Cytokine Profiling Plays a Crucial Role in Activating Immune System to Clear Infectious Pathogens

Muñoz‐Carrillo, José Luis; Contreras-Cordero, Juan Francisco; Gutiérrez-Coronado, Oscar; Villalobos-Gutiérrez, Paola Trinidad; Ramos-Gracia, Luis Guillermo; Hernández-Reyes, Viridiana Elizabeth

doi:10.5772/intechopen.80843

Cited by 54 publications

(52 citation statements)

References 168 publications

(203 reference statements)

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“…By contrast, only the unique type II IFN (IFN II), the IFN-γ, mainly contributes to the clearance of bacterial infections. 3 If IFN I and IFN II are clear signatures associated with viral and bacterial infections, their short life in the body fluids does not allow a robust differentiation. 4 Thus, it appears that it would be useful to study molecules that are more stably expressed downstream of IFN activation.…”

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confidence: 99%

Role of the interferons in CD64 and CD169 expressions in whole blood: Relevance in the balance between viral‐ or bacterial‐oriented immune responses

Bourgoin

Biéchelé

Belkacem

et al. 2020

Immunity Inflam & Disease

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Introduction: CD64 expression increases on neutrophils during bacterial infections. Recently an increase in CD169 expression has been discovered on monocytes during viral infections. Generally, interferons α (IFNsα) andIFNsγ are key drivers of the infectious host immune response. The purpose of this study was to explore if a link exists between these IFNs and both biomarkers. Methods: Whole blood samples from healthy volunteers were stimulated with either IFNs, interleukins, or infectious extracts, to mimic an infectious state. Expressions of CD64 and CD169 were assessed in these samples by multiple flow cytometry methods, over precise kinetics.Results: The expression of CD64 was statistically higher in samples stimulated with IFNγ, and CD169 in those stimulated with IFNα (and all other type I IFNs).Surface expressions are directly induced by their respective IFNs via Janus kinase/ signal transducer and activator of transduction pathways within 6 to 8 hours of incubation. Mixing both types of IFNs seemed to indicate that they partially inhibit each other. Conclusions: The induction of CD169 on monocytes and CD164 on neutrophils by type I and type II IFNs confirms the relevance of these markers for assessing between a viral-vs bacterial-oriented immune response.

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confidence: 99%

Role of the interferons in CD64 and CD169 expressions in whole blood: Relevance in the balance between viral‐ or bacterial‐oriented immune responses

Bourgoin

Biéchelé

Belkacem

et al. 2020

Immunity Inflam & Disease

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“…To evaluate the role of immune regulators and P. aeruginosa infection, we examined IL-6 and IL-1β in BV-2 P. aeruginosa-derived EVs and cell lysates. Interleukins have a key part in systemic immune protection against infections, particularly bacterial infections [57]. Interleukins protect by activating the adaptive immune response that occurs after apoptotic reactions.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pseudomonas aeruginosa on Microglial-Derived Extracellular Vesicle Biogenesis and Composition

et al. 2019

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The packaging of molecular constituents inside extracellular vesicles (EVs) allows them to participate in intercellular communication and the transfer of biological molecules, however the role of EVs during bacterial infection is poorly understood. The goal of this study was to examine the effects of Pseudomonas aeruginosa (P. aeruginosa) infection on the biogenesis and composition of EVs derived from the mouse microglia cell line, BV-2. BV-2 cells were cultured in exosome-free media and infected with 0, 1.3 × 104, or 2.6 × 104 colony forming units per milliliter P. aeruginosa for 72 h. The results indicated that compared with the control group, BV-2 cell viability significantly decreased after P. aeruginosa infection and BV-2-derived EVs concentration decreased significantly in the P. aeruginosa-infected group. P. aeruginosa infection significantly decreased chemokine ligand 4 messenger RNA in BV-2-derived infected EVs, compared with the control group (p ≤ 0.05). This study also revealed that heat shock protein 70 (p ≤ 0.05) and heat shock protein 90β (p ≤ 0.001) levels of expression within EVs increased after P. aeruginosa infection. EV treatment with EVs derived from P. aeruginosa infection reduced cell viability of BV-2 cells. P. aeruginosa infection alters the expression of specific proteins and mRNA in EVs. Our study suggests that P. aeruginosa infection modulates EV biogenesis and composition, which may influence bacterial pathogenesis and infection.

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“…The inflammatory response consists of four main components: (1) endogenous or exogenous factors, such as molecular patterns associated with pathogens (PAMP) and damage (DAMP), which are derived from bacteria, viruses, fungi, parasites, and cell damage, as well as toxic cellular components or any other harmful condition; (2) cellular receptors that recognize these molecular patterns (PRR), for example, Toll-like receptors (TLR); (3) proinflammatory mediators, such as cytokines, chemokines, the complement system, etc. ; and (4) target cells and tissues, where these proinflammatory mediators act [20,21]. The inflammatory response is mainly characterized by four successive phases: (1) silent phase, where the cells synthesize and release the first proinflammatory mediators; (2) vascular phase, characterized by an increase in vascular permeability and dilatation; (3) cellular Pathogenesis of Periodontal Disease DOI: http://dx.doi.org /10.5772/intechopen.86548 phase, characterized by the infiltration of inflammatory cells at the site of injury; and (4) the resolution of the inflammatory response [22].…”

Section: Innate Immune Response In Periodontal Diseasementioning

confidence: 99%

Pathogenesis of Periodontal Disease

Muñoz‐Carrillo¹,

Hernández-Reyes²,

García-Huerta³

et al. 2020

Periodontal Disease - Diagnostic and Adjunctive Non-Surgical Considerations

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Inflammation is a physiological response of the innate immune system against several endogenous or exogenous stimuli. Inflammation begins with an acute pattern; however, it can become chronic by activating the adaptive immune response through cellular and noncellular mechanisms. The main etiologic factor of periodontal disease is bacteria which substantially harbor the human oral cavity. The most common periodontal diseases are gingivitis and periodontitis, whose main characteristic is inflammation. The knowledge of how immune mechanisms and inflammatory responses are regulated is fundamental to understanding the pathogenesis of periodontal disease. The purpose of this chapter is to show the current panorama of the immunological mechanisms involved in the pathogenesis of periodontal disease.

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Cytokine Profiling Plays a Crucial Role in Activating Immune System to Clear Infectious Pathogens

Cited by 54 publications

References 168 publications

Role of the interferons in CD64 and CD169 expressions in whole blood: Relevance in the balance between viral‐ or bacterial‐oriented immune responses

Role of the interferons in CD64 and CD169 expressions in whole blood: Relevance in the balance between viral‐ or bacterial‐oriented immune responses

Effects of Pseudomonas aeruginosa on Microglial-Derived Extracellular Vesicle Biogenesis and Composition

Pathogenesis of Periodontal Disease

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