scholarly journals Immune defects in patients with pulmonary Mycobacterium abscessus disease without cystic fibrosis

2020 ◽  
Vol 6 (4) ◽  
pp. 00590-2020
Author(s):  
Milou M.F. Schuurbiers ◽  
Mariolina Bruno ◽  
Sanne M.H. Zweijpfenning ◽  
Cecile Magis-Escurra ◽  
Martin Boeree ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Immune Response ◽  
Pulmonary Disease ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Adaptive Immune Response ◽  
Mycobacterium Abscessus ◽  
Adaptive Immune ◽  
Ifn Γ ◽  
Immune Defects

The prevalence of Mycobacterium abscessus infections in non-cystic fibrosis (CF) patients has increased in recent years. In this study, we investigate whether immune defects explain the apparent susceptibility to this opportunistic infection in non-CF patients.We performed stimulations of peripheral blood mononuclear cells and whole blood from 13 patients with M. abscessus pulmonary disease and 13 healthy controls to investigate their cytokine production after 24 h and 7 days.Patients were predominantly women (54%) with a mean age of 59 years; 62% had nodular bronchiectatic disease. Many patients had predisposing pulmonary diseases, such as COPD (46%), and asthma (23%). Patients with COPD showed an impaired interleukin (IL)-6 response to M. abscessus and a reduced IL-17 response to Candida, together with a M. abscessus-specific enhanced IL-22 production. Patients without COPD showed higher levels of interleukin-1 receptor antagonist (IL-1Ra), an anti-inflammatory molecule. Within the non-COPD patients, those with bronchiectasis showed defective interferon (IFN)-γ production in response to Candida albicans.In conclusion, susceptibility to M. abscessus is likely determined by a combination of immunological defects and predisposing pulmonary disease. The main defect in the innate immune response was a shift of the ratio of IL-1β to IL-1Ra, which decreased the bioactivity of this pathway in the adaptive immune response. In the adaptive immune response there was defective IL-17 and IFN-γ production. Patients with COPD and bronchiectasis showed different cytokine defects. It is therefore crucial to interpret the immunological results within the clinical background of the patients tested.

Adaptive Immune Response to Mycobacterium abscessus Complex and Cross-Reactivity of BCG Vaccination

2021 ◽  
Author(s):  
Renan Marrichi Mauch ◽  
Peter Østrup Jensen ◽  
Tavs Qvist ◽  
Mette Kolpen ◽  
Claus Moser ◽  
...  
Keyword(s):  
Immune Response ◽  
Adaptive Immune Response ◽  
Cross Reactivity ◽  
Mycobacterium Abscessus ◽  
Bcg Vaccination ◽  
Adaptive Immune

scholarly journals Polyphenol Effects on Splenic Cytokine Response in Post-Weaning Contactin 1-Overexpressing Transgenic Mice

Molecules ◽  
2019 ◽  
Vol 24 (12) ◽  
pp. 2205 ◽  
Author(s):  
Thea Magrone ◽  
Anna Spagnoletta ◽  
Antonella Bizzoca ◽  
Matteo Antonio Russo ◽  
Emilio Jirillo ◽  
...  
Keyword(s):  
Immune Response ◽  
Adaptive Immune Response ◽  
Immune Development ◽  
Adaptive Immune ◽  
Tnf Α ◽  
Pregnant Mice ◽  
Ifn Γ ◽  
Delayed Maturation ◽  
Red Grape ◽  
Necrosis Factor

Background: In mice, postnatal immune development has previously been investigated, and evidence of a delayed maturation of the adaptive immune response has been detected. Methods: In this study, the effects of red grape polyphenol oral administration on the murine immune response were explored using pregnant mice (TAG/F3 transgenic and wild type (wt) mice) as the animal model. The study was performed during pregnancy as well as during lactation until postnatal day 8. Suckling pups from polyphenol-administered dams as well as day 30 post-weaning pups (dietary-administered with polyphenols) were used. Polyphenol effects were evaluated, measuring splenic cytokine secretion. Results: Phorbol myristate acetate-activated splenocytes underwent the highest cytokine production at day 30 in both wt and TAG/F3 mice. In the latter, release of interferon (IFN)-γ and tumor necrosis factor (TNF)-α was found to be higher than in the wt counterpart. In this context, polyphenols exerted modulating activities on day 30 TAG/F3 mice, inducing release of interleukin (IL)-10 in hetero mice while abrogating release of IL-2, IFN-γ, TNF-α, IL-6, and IL-4 in homo and hetero mice. Conclusion: Polyphenols are able to prevent the development of an inflammatory/allergic profile in postnatal TAG/F3 mice.

scholarly journals The Innate Immune Responses of Colonic Epithelial Cells to Trichuris muris Are Similar in Mouse Strains That Develop a Type 1 or Type 2 Adaptive Immune Response

