scholarly journals Lactiplantibacillus plantarum as a Potential Adjuvant and Delivery System for the Development of SARS-CoV-2 Oral Vaccines

2021 ◽  
Vol 9 (4) ◽  
pp. 683
Author(s):  
Julio Villena ◽  
Chang Li ◽  
Maria Guadalupe Vizoso-Pinto ◽  
Jacinto Sacur ◽  
Linzhu Ren ◽  
...  
Keyword(s):  
Immune Responses ◽  
Oral Administration ◽  
Molecular Mechanisms ◽  
Spike Protein ◽  
Heterologous Proteins ◽  
Oral Vaccines ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Viral Antigens ◽  
Mucosal Infection

The most important characteristics regarding the mucosal infection and immune responses against the Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) as well as the current vaccines against coronavirus disease 2019 (COVID-19) in development or use are revised to emphasize the opportunity for lactic acid bacteria (LAB)-based vaccines to offer a valid alternative in the fight against this disease. In addition, this article revises the knowledge on: (a) the cellular and molecular mechanisms involved in the improvement of mucosal antiviral defenses by beneficial Lactiplantibacillus plantarum strains, (b) the systems for the expression of heterologous proteins in L. plantarum and (c) the successful expressions of viral antigens in L. plantarum that were capable of inducing protective immune responses in the gut and the respiratory tract after their oral administration. The ability of L. plantarum to express viral antigens, including the spike protein of SARS-CoV-2 and its capacity to differentially modulate the innate and adaptive immune responses in both the intestinal and respiratory mucosa after its oral administration, indicates the potential of this LAB to be used in the development of a mucosal COVID-19 vaccine.

scholarly journals MicroRNA profiling of mouse liver in response to DENV-1 infection by deep sequencing

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6697 ◽  
Author(s):  
Lian Yih Pong ◽  
Sinikka Parkkinen ◽  
Amreeta Dhanoa ◽  
Han Ming Gan ◽  
Indeevari Abisheka Chiharu Wickremesinghe ◽  
...  
Keyword(s):  
Immune Responses ◽  
Infected Mouse ◽  
Deep Sequencing ◽  
Molecular Mechanisms ◽  
Fold Change ◽  
Differentially Expressed ◽  
Pathway Enrichment Analysis ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Mirna Sequencing

BackgroundDengue caused by dengue virus (DENV) serotypes −1 to −4 is the most important mosquito-borne viral disease in the tropical and sub-tropical countries worldwide. Yet many of the pathophysiological mechanisms of host responses during DENV infection remain largely unknown and incompletely understood.MethodsUsing a mouse model, the miRNA expressions in liver during DENV-1 infection was investigated using high throughput miRNA sequencing. The differential expressions of miRNAs were then validated by qPCR, followed by target genes prediction. The identified miRNA targets were subjected to gene ontology (GO) annotation and pathway enrichment analysis to elucidate the potential biological pathways and molecular mechanisms associated with DENV-1 infection.ResultsA total of 224 and 372 miRNAs out of 433 known mouse miRNAs were detected in the livers of DENV-1-infected and uninfected mice, respectively; of these, 207 miRNAs were present in both libraries. The miR-148a-3p and miR-122-5p were the two most abundant miRNAs in both groups. Thirty-one miRNAs were found to have at least 2-fold change in upregulation or downregulation, in which seven miRNAs were upregulated and 24 miRNAs were downregulated in the DENV-1-infected mouse livers. The miR-1a-3p was found to be the most downregulated miRNA in the DENV-1-infected mouse livers, with a significant fold change of 0.10. To validate the miRNA sequencing result, the expression pattern of 12 miRNAs, which were highly differentially expressed or most abundant, were assessed by qPCR and nine of them correlated positively with the one observed in deep sequencing.In silicofunctional analysis revealed that the adaptive immune responses involving TGF-beta, MAPK, PI3K-Akt, Rap1, Wnt and Ras signalling pathways were modulated collectively by 23 highly differentially expressed miRNAs during DENV-1 infection.ConclusionThis study provides the first insight into the global miRNA expressions of mouse livers in response to DENV-1 infectionin vivoand the possible roles of miRNAs in modulating the adaptive immune responses during DENV-1 infection.

scholarly journals Comparison of intestinal APC subsets from homeostatic and immunostimulatory environments

