MicroRNA profiling of mouse liver in response to DENV-1 infection by deep 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.

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

Microorganisms ◽

10.3390/microorganisms9040683 ◽

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.

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

Blood ◽

10.1182/blood-2009-09-242784 ◽

2010 ◽

Vol 115 (10) ◽

pp. 1865-1872 ◽

Cited By ~ 106

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.

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

Tick-borne encephalitis - The Book ◽

10.33442/26613980_4-3 ◽

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.

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

Tick-borne encephalitis - The Book ◽

10.33442/978-981-14-0914-1_4 ◽

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.

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

Tick-borne encephalitis - The Book ◽

10.33442/26613980_4-4 ◽

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

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PSII-1 Beef steers divergent in average daily gain have differential expressions of immunity-related genes in whole blood

Journal of Animal Science ◽

10.1093/jas/skaa278.702 ◽

2020 ◽

Vol 98 (Supplement_4) ◽

pp. 399-400

Author(s):

Ibukun M Ogunade

Keyword(s):

Immune Responses ◽

Whole Blood ◽

Average Daily Gain ◽

Differentially Expressed ◽

Beef Steers ◽

Adaptive Immune Responses ◽

Viral Pathogen ◽

Immune Genes ◽

Adaptive Immune ◽

Daily Gain

Abstract We evaluated the whole-blood immune-related gene expression profiles in beef steers divergent in average daily gain (ADG). Forty-eight healthy Angus crossbred beef steers (21 d post-weaning; 210 ± 12 kg of BW) from a single source were housed in individual slatted floor pens and were fed similar corn silage-based total mixed ration ad libitum. After 42 days of feeding, the steers were assigned into two groups with lowest ADG (LF: n = 8) and highest (HF: n = 8) ADG. The average daily DM intake of the steers in LF and HF were 6.08 kg ± 0.57 and 6.04 kg ± 0.42, respectively, and was similar between the two groups (P = 0.72). Whole blood samples were taken from both LF and HF steers and were immediately processed for RNA extraction. Messenger RNA expressions of 84 genes related to innate and adaptive immune responses were analyzed using the RT2 Profiler cow innate and adaptive immune responses PCR Array (PABT-052ZA; Qiagen). Immune genes with FC ≥ 1.2 or ≤ 0.83 having P-value ≤ 0.05 were considered to be differentially expressed. A total number of 11 immune genes were differentially expressed between HF and LF steers. The mRNA expressions of 10 immune genes (IRF3, TLR3, CCR4, MAPK3, TYK2, STAT3, STAT4, STAT6, CCR8, and GATA3) were upregulated in HF steers; these genes were involved in viral pathogen recognition and eradication, defense against intracellular and extracellular pathogens and parasites, and immune response homeostasis. A pro-inflammatory cytokine, IL-2, was upregulated in LF steers. These findings demonstrate that beef steers with divergent ADG had differential expressions of immune-related genes in the blood and future studies are needed to evaluate the mechanisms that cause differences in the expression of these immune genes and how these mechanisms can be employed to drive improved animal performance.

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