2006 ◽  
Vol 74 (11) ◽  
pp. 6280-6286 ◽  
Author(s):  
Matthew L. deSchoolmeester ◽  
Harinder Manku ◽  
Kathryn J. Else
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Adaptive Immune Response ◽  
Subsequent Development ◽  
Trichuris Muris ◽  
Adaptive Immune ◽  
Ifn Γ

ABSTRACT Trichuris muris resides in intimate contact with its host, burrowing within cecal epithelial cells. However, whether the enterocyte itself responds innately to T. muris is unknown. This study investigated for the first time whether colonic intestinal epithelial cells (IEC) produce cytokines or chemokines following T. muris infection and whether divergence of the innate response could explain differentially polarized adaptive immune responses in resistant and susceptible mice. Increased expression of mRNA for the proinflammatory cytokines gamma interferon (IFN-γ) and tumor necrosis factor and the chemokine CCL2 (MCP-1) were seen after infection of susceptible and resistant strains, with the only difference in expression being a delayed increase in CCL2 in BALB/c IEC. These increases were ablated in MyD88−/− mice, and NF-κB p65 was phosphorylated in response to T. muris excretory/secretory products in the epithelial cell line CMT-93, suggesting involvement of the MyD88-NF-κB signaling pathway in IEC cytokine expression. These data reveal that IEC respond innately to T. muris. However, the minor differences identified between resistant and susceptible mice are unlikely to underlie the subsequent development of a susceptible type 1 (IFN-γ-dominated) or resistant type 2 (interleukin-4 [IL-4]/IL-13-dominated) adaptive immune response.

scholarly journals The Dynamics of Innate and Adaptive Immune Response to Sars Cov-2 Infection and Its Limitations in Human Beings

2021 ◽  
pp. 10-25
Author(s):  
Akpanda Etido ◽  
Emmanuel Ifeanyi Obeagu ◽  
Chukwuma J. Okafor ◽  
Udunma Olive Chijioke ◽  
C. C. N. Vincent ◽  
...  
Keyword(s):  
Immune Response ◽  
Severe Acute Respiratory Syndrome ◽  
Interleukin 1 ◽  
Adaptive Immune Response ◽  
Infection Process ◽  
Host Cells ◽  
Human Beings ◽  
Infected People ◽  
Adaptive Immune ◽  
Cell Immunity

This article deals with the dynamics of the innate and adaptive immune response to severe acute respiratory syndrome coronavirus 2 (SARSCoV2) infection. SARSCoV2 is the viral factor that causes the current global coronavirus pandemic disease 2019 (COVID2019). In terms of person-to-person transmission, it is contacted by inhaling the sneeze droplets of infected people. Severe acute respiratory syndrome Coronavirus 2 attacks lung cells first in its binding mechanism because there are many conservative receptor entries, such as angiotensin converting enzyme 2. The presence of this virus in host cells triggers a variety of protective immune responses, resulting in leads to pneumonia and acute respiratory distress syndrome. In the SarsCoV2 infection process, virus replication, immune response, and inflammatory response are dynamic events that can change rapidly; leading to different results, involving the dynamic expression of pro-inflammatory genes, peaking after the lowest point of respiratory function and leading to a cytokine storm, research on the interleukin 1 (IL1) pathway has shown that it is a factor related in severe respiratory diseases. The weakened expression of cytokines associated with mild infections will also delay T cell immunity to SARSCoV2, thereby prolonging the infection time; this indicates that such afebrile (afebrile) infections and undifferentiated COVID19 cases may promote the virus in the community Spread. This review aims to provide a general overview of the dynamics involved in the human immune response to this viral infection. It also includes a brief description of its structure, discovery history and pathogenesis to facilitate the understanding of this article.

scholarly journals Pseudomonas aeruginosa colonization causes PD-L1 overexpression on monocytes, impairing the adaptive immune response in patients with cystic fibrosis

2019 ◽  
Vol 18 (5) ◽  
pp. 630-635 ◽  
Author(s):  
José Avendaño-Ortiz ◽  
Emilio Llanos-González ◽  
Víctor Toledano ◽  
Rosa del Campo ◽  
Carolina Cubillos-Zapata ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Immune Response ◽  
Pseudomonas Aeruginosa ◽  
Adaptive Immune Response ◽  
Adaptive Immune

scholarly journals Mi-2β-targeted inhibition induces immunotherapy response in melanoma

2020 ◽  
Author(s):  
Bo Zhu ◽  
Zhengyu Wang ◽  
Licheng Yao ◽  
Xingyu Lin ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Checkpoint ◽  
Checkpoint Inhibitors ◽  
Adaptive Immune Response ◽  
Underlying Mechanism ◽  
Adaptive Immune ◽  
Melanoma Patients ◽  
Ifn Γ ◽  
Targeted Inhibition

