Interleukin-37 Attenuates Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice

Li, Yan; Gao, Qiaoyan; Xu, Keye; Xiao, Peng; Yuan, Xianli; Jiang, Wenwen; Li, Mingcai

doi:10.1007/s10753-018-0820-9

Cited by 20 publications

(9 citation statements)

References 41 publications

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“…More and more data suggested that inflammation involved in the pathogenesis of CAP, promoted the occurrence and development of CAP (27,28). Several inflammatory cytokines were increased and inflammatory signaling pathways were activated in the progress of CAP (17,29). The levels of proinflammatory cytokines were compared between two groups in our research.…”

Section: The Association Between Serum Il-37 and The Prognosis In Cap Patientsmentioning

confidence: 82%

“…In addition, an experimental study in vivo found that IL-37 transgenic mice evoked excessive inflammation and tissue damage in murine pneumococcal pneumonia (16). Moreover, mounting evidences revealed that IL-37 plays a crucial protective role in non-small cell lung cancer, murine allergic asthma, fibrosis, and airway inflammation by alleviating inflammation (17)(18)(19). These results indicated that IL-37 may involve in the pathophysiological process of several pulmonary diseases.…”

Section: Introductionmentioning

confidence: 95%

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The Associations of Serum IL-37 With the Severity and Prognosis in Patients With Community-Acquired Pneumonia: A Retrospective Cohort Study

Wang

Chen

et al. 2021

Front. Immunol.

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BackgroundRecent evidences suggested that IL-37 may participate in the pathophysiology of community-acquired pneumonia (CAP). Nevertheless, its exact biological role was unknown. The objective of this study was to determine the associations of serum IL-37 with the severity and prognosis in CAP patients based on a retrospective cohort study.MethodsThe whole of 120 healthy subjects and 240 CAP patients were summoned. Peripheral blood was collected and IL-37 was detected using ELISA.ResultsSerum IL-37 was obviously decreased in CAP patients on admission. In addition, serum IL-37 was gradually decreased in parallel with CAP severity scores. Correlative analysis revealed that serum IL-37 was negatively associated with CAP severity scores and inflammatory cytokines. Further logistical regression found that reduction of serum IL-37 augmented the severity of CAP patients. Moreover, the follow-up research was performed in CAP patients. Serum lower IL-37 on admission prolonged the hospital stay in CAP patients. Serum IL-37 combination with PSI and CURB-65 had a stronger predictive capacity for death than IL-37 and CAP severity score alone in CAP patients.ConclusionThere are remarkably negative correlations between serum IL-37 with the severity and prognosis in CAP patients. Serum IL-37 on admission prolongs the hospital stay, demonstrating that IL-37 may involve in the process of CAP. Serum IL-37 may be regarded as a biomarker for diagnosis and prognosis for CAP patients.

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Section: The Association Between Serum Il-37 and The Prognosis In Cap Patientsmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 95%

The Associations of Serum IL-37 With the Severity and Prognosis in Patients With Community-Acquired Pneumonia: A Retrospective Cohort Study

Wang

Chen

et al. 2021

Front. Immunol.

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“…Accordingly, we measured lower TGF-β mRNA levels in livers of IL-37tg mice after CCl 4treatment. Li et al also showed that intranasal administration of a lentivirus expressing IL-37 improved survival, attenuated pulmonary inflammation and collagen deposition in bleomycintreated mice (52). In summary, these reports lead us to speculate that, beside limiting the inflammatory response, IL-37 directly impacts HSC-mediated liver fibrogenesis by interacting with TGF-β dependent pathways.…”

Section: Figure 7 |mentioning

confidence: 95%

Modulation of Liver Inflammation and Fibrosis by Interleukin-37

et al. 2021

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Background and Aims: Chronic inflammation induces liver fibrosis, cirrhosis and potentially liver cancer. Kupffer cells modulate hepatic stellate cells by secreting immunologically active proteins as TGF-β. TGF-β promotes liver fibrosis via the activation of Sma- and Mad-related protein 3. IL-37 broadly suppresses innate and adaptive immune responses. Intracellular IL-37 interacts with Smad3. We hypothesize that IL-37 downregulates the activation of hepatic Kupffer and stellate cells and interferes with the TGF-β signaling cascade to modulate liver fibrogenesis.Methods: The role of IL-37 on liver inflammation and fibrogenesis was assessed in three mouse models as well as isolated Kupffer- and stellate cells. Serum IL-37 was tested by ELISA in a clinical cohort and correlated with liver disease severity.Results: Transgene expression of IL-37 in mice extends survival, reduces hepatic damage, expression of early markers of fibrosis and histologically assessed liver fibrosis after bile duct ligation. IL-37tg mice were protected against CCl4-induced liver inflammation. Colitis-associated liver inflammation and fibrosis was less severe in IL-10 knockout IL-37tg mice. Spontaneous and LPS/TGF-β-induced cytokine release and profibrogenic gene expression was lower in HSC and KC isolated from IL-37tg mice and IL-37 overexpressing, IL-1β stimulated human LX-2 stellate cells. However, administration of recombinant human IL-37 did not modulate fibrosis pathways after BDL in mice, LX2 cells or murine HSCs. In a large clinical cohort, we observed a positive correlation of serum IL-37 levels with disease severity in liver cirrhosis.Conclusions: Predominantly intracellular IL-37 downregulates liver inflammation and fibrosis. The correlation of serum IL-37 with disease severity in cirrhosis suggests its potential as a novel target modulating the course of liver fibrosis.

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“…Treatment with the anti-inflammatory cytokine IL-37 attenuated BLM-induced PF by inhibiting collagen deposition and inflammatory infiltration into the lungs. IL-37 treatment reduced MCP-1, IL-6, and TNF-α expression and induced IFN-γ expression in lung tissue [ 89 ].…”

Section: Soluble Immune Modulators In Pulmonary Fibrosismentioning

confidence: 99%

Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis

Hasan

Paul

et al. 2022

Molecules

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Pulmonary fibrosis (PF) is a disease-refractive lung condition with an increased rate of mortality. The potential factors causing PF include viral infections, radiation exposure, and toxic airborne chemicals. Idiopathic PF (IPF) is related to pneumonia affecting the elderly and is characterized by recurring scar formation in the lungs. An impaired wound healing process, defined by the dysregulated aggregation of extracellular matrix components, triggers fibrotic scar formation in the lungs. The potential pathogenesis includes oxidative stress, altered cell signaling, inflammation, etc. Nintedanib and pirfenidone have been approved with a conditional endorsement for the management of IPF. In addition, natural product-based treatment strategies have shown promising results in treating PF. In this study, we reviewed the recently published literature and discussed the potential uses of natural products, classified into three types—isolated active compounds, crude extracts of plants, and traditional medicine, consisting of mixtures of different plant products—in treating PF. These natural products are promising in the treatment of PF via inhibiting inflammation, oxidative stress, and endothelial mesenchymal transition, as well as affecting TGF-β-mediated cell signaling, etc. Based on the current review, we have revealed the signaling mechanisms of PF pathogenesis and the potential opportunities offered by natural product-based medicine in treating PF.

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Interleukin-37 Attenuates Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice

Cited by 20 publications

References 41 publications

The Associations of Serum IL-37 With the Severity and Prognosis in Patients With Community-Acquired Pneumonia: A Retrospective Cohort Study

The Associations of Serum IL-37 With the Severity and Prognosis in Patients With Community-Acquired Pneumonia: A Retrospective Cohort Study

Modulation of Liver Inflammation and Fibrosis by Interleukin-37

Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis

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