2021 ◽  
Author(s):  
◽  
Kerry Hilligan
Keyword(s):  
T Cells ◽  
Food Allergy ◽  
Immune Responses ◽  
Oral Administration ◽  
Mesenteric Lymph Nodes ◽  
Adaptive Immune Responses ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Adaptive Immune ◽  
Inflammatory Bowel

<p>Antigen presenting cells (APC) including dendritic cells (DC) play a key role in the initiation and direction of adaptive immune responses. Acting as sentinels in the tissue, DC sample antigen and traffic to the local lymph node where they present antigen to naïve T cells. The signals DC provide to naïve T cells determines the functional fate of the T cell and therefore, the type of immune response generated. At mucosal sites, such as the intestine, immune responses need to be carefully regulated due to the high antigenic load. For this reason, intestinal immune cells are highly specialised to prevent immune activation to innocuous antigens while still holding the capacity to induce potent responses to pathogenic microbes and helminths. Oral administration of antigen is associated with tolerance and the generation of FoxP3+ regulatory T cells (Tregs). Specialised lamina propria (LP) resident APC are required for the initiation of Treg differentiation in the mesenteric lymph nodes (MLN) through production of chemical mediators such as retinoic acid (RA). Ablation of these populations or restricted trafficking prevents the development of Tregs in mouse models thus supporting the essential role of APC in maintaining intestinal homeostasis. During infection, APC promote the induction of adaptive immune responses which neutralise threats. However, the APC subsets involved in this are not well defined. Pathologies such as food allergy and inflammatory bowel disease are thought to arise due to the development of aberrant immune responses. Food allergy can be modelled in mice using the mucosal adjuvant cholera toxin (CT) which has been shown to drive immunity to co-delivered antigens and is associated with the generation of IL-4 producing T helper 2 cells. Understanding the APC subsets involved in the initiation of intestinal immune responses could help in the development of targeted therapies for inflammatory bowel conditions. In this thesis, I show that oral administration of CT is followed by the appearance of a novel phenotype of DC in the intestinal LP and MLN. These DC differ functionally from DC at steady-state and may contribute to the generation of IL-4 producing T cells observed in the LP, MLN and spleen following oral administration of CT.</p>

Graft-versus-host disease: regulation by microbe-associated molecules and innate immune receptors

Blood ◽  
2010 ◽  
Vol 115 (10) ◽  
pp. 1865-1872 ◽  
Author(s):  
Olaf Penack ◽  
Ernst Holler ◽  
Marcel R. M. van den Brink
Keyword(s):  
Immune Responses ◽  
Graft Versus Host Disease ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Adaptive Immune Responses ◽  
Hematopoietic Stem ◽  
Host Disease ◽  
Graft Versus Host ◽  
Adaptive Immune ◽  
Immune Receptors

Abstract Acute graft-versus-host disease (GVHD) remains the major obstacle to a more favorable therapeutic outcome of allogeneic hematopoietic stem cell transplantation (HSCT). GVHD is characterized by tissue damage in gut, liver, and skin, caused by donor T cells that are critical for antitumor and antimicrobial immunity after HSCT. One obstacle in combating GVHD used to be the lack of understanding the molecular mechanisms that are involved in the initiation phase of this syndrome. Recent research has demonstrated that interactions between microbial-associated molecules (pathogen-associated molecular patterns [PAMPs]) and innate immune receptors (pathogen recognition receptors [PRRs]), such as NOD-like receptors (NLRs) and Toll-like receptors (TLRs), control adaptive immune responses in inflammatory disorders. Polymorphisms of the genes encoding NOD2 and TLR4 are associated with a higher incidence of GVHD in HSC transplant recipients. Interestingly, NOD2 regulates GVHD through its inhibitory effect on antigen-presenting cell (APC) function. These insights identify important mechanisms regarding the induction of GVHD through the interplay of microbial molecules and innate immunity, thus opening a new area for future therapeutic approaches. This review covers current knowledge of the role of PAMPs and PRRs in the control of adaptive immune responses during inflammatory diseases, particularly GVHD.

