scholarly journals Staphylococcus aureus Internalization in Osteoblast Cells: Mechanisms, Interactions and Biochemical Processes. What Did We Learn from Experimental Models?

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 239
Author(s):  
Stefano Stracquadanio ◽  
Nicolò Musso ◽  
Angelita Costantino ◽  
Lorenzo Mattia Lazzaro ◽  
Stefania Stefani ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune System ◽  
Current Knowledge ◽  
Bacterial Species ◽  
Joint Infection ◽  
Experimental Models ◽  
System Response ◽  
Osteoblastic Cell ◽  
Host Immune System ◽  
Osteoblastic Cell Line

Bacterial internalization is a strategy that non-intracellular microorganisms use to escape the host immune system and survive inside the human body. Among bacterial species, Staphylococcus aureus showed the ability to interact with and infect osteoblasts, causing osteomyelitis as well as bone and joint infection, while also becoming increasingly resistant to antibiotic therapy and a reservoir of bacteria that can make the infection difficult to cure. Despite being a serious issue in orthopedic surgery, little is known about the mechanisms that allow bacteria to enter and survive inside the osteoblasts, due to the lack of consistent experimental models. In this review, we describe the current knowledge about S. aureus internalization mechanisms and various aspects of the interaction between bacteria and osteoblasts (e.g., best experimental conditions, bacteria-induced damages and immune system response), focusing on studies performed using the MG-63 osteoblastic cell line, the best traditional (2D) model for the study of this phenomenon to date. At the same time, as it has been widely demonstrated that 2D culture systems are not completely indicative of the dynamic environment in vivo, and more recent 3D models—representative of bone infection—have also been investigated.

scholarly journals Staphylococcus aureus Internalization in Osteoblast Cells: Mechanisms, Interactions and Biochemical Processes. What did We Learn from Experimental Models?

2020 ◽  
Author(s):  
Nicolò Musso ◽  
Stefano Stracquadanio ◽  
Angelita Costantino ◽  
Lorenzo Mattia Lazzaro ◽  
Stefania Stefani ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune System ◽  
Current Knowledge ◽  
Joint Infection ◽  
Experimental Models ◽  
System Response ◽  
Osteoblastic Cell ◽  
Host Immune System ◽  
Experimental Conditions ◽  
Osteoblastic Cell Line

Bacterial internalization is a strategy that non-intracellular microorganisms use to escape the host immune system and survive inside the human body. Among bacteria species, Staphylococcus aureus showed ability to interact and infect osteoblasts causing osteomyelitis as well as bone and joint infection, while also becoming increasingly resistant to antibiotic therapy and a reservoir of bacteria that can make the infection difficult to cure. Despite being a serious issue in orthopedic surgery, little is known about the mechanisms that allow bacteria to enter and survive inside the osteoblasts, also due to the lack of consistent experimental models. In this review, we describe the current knowledge about S. aureus internalization mechanisms and various aspects of the interaction between bacteria and osteoblasts (e.g. best experimental conditions, bacteria-induced damages and immune system response), focusing on studies performed using the MG-63 osteoblastic cell line, so far the best model for the study of this phenomenon.

scholarly journals Genotypic diversity between surgical and nasal Staphylococcus aureus isolates

2020 ◽  
Author(s):  
Dongzhu Ma ◽  
Patrick L. Maher ◽  
Kimberly M. Brothers ◽  
Nathan J. Phillips ◽  
Deborah Simonetti ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Joint Infection ◽  
Parallel Evolution ◽  
Genotypic Diversity ◽  
Nasal Carriage ◽  
Host Immune System ◽  
Host Status ◽  
Fibronectin Binding ◽  
Two Populations ◽  
Atypical Strains

AbstractStaphylococcus aureus is a common organism in periprosthetic joint infection (PJI). Little is known about S. aureus genetic diversity in PJI as compared to nasal carriage. We hypothesized PJI S. aureus strains would be associated with increased virulence as compared to those from nasal carriage. Whole genome sequencing and multilocus sequence typing (MLST) was performed to genotype these two populations at high resolution. MLST revealed a variety of genotypes in both populations but many belonged to the most common clonal complexes. In nasal cultures, 69% of strains were of clonal complexes CC5, CC8, and CC30. In PJI cultures, only 51% could be classified in these common clonal complexes. Remaining strains were atypical, and these atypical strains in PJI were associated with poor host status and compromised immune conditions. Mutations in genes involved in fibronectin binding (ebh, fnbA, clfA, clfB) systematically distinguished later PJI isolates from the first PJI isolate from each patient. S. aureus isolated from nasal carriage and PJI specimens differ significantly, with the latter being more diverse. Strains associated with lower pathogenicity tended to be found in immunocompromised patients, suggesting the host immune system plays an important role in preventing PJI. Repeated mutations in S. aureus genes associated with extracellular matrix binding were identified suggesting an adaptive, parallel evolution in S. aureus during the development of PJI.

