The crucial regulatory role of type I interferon in inflammatory diseases

Ji, Ling; Li, Tianle; Chen, Huimin; Yang, Yanqi; Lu, Eryi; Liu, Jieying; Qiao, Wei; Chen, Hui

doi:10.1186/s13578-023-01188-z

Cited by 7 publications

(4 citation statements)

References 255 publications

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“…However, the IFNA2 USR signature had a negative z-score (Fig. 6b, Anti-viral), suggesting reduced inflammation, with type I IFNs major drivers of inflammation [117]. A reduced type I IFN signature is consistent with the lower viral loads at 2 dpi (Fig.…”

Section: Iron Deficient Vs Control Diet; Lung Rna-seq At 6 Dpimentioning

confidence: 77%

The effects of iron deficient and high iron diets on SARS-CoV-2 lung infection and disease

Carolin,

Frazer,

Yan

et al. 2024

Preprint

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The severity of Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is often dictated by a range of comorbidities. A considerable literature suggests iron deficiency and iron overload may contribute to increased infection, inflammation and disease severity, although direct causal relationships have been difficult to establish. Here we generate iron deficient and iron loaded C57BL/6J mice by feeding low and high iron diets, with mice on a normal iron diet representing controls. All mice were infected with a primary omicron XXB SARS-CoV-2 isolate and lung inflammatory responses were analyzed by histology, immunohistochemistry and RNA-Seq. Compared with controls, iron deficient mice showed no significant changes in lung viral loads or histopathology, whereas, iron loaded mice showed slightly, but significantly, reduced lung viral loads and histopathology. Transcriptional changes were modest, but illustrated widespread dysregulation of inflammation signatures for both iron deficient vs. controls, and iron loaded vs. controls. Some of these changes could be associated with detrimental outcomes, whereas others would be viewed as beneficial. Diet-associated iron deficiency or overload thus induced modest modulations of inflammatory signatures, but no significant histopathologically detectable disease exacerbations.Author summaryA diet deficient in iron can lead to anemia, a widespread problem worldwide. A diet with excessive iron is less common, but can be associated with excessive consumption of iron supplements. We investigate herein using a mouse model, whether low or high iron diets predispose to detrimental outcomes in the lungs after infection with SARS-CoV-2. A considerable literature suggests iron dysregulation would promote infection and inflammation. However, we found, although inflammatory responses showed modest modulations, viral loads were unaffected or slightly reduced, and lung histopathology was either unaffected or indicated slightly less severe disease. These findings do not support a view that low or high iron diets represent comorbidities predisposing to overt detrimental outcomes for acute COVID-19 lung disease.

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Section: Iron Deficient Vs Control Diet; Lung Rna-seq At 6 Dpimentioning

confidence: 77%

The effects of iron deficient and high iron diets on SARS-CoV-2 lung infection and disease

Carolin,

Frazer,

Yan

et al. 2024

Preprint

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“…The HER2 high group exhibited six unique pathways, including EGF, WNT, EDA, AGT, PMCH, and BRADYKININ. Notably, the common pathways between the HER2 low and negative groups were LIFR, IL10, IFN-I, ENHO, CALCR, which are inflammation-relevant factors 67 , underscoring shared inflammation features in these groups. There is no shared pathway among all three HER2 groups ( Figure 6B ).…”

Section: Resultsmentioning

confidence: 93%

HER2 Prognostic Significance and Therapeutic Implications in Gastric Cardia Adenocarcinoma: Insights from Multi-Omics Profiling

Wang,

Xing,

Zhao

et al. 2024

Preprint

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Therapeutic targets for Gastric Cardia Adenocarcinoma (GCA), particularly for HER2-negative patients, are lacking. Here, we conducted multi-omics profiling on 128 GCA patients using mass spectrometry, whole-exome sequencing, RNA-Seq, and metabolomics. We found HER2 to be a favorable prognostic marker for GCA. Employing molecular counting, we categorized patients into HER2-high, -low, and -negative groups. We uncovered an enrichment of DNA repair features in the HER2-high group, while HER2-low and -negative groups exhibited strong inflammation. We found that tumor mutation burden may not be the distinguishing factor among these three groups. We revealed that the HER2-negative and -low groups have a tumor-suppressive immune microenvironment, and HER2 expression is associated with fatty acid metabolic profiles and inflammation in the blood of patients. Our study revealed anti-inflammatory and immune checkpoint inhibition, targeting PD-L2 and the CD47/SIRPA pair, as therapeutic strategies for HER2-negative GCA patients. These findings highlight promising avenues for personalized treatment for GCA.

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“…A variety of immune cells in the body, such as macrophages and dendritic cells (DCs), could produce IFN-α in response to pathogen stimulation of pattern recognition receptors (PRRs). 51 Dysregulated IFN-α signaling could cause inflammatory diseases, including autoimmune diseases and chronic infections. 52 , 53 In autoimmune diseases, IFN-α may exert anti-inflammatory effects by inhibiting neutrophil recruitment and reducing the release of reactive oxygen species (ROS) and proteases.…”

Section: Discussionmentioning

confidence: 99%

Construction of a Multi-Indicator Model for Abscess Prediction in Granulomatous Lobular Mastitis Using Inflammatory Indicators

Du,

Feng,

Shao

et al. 2024

JIR

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Background Granulomatous lobular mastitis (GLM) is a chronic inflammatory breast disease, and abscess formation is a common complication of GLM. The process of abscess formation is accompanied by changes in multiple inflammatory markers. The present study aimed to construct a diagnosis model for the early of GLM abscess formation based on multiple inflammatory parameters. Methods Based on the presence or absence of abscess formation on breast magnetic resonance imaging (MRI), 126 patients with GLM were categorised into an abscess group (85 patients) and a non-abscess group (41 patients). Demographic characteristics and the related laboratory results for the 9 inflammatory markers were collected. Logistics univariate analysis and collinearity test were used for selecting independent variables. A regression model to predict abscess formation was constructed using Logistics multivariate analysis. Results The univariate and multivariate analysis showed that the N, ESR, IL-4, IL-10 and INF-α were independent diagnostic factors of abscess formation in GLM ( P <0. 05). The nomogram was drawn on the basis of the logistics regression model. The area under the curve (AUC) of the model was 0.890, which was significantly better than that of a single indicator and the sensitivity and specificity of the model were high (81.2% and 85.40%, respectively). These results predicted by the model were highly consistent with the actual diagnostic results. The results of this calibration curve indicated that the model had a good value and stability in predicting abscess formation in GLM. The decision curve analysis (DCA) demonstrated a satisfactory positive net benefit of the model. Conclusion A predictive model for abscess formation in GLM based on inflammatory markers was constructed in our study, which may provide a new strategy for early diagnosis and treatment of the abscess stage of GLM.

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The crucial regulatory role of type I interferon in inflammatory diseases

Cited by 7 publications

References 255 publications

The effects of iron deficient and high iron diets on SARS-CoV-2 lung infection and disease

The effects of iron deficient and high iron diets on SARS-CoV-2 lung infection and disease

HER2 Prognostic Significance and Therapeutic Implications in Gastric Cardia Adenocarcinoma: Insights from Multi-Omics Profiling

Construction of a Multi-Indicator Model for Abscess Prediction in Granulomatous Lobular Mastitis Using Inflammatory Indicators

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