Chapter 4: Pathogenesis of TBE with a focus on molecular mechanisms

2020 ◽  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Reverse Genetics ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Adaptive Immune Responses ◽  
Knock Out ◽  
Adaptive Immune ◽  
Tick Borne Encephalitis ◽  
Tick Borne Encephalitis Virus

In this chapter we describe the pathogenesis of tick-borne encephalitis virus (TBEV). To cause infection, TBEV needs to cross three different barriers; the physical, the innate and adaptive and the blood-brain barrier. The trigger of innate immune and adaptive immune responses, by TBEV is necessary to clear the infection. TBEV employs strategies to evade the innate immune response. Tools to study TBEV pathogenicity such as mouse knock-out models and reverse genetics are also discussed.

scholarly journals Comparison of intestinal APC subsets from homeostatic and immunostimulatory environments

2021 ◽  
Author(s):  
◽  
Kerry Hilligan
Keyword(s):  
T Cells ◽  
Food Allergy ◽  
Immune Responses ◽  
Oral Administration ◽  
Mesenteric Lymph Nodes ◽  
Adaptive Immune Responses ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Adaptive Immune ◽  
Inflammatory Bowel

<p>Antigen presenting cells (APC) including dendritic cells (DC) play a key role in the initiation and direction of adaptive immune responses. Acting as sentinels in the tissue, DC sample antigen and traffic to the local lymph node where they present antigen to naïve T cells. The signals DC provide to naïve T cells determines the functional fate of the T cell and therefore, the type of immune response generated. At mucosal sites, such as the intestine, immune responses need to be carefully regulated due to the high antigenic load. For this reason, intestinal immune cells are highly specialised to prevent immune activation to innocuous antigens while still holding the capacity to induce potent responses to pathogenic microbes and helminths. Oral administration of antigen is associated with tolerance and the generation of FoxP3+ regulatory T cells (Tregs). Specialised lamina propria (LP) resident APC are required for the initiation of Treg differentiation in the mesenteric lymph nodes (MLN) through production of chemical mediators such as retinoic acid (RA). Ablation of these populations or restricted trafficking prevents the development of Tregs in mouse models thus supporting the essential role of APC in maintaining intestinal homeostasis. During infection, APC promote the induction of adaptive immune responses which neutralise threats. However, the APC subsets involved in this are not well defined. Pathologies such as food allergy and inflammatory bowel disease are thought to arise due to the development of aberrant immune responses. Food allergy can be modelled in mice using the mucosal adjuvant cholera toxin (CT) which has been shown to drive immunity to co-delivered antigens and is associated with the generation of IL-4 producing T helper 2 cells. Understanding the APC subsets involved in the initiation of intestinal immune responses could help in the development of targeted therapies for inflammatory bowel conditions. In this thesis, I show that oral administration of CT is followed by the appearance of a novel phenotype of DC in the intestinal LP and MLN. These DC differ functionally from DC at steady-state and may contribute to the generation of IL-4 producing T cells observed in the LP, MLN and spleen following oral administration of CT.</p>

Chapter 4: Pathogenesis of TBE with a focus on molecular mechanisms

2019 ◽  
Author(s):  
Andrea Kröger ◽  
Anna K. Överby
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Reverse Genetics ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Adaptive Immune Responses ◽  
Knock Out ◽  
Adaptive Immune ◽  
Tick Borne Encephalitis ◽  
Tick Borne Encephalitis Virus

• In this chapter we describe the pathogenesis of tick-borne encephalitis virus (TBEV). • To cause infection, TBEV needs to cross three different barriers; the physical, the innate and adaptive, and the blood-brain barrier. • The trigger of innate immune and adaptive immune responses, by TBEV is necessary to clear the infection. • TBEV employs strategies to evade the innate immune response. • Tools to study TBEV pathogenicity such as mouse knock-out models and reverse genetics are also discussed.

Chapter 4: Pathogenesis of TBE with a focus on molecular mechanisms

2021 ◽  
Author(s):  
Andrea Kröger ◽  
Anna K Överby
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Reverse Genetics ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Adaptive Immune Responses ◽  
Knock Out ◽  
Adaptive Immune ◽  
Tick Borne Encephalitis ◽  
Tick Borne Encephalitis Virus

In this chapter we describe the pathogenesis of tick-borne encephalitis virus (TBEV). To cause infection, TBEV needs to cross three different barriers; the physical, the innate and adaptive and the blood-brain barrier. The trigger of innate immune and adaptive immune responses, by TBEV is necessary to clear the infection. TBEV employs strategies to evade the innate immune response. Tools to study TBEV pathogenicity such as mouse knock-out models and reverse genetics are also discussed.

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