scholarly journals The Interplay between Host Innate Immunity and Hepatitis E Virus

Viruses ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 541 ◽  
Author(s):  
Yang Li ◽  
Changbo Qu ◽  
Peifa Yu ◽  
Xumin Ou ◽  
Qiuwei Pan ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Hepatitis E Virus ◽  
Inflammatory Responses ◽  
Hepatitis E ◽  
Experimental Models ◽  
Innate Immune ◽  
Host Immune System ◽  
Global Health Issue ◽  
Host Innate Immunity

Hepatitis E virus (HEV) infection represents an emerging global health issue, whereas the clinical outcomes vary dramatically among different populations. The host innate immune system provides a first-line defense against the infection, but dysregulation may partially contribute to severe pathogenesis. A growing body of evidence has indicated the active response of the host innate immunity to HEV infection both in experimental models and in patients. In turn, HEV has developed sophisticated strategies to counteract the host immune system. In this review, we aim to comprehensively decipher the processes of pathogen recognition, interferon, and inflammatory responses, and the involvement of innate immune cells in HEV infection. We further discuss their implications in understanding the pathogenic mechanisms and developing antiviral therapies.

scholarly journals Mutual Interplay of Host Immune System and Gut Microbiota in the Immunopathology of Atherosclerosis

2020 ◽  
Vol 21 (22) ◽  
pp. 8729 ◽  
Author(s):  
Chih-Fan Yeh ◽  
Ying-Hsien Chen ◽  
Sheng-Fu Liu ◽  
Hsien-Li Kao ◽  
Ming-Shiang Wu ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Cytokine Production ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Inflammasome Activation ◽  
Host Immune System ◽  
Gut Permeability ◽  
And Function ◽  
Progression Of Atherosclerosis

Inflammation is the key for the initiation and progression of atherosclerosis. Accumulating evidence has revealed that an altered gut microbiome (dysbiosis) triggers both local and systemic inflammation to cause chronic inflammatory diseases, including atherosclerosis. There have been some microbiome-relevant pro-inflammatory mechanisms proposed to link the relationships between dysbiosis and atherosclerosis such as gut permeability disruption, trigger of innate immunity from lipopolysaccharide (LPS), and generation of proatherogenic metabolites, such as trimethylamine N-oxide (TMAO). Meanwhile, immune responses, such as inflammasome activation and cytokine production, could reshape both composition and function of the microbiota. In fact, the immune system delicately modulates the interplay between microbiota and atherogenesis. Recent clinical trials have suggested the potential of immunomodulation as a treatment strategy of atherosclerosis. Here in this review, we present current knowledge regarding to the roles of microbiota in contributing atherosclerotic pathogenesis and highlight translational perspectives by discussing the mutual interplay between microbiota and immune system on atherogenesis.

scholarly journals The Bacterium Frischella perrara Causes Scab Formation in the Gut of its Honeybee Host

mBio ◽  
2015 ◽  
Vol 6 (3) ◽  
Author(s):  
Philipp Engel ◽  
Kelsey D. Bartlett ◽  
Nancy A. Moran
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Gut Microbiota ◽  
Bacterial Colonization ◽  
Bacterial Species ◽  
Host Immune System ◽  
Natural Ecosystems ◽  
Epithelial Surface ◽  
Host Interactions ◽  
Key Species