Abstract Recent development of some new immune checkpoint inhibitors has been particularly successfully in melanoma, but the majority of melanoma patients exhibit resistance. Understanding and targeting the potential underlying mechanism/targets, especially the tumor-intrinsic modulators to convert resistant melanomas to immunotherapy sensitivity will potentially provide a significant improvement in patient outcome. Here, Mi-2β, a chromatin remodeling enzyme was identified as a key melanoma-intrinsic effector regulating the adaptive anti-tumor immune response. Loss of Mi-2β rescued the immune response to immunotherapy in vivo. Mechanistically, targeting Mi-2β induced the adaptive immune response by transcriptionally enhancing expression of a set of IFN-γ-responsive genes including CXCL9, CXCL10 and IRF1. Finally, we developed a Mi-2β-targeted inhibitor Z36-MP5, which specifically and effectively induced a response to immune checkpoint blockades in otherwise resistant melanomas. Our work provides a new insight into the epigenetic regulation in adaptive immune response, and highlights a viable strategy to improve immunotherapies in melanoma.

scholarly journals Time-Resolved Gene Expression Analysis Monitors the Regulation of Inflammatory Mediators and Attenuation of Adaptive Immune Response by Vitamin D

2022 ◽  
Vol 23 (2) ◽  
pp. 911
Author(s):  
Andrea Hanel ◽  
Carsten Carlberg
Keyword(s):  
Gene Expression ◽  
Vitamin D ◽  
Immune Response ◽  
Immune System ◽  
Calcium Binding ◽  
Target Genes ◽  
Mononuclear Cells ◽  
Adaptive Immune Response ◽  
Time Resolved ◽  
Adaptive Immune

Peripheral blood mononuclear cells (PBMCs) belong to the innate and adaptive immune system and are highly sensitive and responsive to changes in their systemic environment. In this study, we focused on the time course of transcriptional changes in freshly isolated human PBMCs 4, 8, 24 and 48 h after onset of stimulation with the active vitamin D metabolite 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3). Taking all four time points together, 662 target genes were identified and segregated either by time of differential gene expression into 179 primary and 483 secondary targets or by driver of expression change into 293 direct and 369 indirect targets. The latter classification revealed that more than 50% of target genes were primarily driven by the cells' response to ex vivo exposure than by the nuclear hormone and largely explained its down-regulatory effect. Functional analysis indicated vitamin D’s role in the suppression of the inflammatory and adaptive immune response by down-regulating ten major histocompatibility complex class II genes, five alarmins of the S100 calcium binding protein A family and by affecting six chemokines of the C-X-C motif ligand family. Taken together, studying time-resolved responses allows to better contextualize the effects of vitamin D on the immune system.

scholarly journals Human Dendritic Cells Are Activated by Dengue Virus Infection: Enhancement by Gamma Interferon and Implications for Disease Pathogenesis

2001 ◽  
Vol 75 (8) ◽  
pp. 3501-3508 ◽  
Author(s):  
Daniel H. Libraty ◽  
Sathit Pichyangkul ◽  
Chuanpis Ajariyakhajorn ◽  
Timothy P. Endy ◽  
Francis A. Ennis
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Virus Infection ◽  
Dengue Virus ◽  
Adaptive Immune Response ◽  
Interleukin 12 ◽  
Cell Mediated Immunity ◽  
Dengue Virus Infection ◽  
Adaptive Immune ◽  
Ifn Γ

ABSTRACT The ability of dendritic cells (DCs) to shape the adaptive immune response to viral infection is mediated largely by their maturation and activation state as determined by the surface expression of HLA molecules, costimulatory molecules, and cytokine production. Dengue is an emerging arboviral disease where the severity of illness is influenced by the adaptive immune response to the virus. In this report, we have demonstrated that dengue virus infects and replicates in immature human myeloid DCs. Exposure to live dengue virus led to maturation and activation of both the infected and surrounding, uninfected DCs and stimulated production of tumor necrosis factor alpha (TNF-α) and alpha interferon (IFN-α). Activation of the dengue virus-infected DCs was blunted compared to the surrounding, uninfected DCs, and dengue virus infection induced low-level release of interleukin-12 p70 (IL-12 p70), a key cytokine in the development of cell-mediated immunity (CMI). Upon the addition of IFN-γ, there was enhanced activation of dengue virus-infected DCs and enhanced dengue virus-induced IL-12 p70 release. The data suggest a model whereby DCs are the early, primary target of dengue virus in natural infection and the vigor of CMI is modulated by the relative presence or absence of IFN-γ in the microenvironment surrounding the virus-infected DCs. These findings are relevant to understanding the pathogenesis of dengue hemorrhagic fever and the design of new vaccination and therapeutic strategies.

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