Impaired interferon‐α expression in plasmacytoid dendritic cells in asthma

Lin, Ting‐Yu; Lo, Chun‐Yu; Tsao, Kuo‐Chien; Chang, Po‐Jui; Kuo, Chih-His Scott; Lo, Yu‐Lun; Lin, Shu‐Min; Hsieh, Ming‐Ju; Wang, Tsai‐Yu; Hsu, Ping‐Chih; Lin, Horng‐Chyuan

doi:10.1002/iid3.376

Cited by 5 publications

(6 citation statements)

References 49 publications

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“…In several studies, deficiency of various IFN has been verified utilizing cultured human bronchial epithelial cells (HBECs) from asthmatics after RV infection in vitro , which leads to the deficiency of IFN-β and IFN-λ in primary bronchial epithelial cells (PBECs) and deficiency of IFNs (γ, α, β and λ) and IL-15 in bronchoalveolar lavage (BAL) cells ( 23 ). This result is accorded with that of Lin et al, showing the feasibility of utilizing IFN for alleviating RV infection ( 106 ).…”

Section: Utilizations Of Anti-inflammatory Cytokinessupporting

confidence: 90%

Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions

Sang,

Gong,

Huang

et al. 2024

Front. Allergy

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Rhinovirus is a widespread virus associated with several respiratory diseases, especially asthma exacerbation. Currently, there are no accurate therapies for rhinovirus. Encouragingly, it is found that during rhinovirus-induced immunoreactions the levels of certain cytokines in patients' serum will alter. These cytokines may have pivotal pro-inflammatory or anti-inflammatory effects via their specific mechanisms. Thus far, studies have shown that inhibitions of cytokines such as IL-1, IL-4, IL-5, IL-6, IL-13, IL-18, IL-25, and IL-33 may attenuate rhinovirus-induced immunoreactions, thereby relieving rhinovirus infection. Furthermore, such therapeutics for rhinovirus infection can be applied to viruses of other species, with certain practicability.

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Section: Utilizations Of Anti-inflammatory Cytokinessupporting

confidence: 90%

Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions

Sang,

Gong,

Huang

et al. 2024

Front. Allergy

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“…Consistently, a in IFN type I production was observed in patients in which RV was detected in vivo compared to patients without RV in their airways. For the latter group the IFN-a detection was significantly lower (19). In preschool asthmatic children, the same deficiency was found during a nonsymptomatic phase, however during HRV-induced exacerbations there is a delayed, but sufficient IFN-a production measurable (90,92).…”

Section: Interferon Type Imentioning

confidence: 60%

“…Those patients showed a temporal upregulation of IFN-a and IFN-g levels, which also correlated with the clinical parameters assessed by Cold Symptoms Score (CSS) (94). In pDCs as well as in PBMCs it has been shown that TLR-7/8-agonists, for example Resiquimod, and RV infection lead to an upregulation of IFN type I, however in asthmatic patients, this upregulation was found to be deficient (19,95). In infants deficiency in IFN type I production in the first place, also caused increased susceptibility to RV infections and thereby to a higher risk of subsequent asthma development (96).…”

Section: Interferon Type Imentioning

confidence: 68%

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Mechanism of Rhinovirus Immunity and Asthma

et al. 2021

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The majority of asthma exacerbations in children are caused by Rhinovirus (RV), a positive sense single stranded RNA virus of the Picornavirus family. The host has developed virus defense mechanisms that are mediated by the upregulation of interferon-activated signaling. However, the virus evades the immune system by inducing immunosuppressive cytokines and surface molecules like programmed cell death protein 1 (PD-1) and its ligand (PD-L1) on immunocompetent cells. Initially, RV infects epithelial cells, which constitute a physiologic mucosal barrier. Upon virus entrance, the host cell immediately recognizes viral components like dsRNA, ssRNA, viral glycoproteins or CpG-DNA by host pattern recognition receptors (PRRs). Activation of toll like receptors (TLR) 3, 7 and 8 within the endosome and through MDA-5 and RIG-I in the cytosol leads to the production of interferon (IFN) type I and other antiviral agents. Every cell type expresses IFNAR1/IFNAR2 receptors thus allowing a generalized antiviral activity of IFN type I resulting in the inhibition of viral replication in infected cells and preventing viral spread to non-infected cells. Among immune evasion mechanisms of the virus, there is downregulation of IFN type I and its receptor as well as induction of the immunosuppressive cytokine TGF-β. TGF-β promotes viral replication and is associated with induction of the immunosuppression signature markers LAP3, IDO and PD-L1. This article reviews the recent advances on the regulation of interferon type I expression in association with RV infection in asthmatics and the immunosuppression induced by the virus.

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“…Plasmacytoid dendritic cells (pDCs) are the primary cells responsible for producing IFN-α against viruses. Lin et al ( 2020 ) found that after RV stimulation, interferon-α production by pDCs was significantly increased in normal subjects but not in asthmatic patients. This provides further evidence of a defective innate response to RV infection in asthmatic patients.…”

Section: The Role Of Gut Microbial Changes Caused By Respiratory Infe...mentioning

confidence: 99%

The role of gut microbiome in the complex relationship between respiratory tract infection and asthma

Xin

Zhou

et al. 2023

Front. Microbiol.

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Asthma is one of the common chronic respiratory diseases in children, which poses a serious threat to children's quality of life. Respiratory infection is a risk factor for asthma. Compared with healthy children, children with early respiratory infections have a higher risk of asthma and an increased chance of developing severe asthma. Many clinical studies have confirmed the correlation between respiratory infections and the pathogenesis of asthma, but the underlying mechanism is still unclear. The gut microbiome is an important part of maintaining the body's immune homeostasis. The imbalance of the gut microbiome can affect the lung immune function, and then affect lung health and cause respiratory diseases. A large number of evidence supports that there is a bidirectional regulation between intestinal flora and respiratory tract infection, and both are significantly related to the development of asthma. The changes of intestinal microbial components and their metabolites in respiratory tract infection may affect the occurrence and development of asthma through the immune pathway. By summarizing the latest advancements in research, this review aims to elucidate the intricate connection between respiratory tract infections and the progression of asthma by highlighting its bridging role of the gut microbiome. Furthermore, it offers novel perspectives and ideas for future investigations into the mechanisms that underlie the relationship between respiratory tract infections and asthma.

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Impaired interferon‐α expression in plasmacytoid dendritic cells in asthma

Cited by 5 publications

References 49 publications

Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions

Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions

Mechanism of Rhinovirus Immunity and Asthma

The role of gut microbiome in the complex relationship between respiratory tract infection and asthma

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