ABSTRACT Honeybees harbor well-defined bacterial communities in their guts. The major members of these communities appear to benefit the host, but little is known about how they interact with the host and specifically how they interface with the host immune system. In the pylorus, a short region between the midgut and hindgut, honeybees frequently exhibit scab-like structures on the epithelial gut surface. These structures are reminiscent of a melanization response of the insect immune system. Despite the wide distribution of this phenotype in honeybee populations, its cause has remained elusive. Here, we show that the presence of a common member of the bee gut microbiota, the gammaproteobacterium Frischella perrara, correlates with the appearance of the scab phenotype. Bacterial colonization precedes scab formation, and F. perrara specifically localizes to the melanized regions of the host epithelium. Under controlled laboratory conditions, we demonstrate that exposure of microbiota-free bees to F. perrara but not to other bacteria results in scab formation. This shows that F. perrara can become established in a spatially restricted niche in the gut and triggers a morphological change of the epithelial surface, potentially due to a host immune response. As an intermittent colonizer, this bacterium holds promise for addressing questions of community invasion in a simple yet relevant model system. Moreover, our results show that gut symbionts of bees engage in differential host interactions that are likely to affect gut homeostasis. Future studies should focus on how these different gut bacteria impact honeybee health. IMPORTANCE As pollinators, honeybees are key species for agricultural and natural ecosystems. Their guts harbor simple communities composed of characteristic bacterial species. Because of these features, bees are ideal systems for studying fundamental aspects of gut microbiota-host interactions. However, little is known about how these bacteria interact with their host. Here, we show that a common member of the bee gut microbiota causes the formation of a scab-like structure on the gut epithelium of its host. This phenotype was first described in 1946, but since then it has not been much further characterized, despite being found in bee populations worldwide. The scab phenotype is reminiscent of melanization, a conserved innate immune response of insects. Our results show that high abundance of one member of the bee gut microbiota triggers this specific phenotype, suggesting that the gut microbiota composition can affect the immune status of this key pollinator species.

Expression of heat shock proteins 27 and 72 correlates with specific commensal microbes in different regions of porcine gastrointestinal tract

2014 ◽  
Vol 306 (12) ◽  
pp. G1033-G1041 ◽  
Author(s):  
Hao-Yu Liu ◽  
Johan Dicksved ◽  
Torbjörn Lundh ◽  
Jan Erik Lindberg
Keyword(s):  
Immune System ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Bacterial Species ◽  
Host Immune System ◽  
Gi Tract ◽  
Microbe Interactions ◽  
Cell Type Specific ◽  
Host Microbe Interactions ◽  
Shock Proteins

The gastrointestinal (GI) tract of mammals is inhabited by trillions of microorganisms, resulting in exceedingly complex networking. The interaction between distinct bacterial species and the host immune system is essential in maintaining homeostasis in the gut ecosystem. For instance, the gut commensal microbiota dictates intestinal mucosa maturation and its abundant immune components, such as cytoprotective heat shock proteins (HSP). Here we examined physiological expression of HSP in the normal porcine GI tract and found it to be gut region- and cell type-specific in response to dietary components, microbes, and microbial metabolites to which the mucosa surface is exposed. Correlations between HSP72 expression and ileal Lactobacillus spp. and colonic clostridia species, and between HSP27 expression and uronic acid ingestion, were important interplays identified here. Thus this study provides novel insights into host-microbe interactions shaping the immune system that are modifiable by dietary regime.

scholarly journals Improving the Efficacy of Antimicrobials against Biofilm-Embedded Bacteria Using Bovine Hyaluronidase Azoximer (Longidaza®)

Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1740
Author(s):  
Elena Trizna ◽  
Diana Baidamshina ◽  
Anna Gorshkova ◽  
Valentin Drucker ◽  
Mikhail Bogachev ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Immune System ◽  
Side Effects ◽  
Klebsiella Pneumoniae ◽  
Chronic Infection ◽  
Bacterial Species ◽  
Biofilm Bacteria ◽  
Biofilm Structure

While in a biofilm, bacteria are extremely resistant to both antimicrobials and the immune system, leading to the development of chronic infection. Here, we show that bovine hyaluronidase fused with a copolymer of 1,4-ethylenepiperazine N-oxide and (N-carboxymethyl) -1,4-ethylenepiperazinium bromide (Longidaza®) destroys both mono- and dual-species biofilms formed by various bacteria. After 4 h of treatment with 750 units of the enzyme, the residual biofilms of Staphylococcus aureus, Enterococcus faecalis, Escherichia coli, Pseudomonas aeruginosa and Klebsiella pneumoniae preserved about 50–70% of their initial mass. Biomasses of dual-species biofilms formed by S. aureus and the four latter species were reduced 1.5-fold after 24 h treatment, while the significant destruction of S. aureus–P. aeruginosa and S. aureus–K. pneumoniae was also observed after 4 h of treatment with Longidaza®. Furthermore, when applied in combination, Longidaza® increased the efficacy of various antimicrobials against biofilm-embedded bacteria, although with various increase-factor values depending on both the bacterial species and antimicrobials chosen. Taken together, our data indicate that Longidaza® destroys the biofilm structure, facilitating the penetration of antimicrobials through the biofilm, and in this way improving their efficacy, lowering the required dose and thus also potentially reducing the associated side effects.

