage and repair, we show that IL-36γ is a potent inducer of IL-23 both in vitro and in vivo. IL-36γ–induced IL-23 required Notch2-dependent (CD11b+CD103+) dendritic cells (DCs), but not Batf3-dependent (CD11b−CD103+) DCs or CSF1R-dependent macrophages. The intracellular signaling cascade linking IL-36 receptor (IL-36R) to IL-23 production by DCs involved MyD88 and the NF-κB subunits c-Rel and p50. Consistent with in vitro observations, IL-36R– and IL-36γ–deficient mice exhibited dramatically reduced IL-23, IL-22, and AMP levels, and consequently failed to recover from acute intestinal damage. Interestingly, impaired recovery of mice deficient in IL-36R or IL-36γ could be rescued by treatment with exogenous IL-23. This recovery was accompanied by a restoration of IL-22 and AMP expression in the colon. Collectively, these data define a cytokine network involving IL-36γ, IL-23, and IL-22 that is activated in response to intestinal barrier damage and involved in providing critical host defense.

scholarly journals Shiga toxin suppresses noncanonical inflammasome responses to cytosolic LPS

2020 ◽  
Vol 5 (53) ◽  
pp. eabc0217
Author(s):  
Morena S. Havira ◽  
Atri Ta ◽  
Puja Kumari ◽  
Chengliang Wang ◽  
Ashley J. Russo ◽  
...  
Keyword(s):  
Host Defense ◽  
Shiga Toxin ◽  
Interleukin 1 ◽  
Immune Surveillance ◽  
Bacterial Toxin ◽  
Human Pathogen ◽  
Lps Challenge ◽  
Phage Protein ◽  
Uremic Syndrome

Inflammatory caspase–dependent cytosolic lipopolysaccharide (LPS) sensing is a critical arm of host defense against bacteria. How pathogens overcome this pathway to establish infections is largely unknown. Enterohemorrhagic Escherichia coli (EHEC) is a clinically important human pathogen causing hemorrhagic colitis and hemolytic uremic syndrome. We found that a bacteriophage-encoded virulence factor of EHEC, Shiga toxin (Stx), suppresses caspase-11–mediated activation of the cytosolic LPS sensing pathway. Stx was essential and sufficient to inhibit pyroptosis and interleukin-1 (IL-1) responses elicited specifically by cytosolic LPS. The catalytic activity of Stx was necessary for suppression of inflammasome responses. Stx impairment of inflammasome responses to cytosolic LPS occurs at the level of gasdermin D activation. Stx also suppresses inflammasome responses in vivo after LPS challenge and bacterial infection. Overall, this study assigns a previously undescribed inflammasome-subversive function to a well-known bacterial toxin, Stx, and reveals a new phage protein-based pathogen blockade of cytosolic immune surveillance.

scholarly journals Reprogramming Immune Cells for Enhanced Cancer Immunotherapy: Targets and Strategies

2021 ◽  
Vol 12 ◽  
Author(s):  
Yan Dong ◽  
Zhuo Wan ◽  
Xiaotong Gao ◽  
Guodong Yang ◽  
Li Liu
Keyword(s):  
Immune Cells ◽  
Causes Of Death ◽  
Immune Cell ◽  
Ex Vivo ◽  
Immune Surveillance ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
The Past ◽  
Cancer Types

Cancer is one of the leading causes of death and a major public health problem all over the world. Immunotherapy is becoming a revolutionary clinical management for various cancer types. Restoration of aberrant immune surveillance on cancers has achieved markable progress in the past years by either in vivo or ex vivo engineering of the immune cells. Here, we summarized the central roles of immune cells in tumor progression and regression, and the existing and emerging strategies for different immune cell-based immunotherapies. In addition, the current challenges and the potential solutions in translating the immunotherapies into the clinic are also discussed.

scholarly journals Review of the speculative role of co-infections in Streptococcus suis-associated diseases in pigs

