The IL-33 Receptor ST2 Regulates Pulmonary Inflammation and Fibrosis to Bleomycin

Fanny, Manoussa; Nascimento, Mégane; Baron, Ludivine; Schricke, Corinne; Maillet, Isabelle; Akbal, Myriam; Riteau, Nicolas; Bert, Marc; Quesniaux, Valérie; Ryffel, Bernhard; Gombault, Aurélie; Même, Sandra; Même, William; Couillin, Isabelle

doi:10.3389/fimmu.2018.01476

Cited by 34 publications

(27 citation statements)

References 36 publications

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“…23 IL-33 has been declared to be associated with disease severity in allergic and pulmonary inflammation including asthma. 6,[9][10][11]24 Increased IL-33 levels have been suggested to be associated with airway and systemic inflammation in COPD, in addition to the pathogenesis and progression of COPD. 7 Postnatal immune maturation and lung development in the process of BPD are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

A Novel Diagnostic Marker for the Severity of Bronchopulmonary Dysplasia in Very Low Birth Weight Infants: Interleukin-33

Çakır

Tayman

Yücel

2019

Pediatric Allergy, Immunology, and Pulmonology

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Background: Bronchopulmonary dysplasia (BPD) is an important clinical problem for premature infants. Previously, some biomarkers associated with severity of BPD have been studied. In our study, we aimed to investigate the value of interleukin-33 (IL-33) levels as a new biomarker in the follow-up of BPD severity and response to treatment. Materials and Methods: Premature infants of <32 weeks of gestational age and birth weight <1,500 g were included in the study. Infants with BPD were divided into moderate and severe BPD groups. Infants without BPD were assigned as the control group. Cord blood samples were taken from both groups immediately after birth. In addition, blood samples were obtained at the time of diagnosis of BPD and after the end of hydrocortisone (HC) treatment to measure IL-33 values in the serum. Results: During the study period, a total of 192 infants were eligible: 96 infants in the BPD group and 96 in the control group. Cord IL-33 values were similar between control (1.29-0.68 pg/mL) and BPD (moderate/severe) (1.31-0.84 pg/mL) groups (P = 0.813). The levels of IL-33 were higher in BPD group (3.43-0.98 pg/mL) than in the control group (0.98-0.51 pg/mL) (P < 0.001). IL-33 values decreased significantly after HC treatment (pretreatment: 3.43-0.98 pg/mL versus post-treatment: 2.97-0.28 pg/mL) (P < 0.001). In addition, IL-33 levels were significantly higher in severe BPD (3.91-1.22 pg/mL) than in moderate BPD (2.82-0.74) group (P < 0.001). Conclusions: Although the IL-33 level was not predictive of the development of BPD immediately after birth, it may be used as a new biomarker to diagnose, monitor, and follow the response to treatment of BPD.

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Section: Discussionmentioning

confidence: 99%

A Novel Diagnostic Marker for the Severity of Bronchopulmonary Dysplasia in Very Low Birth Weight Infants: Interleukin-33

Çakır

Tayman

Yücel

2019

Pediatric Allergy, Immunology, and Pulmonology

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“…IL-33 is dependent on ST2 for MCD diet-induced liver fibrogenesis (120). In addition, IL-33/ST2 is also involved in BLM and E. coli-induced fibrogenesis (121). In BLM-induced fibrogenesis, IL-33/ST2 through B7 homology 3 (B7H3), polarizes bone marrow (BM) cells to M2 cells, secreting IL-13 and TGF-b (122,123).…”

Section: Il-33 In Fibrosismentioning

confidence: 99%

Inflammasomes and Fibrosis

et al. 2021

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Fibrosis is the final common pathway of inflammatory diseases in various organs. The inflammasomes play an important role in the progression of fibrosis as innate immune receptors. There are four main members of the inflammasomes, such as NOD-like receptor protein 1 (NLRP1), NOD-like receptor protein 3 (NLRP3), NOD-like receptor C4 (NLRC4), and absent in melanoma 2 (AIM2), among which NLRP3 inflammasome is the most studied. NLRP3 inflammasome is typically composed of NLRP3, ASC and pro-caspase-1. The activation of inflammasome involves both “classical” and “non-classical” pathways and the former pathway is better understood. The “classical” activation pathway of inflammasome is that the backbone protein is activated by endogenous/exogenous stimulation, leading to inflammasome assembly. After the formation of “classic” inflammasome, pro-caspase-1 could self-activate. Caspase-1 cleaves cytokine precursors into mature cytokines, which are secreted extracellularly. At present, the “non-classical” activation pathway of inflammasome has not formed a unified model for activation process. This article reviews the role of NLRP1, NLRP3, NLRC4, AIM2 inflammasome, Caspase-1, IL-1β, IL-18 and IL-33 in the fibrogenesis.

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“…IL-33 and IL-25 levels are elevated in bronchoalveolar lavage fluid (BALF) samples of IPF patients, which is mirrored by an increase in ILC2s in both BALF and lung tissue [77,78]. The IL-33/ST2 axis in the context of ILC2s is further implicated in several studies that explore a bleomycin-induced mouse model of IPF [78][79][80]. ST2-deficient mice show decreased lung inflammation and attenuated fibrosis in response to bleomycin treatment both in the case of systemic ST2 gene inactivation as well as more selective ST2 gene inactivation in hematopoietic cells.…”

Section: Lung Fibrosismentioning

confidence: 99%

Group 2 Innate Lymphoid Cells: Central Players in a Recurring Theme of Repair and Regeneration

Messing

Jan-Abu

McNagny

2020

IJMS

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Innate lymphoid cells (ILCs) are recently discovered innate counterparts to the well-established T helper cell subsets and are most abundant at barrier surfaces, where they participate in tissue homeostasis and inflammatory responses against invading pathogens. Group 2 innate lymphoid cells (ILC2s) share cytokine and transcription factor expression profiles with type-2 helper T cells and are primarily associated with immune responses against allergens and helminth infections. Emerging data, however, suggests that ILC2s are also key regulators in other inflammatory settings; both in a beneficial context, such as the establishment of neonatal immunity, tissue repair, and homeostasis, and in the context of pathological tissue damage and disease, such as fibrosis development. This review focuses on the interactions of ILC2s with stromal cells, eosinophils, macrophages, and T regulatory cells that are common to the different settings in which type-2 immunity has been explored. We further discuss how an understanding of these interactions can reveal new avenues of therapeutic tissue regeneration, where the role of ILC2s is yet to be fully established.

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The IL-33 Receptor ST2 Regulates Pulmonary Inflammation and Fibrosis to Bleomycin

Cited by 34 publications

References 36 publications

A Novel Diagnostic Marker for the Severity of Bronchopulmonary Dysplasia in Very Low Birth Weight Infants: Interleukin-33

A Novel Diagnostic Marker for the Severity of Bronchopulmonary Dysplasia in Very Low Birth Weight Infants: Interleukin-33

Inflammasomes and Fibrosis

Group 2 Innate Lymphoid Cells: Central Players in a Recurring Theme of Repair and Regeneration

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