scholarly journals Glances in Immunology of HIV and HCV Infection

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Maria Giovanna Quaranta ◽  
Benedetta Mattioli ◽  
Stefano Vella
Keyword(s):  
Immune System ◽  
Immune Escape ◽  
Current Knowledge ◽  
Research Field ◽  
New Drugs ◽  
Host Immune System ◽  
Immune Recognition ◽  
Genetic Associations ◽  
Efficient Treatment ◽  
Adaptive Immune

Since the identification of HIV and HCV much progress has been made in the understanding of their life cycle and interaction with the host immune system. Despite these viruses markedly differ in their virological properties and in their pathogenesis, they share many common features in their immune escape and survival strategy. Both viruses have developed sophisticated ways to subvert and antagonize host innate and adaptive immune responses. In the last years, much effort has been done in the study of the AIDS pathogenesis and in the development of efficient treatment strategies, and a fatal infection has been transformed in a potentially chronic pathology. Much of this knowledge is now being transferred in the HCV research field, especially in the development of new drugs, although a big difference still remains between the outcome of the two infections, being HCV eradicable after treatment, whereas HIV eradication remains at present unachievable due to the establishment of reservoirs. In this review, we present current knowledge on innate and adaptive immune recognition and activation during HIV and HCV mono-infections and evasion strategies. We also discuss the genetic associations between components of the immune system, the course of infection, and the outcome of the therapies.

scholarly journals 3D Cocultures of Osteoblasts and Staphylococcus aureus on Biomimetic Bone Scaffolds as a Tool to Investigate the Host–Pathogen Interface in Osteomyelitis

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 837
Author(s):  
Raffaella Parente ◽  
Valentina Possetti ◽  
Maria Lucia Schiavone ◽  
Elisabetta Campodoni ◽  
Ciro Menale ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Opportunistic Pathogen ◽  
Bone Architecture ◽  
Osteoblastic Cell ◽  
Bone Homeostasis ◽  
Osteoblastic Cell Line ◽  
Host Pathogen

Osteomyelitis (OM) is an infectious disease of the bone primarily caused by the opportunistic pathogen Staphylococcus aureus (SA). This Gram-positive bacterium has evolved a number of strategies to evade the immune response and subvert bone homeostasis, yet the underlying mechanisms remain poorly understood. OM has been modeled in vitro to challenge pathogenetic hypotheses in controlled conditions, thus providing guidance and support to animal experimentation. In this regard, traditional 2D models of OM inherently lack the spatial complexity of bone architecture. Three-dimensional models of the disease overcome this limitation; however, they poorly reproduce composition and texture of the natural bone. Here, we developed a new 3D model of OM based on cocultures of SA and murine osteoblastic MC3T3-E1 cells on magnesium-doped hydroxyapatite/collagen I (MgHA/Col) scaffolds that closely recapitulate the bone extracellular matrix. In this model, matrix-dependent effects were observed in proliferation, gene transcription, protein expression, and cell–matrix interactions both of the osteoblastic cell line and of bacterium. Additionally, these had distinct metabolic and gene expression profiles, compared to conventional 2D settings, when grown on MgHA/Col scaffolds in separate monocultures. Our study points to MgHA/Col scaffolds as biocompatible and bioactive matrices and provides a novel and close-to-physiology tool to address the pathogenetic mechanisms of OM at the host–pathogen interface.

scholarly journals Immunopathogenesis of severe acute respiratory syndrome coronavirus-2: evolving knowledge and its current statuss

2021 ◽  
Author(s):  
Nitin Saksena ◽  
Srinivasa Reddy Bonam ◽  
Monica Miranda-Saksena
Keyword(s):  
Immune System ◽  
Severe Acute Respiratory Syndrome ◽  
Current Knowledge ◽  
Host Immune System ◽  
The Past ◽  
Short Space ◽  
Shed Light ◽  
Global Research

As the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 is a new virus, the current knowledge on the immunopathogenesis of this newly emerged SARS-CoV-2 is beginning to unravel with intensive ongoing global research efforts. Although a plethora of new studies have been published in a short space of time describing how the virus causes disease and incurs insults on the host immune system and the underlying immunopathogenic mechanisms remain to be elucidated. Thus, the discussion in this review is based on the most current knowledge on the immunopathogenesis of SARS-CoV-2 that has emerged in the past 12 months. The main objective is to shed light on the most current concepts in immunopathological aspects of the lung, bloodstream, and brain caused by the SARS-CoV-2, which has led to the current pandemic resulting in > 100 million infections and > 2 million deaths, and ongoing.

Sign in / Sign up

Export Citation Format

Share Document