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Milan R. Obradovic ◽  
Mariela Segura ◽  
Joaquim Segalés ◽  
Marcelo Gottschalk
Keyword(s):  
Respiratory Disease ◽  
Clinical Signs ◽  
Streptococcus Suis ◽  
In Vivo Studies ◽  
Economic Losses ◽  
Upper Respiratory Tract ◽  
Associated Diseases ◽  
Virulent Strains

AbstractStreptococcus suis is one of the most important bacterial swine pathogens affecting post-weaned piglets, causing mainly meningitis, arthritis and sudden death. It not only results in severe economic losses but also raises concerns over animal welfare and antimicrobial resistance and remains an important zoonotic agent in some countries. The definition and diagnosis of S. suis-associated diseases can be complex. Should S. suis be considered a primary or secondary pathogen? The situation is further complicated when referring to respiratory disease, since the pathogen has historically been considered as a secondary pathogen within the porcine respiratory disease complex (PRDC). Is S. suis a respiratory or strictly systemic pathogen? S. suis is a normal inhabitant of the upper respiratory tract, and the presence of potentially virulent strains alone does not guarantee the appearance of clinical signs. Within this unclear context, it has been largely proposed that co-infection with some viral and bacterial pathogens can significantly influence the severity of S. suis-associated diseases and may be the key to understanding how the infection behaves in the field. In this review, we critically addressed studies reporting an epidemiological link (mixed infections or presence of more than one pathogen at the same time), as well as in vitro and in vivo studies of co-infection of S. suis with other pathogens and discussed their limitations and possibilities for improvement and proposed recommendations for future studies.

scholarly journals Draft Genome Sequences of Nine Streptococcus suis Strains Isolated in the United States

2015 ◽  
Vol 3 (6) ◽  
Author(s):  
Samantha J. Hau ◽  
Darrell O. Bayles ◽  
David P. Alt ◽  
Susan L. Brockmeier ◽  
Timothy S. Frana ◽  
...  
Keyword(s):  
Close Contact ◽  
Draft Genome ◽  
Streptococcus Suis ◽  
The United States ◽  
Economic Losses ◽  
Genome Sequences ◽  
Pork Products ◽  
Swine Pathogen ◽  
Severe Infections ◽  
Undercooked Pork

Streptococcus suis is a swine pathogen responsible for economic losses to the pig industry worldwide. Additionally, it is a zoonotic agent that can cause severe infections in those in close contact with infected pigs and/or who consume uncooked or undercooked pork products. Here, we report nine draft genome sequences of S. suis .

scholarly journals Structure and Junctional Complexes of Endothelial, Epithelial and Glial Brain Barriers

2019 ◽  
Vol 20 (21) ◽  
pp. 5372 ◽  
Author(s):  
Mariana Castro Dias ◽  
Josephine A. Mapunda ◽  
Mykhailo Vladymyrov ◽  
Britta Engelhardt
Keyword(s):  
Immune Cells ◽  
Current Knowledge ◽  
Immune Surveillance ◽  
Cellular Composition ◽  
Glia Limitans ◽  
The Central Nervous System ◽  
Junctional Complexes ◽  
The Brain ◽  
Brain Barriers

The homeostasis of the central nervous system (CNS) is ensured by the endothelial, epithelial, mesothelial and glial brain barriers, which strictly control the passage of molecules, solutes and immune cells. While the endothelial blood-brain barrier (BBB) and the epithelial blood-cerebrospinal fluid barrier (BCSFB) have been extensively investigated, less is known about the epithelial and mesothelial arachnoid barrier and the glia limitans. Here, we summarize current knowledge of the cellular composition of the brain barriers with a specific focus on describing the molecular constituents of their junctional complexes. We propose that the brain barriers maintain CNS immune privilege by dividing the CNS into compartments that differ with regard to their role in immune surveillance of the CNS. We close by providing a brief overview on experimental tools allowing for reliable in vivo visualization of the brain barriers and their junctional complexes and thus the respective CNS compartments.

scholarly journals Lrig1 and Wnt dependent niches dictate segregation of resident immune cells and melanocytes in murine tail epidermis

2021 ◽  
Author(s):  
Susanne C. Baess ◽  
Annika Graband ◽  
Kristin Sere ◽  
Martin Zenke ◽  
Catherin Niemann ◽  
...  
Keyword(s):  
Host Defense ◽  
Immune Cells ◽  
Langerhans Cells ◽  
Immune Surveillance ◽  
Cell Types ◽  
First Line ◽  
Interfollicular Epidermis ◽  
Canonical Wnt ◽  
Cellular Hierarchy ◽  
Surveillance Analysis

The barrier-forming, self-renewing mammalian epidermis comprises keratinocytes, pigment-producing melanocytes, and resident immune cells as first-line host defense. In murine tail skin, interfollicular epidermis patterns into pigmented ′scale′ and non-pigmented ′interscale′ epidermis. Why and how mature melanocytes confine to scale epidermis is unresolved. Here, we delineate a cellular hierarchy among epidermal cell types that determines skin patterning. Already during postnatal development, melanocytes co-segregate with newly forming scale compartments. Intriguingly, this process coincides with partitioning of both Langerhans cells and dendritic epidermal T-cells to interscale epidermis, suggesting functional segregation of pigmentation and immune surveillance. Analysis of non-pigmented mice and of mice lacking melanocytes or resident immune cells revealed that immunocyte patterning is melanocyte- and melanin-independent, and, vice versa, immune cells do not control melanocyte localization. Instead, genetically enforced progressive scale fusion upon Lrig1 deletion showed that melanocytes and immune cells dynamically follow epithelial scale:interscale patterns. Importantly, disrupting Wnt-Lef1 function in keratinocytes caused melanocyte mislocalization to interscale epidermis, implicating canonical Wnt signaling in organizing the pigmentation pattern. Together, this work uncovered cellular and molecular principles underlying the compartmentalization of tissue functions in skin.

Abstract 316: Engineering Nanomaterial Morphology for Targeting Immune Cells Within Atherosclerotic Lesions

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Sijia Yi ◽  
Yugang Liu ◽  
Sean Allen ◽  
Fanfan Du ◽  
Xiaomo Li ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Cells ◽  
Near Infrared ◽  
Flow Cytometric Analysis ◽  
Cellular Level ◽  
Mononuclear Phagocyte ◽  
Atherosclerotic Lesions ◽  
Nirf Imaging ◽  
Poly Ethylene

Atherosclerosis is a chronic vascular inflammatory disease, in which several types of immune cells have been identified as playing important roles. Nanomaterials can function as powerful theranostic platforms for diagnostic imaging and controlled delivery of therapeutics in atherosclerosis. Here, we present a detailed investigation into the effects of morphology on the in vivo biodistribution of nanomaterials in naïve mice following intravenous injection. We applied these findings towards the targeting of diverse immune cells within the lesions of atherosclerotic mice. Three different nanostructures of the same surface chemistry were assembled from poly(ethylene glycol)- bl -poly(propylene sulfide) (PEG- bl -PPS) block copolymers: micelles (30 nm), vesicles (120 nm) and filomicelles (50 nm diameter by micron length). To assess the effects of the different morphologies, a multimodal approach was utilized that included 1) near infrared fluorescence (NIRF) imaging to quantify organ targeting, and 2) fluorescent polymer conjugation for subsequent flow cytometric analysis of uptake by immune cells. Of note, vesicles were exceptionally efficient at targeting the spleen and were associated with up to 85% of plasmacytoid dendritic cells. Micelles were associated with up to 90% of macrophages in the liver, and filomicelles were most effective at avoiding uptake by the cells of the mononuclear phagocyte system. Due to their enhanced uptake by dendritic cell subsets relative to other nanostructures, vesicles were selected for targeting cells within aortic lesions of atherosclerotic LDL -/- mice. In addition to associating with macrophages and eosinophils, vesicles were found to target significantly higher percentages of atheroma-resident dendritic cells (25%). In conclusion, differences in morphology can drastically change the biodistribution of nanomaterials at both the organ and cellular level. The ability to target or avoid phagocytic cell subsets will enhance current and future theranostic strategies. Furthermore, the targeting of dendritic cells by vesicular nanostructures within atherosclerotic lesions opens new avenues for immunotherapies in cardiovascular disease.

scholarly journals Characterization of immune cell migration using microfabrication

2021 ◽  
Author(s):  
Doriane Vesperini ◽  
Galia Montalvo ◽  
Bin Qu ◽  
Franziska Lautenschläger
Keyword(s):  
Cell Migration ◽  
Immune Cells ◽  
Immune Cell ◽  
Immune Surveillance ◽  
Advantages And Disadvantages ◽  
Infected Cells ◽  
Immune Cell Migration ◽  
Underlying Mechanisms

AbstractThe immune system provides our defense against pathogens and aberrant cells, including tumorigenic and infected cells. Motility is one of the fundamental characteristics that enable immune cells to find invading pathogens, control tissue damage, and eliminate primary developing tumors, even in the absence of external treatments. These processes are termed “immune surveillance.” Migration disorders of immune cells are related to autoimmune diseases, chronic inflammation, and tumor evasion. It is therefore essential to characterize immune cell motility in different physiologically and pathologically relevant scenarios to understand the regulatory mechanisms of functionality of immune responses. This review is focused on immune cell migration, to define the underlying mechanisms and the corresponding investigative approaches. We highlight the challenges that immune cells encounter in vivo, and the microfabrication methods to mimic particular aspects of their microenvironment. We discuss the advantages and disadvantages of the proposed tools, and provide information on how to access them. Furthermore, we summarize the directional cues that regulate individual immune cell migration, and discuss the behavior of immune cells in a complex environment composed of multiple directional cues.

scholarly journals Thrombin–Fibrin(ogen) Interactions, Host Defense and Risk of Thrombosis

2021 ◽  
Vol 22 (5) ◽  
pp. 2590
Author(s):  
Anne-Marije Hulshof ◽  
H. Coenraad Hemker ◽  
Henri M. H. Spronk ◽  
Yvonne M. C. Henskens ◽  
Hugo ten Cate
Keyword(s):  
Immune System ◽  
Host Defense ◽  
Immune Cells ◽  
Thrombin Generation ◽  
Plasma Fibrinogen ◽  
Future Research ◽  
Complex Interplay ◽  
Vascular Integrity ◽  
Α2 Macroglobulin

Fibrinogen is a well-known risk factor for arterial and venous thrombosis. Its function is not restricted to clot formation, however, as it partakes in a complex interplay between thrombin, soluble plasma fibrinogen, and deposited fibrin matrices. Fibrinogen, like thrombin, participates predominantly in hemostasis to maintain vascular integrity, but executes some important pleiotropic effects: firstly, as observed in thrombin generation experiments, fibrin removes thrombin from free solution by adsorption. The adsorbed thrombin is protected from antithrombins, notably α2-macroglobulin, and remains physiologically active as it can activate factors V, VIII, and platelets. Secondly, immobilized fibrinogen or fibrin matrices activate monocytes/macrophages and neutrophils via Mac-1 interactions. Immobilized fibrin(ogen) thereby elicits a pro-inflammatory response with a reciprocal stimulating effect of the immune system on coagulation. In contrast, soluble fibrinogen prohibits recruitment of these immune cells. Thus, while fibrin matrices elicit a procoagulant response, both directly by protecting thrombin and indirectly through the immune system, high soluble fibrinogen levels might protect patients due to its immune diminutive function. The in vivo influence of the ‘protective’ plasma fibrinogen versus the ‘pro-thrombotic’ fibrin matrices on thrombosis should be explored in future research.

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