Faculty Opinions recommendation of Platelets orchestrate the resolution of pulmonary inflammation in mice by T reg cell repositioning and macrophage education.

Sepsis is the syndrome of systemic inflammatory response caused by infection. Over 20 million people worldwide suffer from sepsis each year, of whom about 6 million die, with a case-fatality rate of more than 25%. Therefore, to develop a rational plan for the management of sepsis, there is an urgent need to understand the mechanism of pathogenesis. Sesamin is a kind of sesame lignin isolated from sesame that exhibits multiple biological functions including antiviral, antidyslipidemic, and antihypertensive to name a few. An antioxidant and anti-inflammatory activity of sesamin appears to be a common denominator in all of its biologic activities. However, the mechanism of sesamin on septic-induced acute pulmonary inflammation still needs further study. Herein, we have established a sepsis model of C57BL/6 mice by cecal ligation and perforation. Using this model, we have shown that sesamin could reduce the levels of several inflammatory factors as well as oxidative stress response. Furthermore, sesamin could repress NLRP3 inflammasome and activate Nrf2/HO-1 pathway, and further inhibit acute pulmonary inflammation. This study reveals the mechanism of the diminution of septic-induced acute pulmonary inflammation by sesamin. This opens a theoretical basis for the development of drugs for treatment of sepsis.

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PROTECTIVE ROLE OF CORTISTATIN IN PULMONARY INFLAMMATION AND FIBROSIS

British Journal of Pharmacology ◽

10.1111/bph.15615 ◽

2021 ◽

Author(s):

Margarita Barriga ◽

Raquel Benitez ◽

Viviane Ferraz‐de‐Paula ◽

Marina Garcia‐Frutos ◽

Marta Caro ◽

...

Keyword(s):

Pulmonary Inflammation ◽

Protective Role

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Selective deletion of SHIP-1 in hematopoietic cells in mice leads to severe lung inflammation involving ILC2 cells

Scientific Reports ◽

10.1038/s41598-021-88677-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Xujun Ye ◽

Fengrui Zhang ◽

Li Zhou ◽

Yadong Wei ◽

Li Zhang ◽

...

Keyword(s):

Lung Inflammation ◽

Airway Remodeling ◽

Pulmonary Inflammation ◽

Hematopoietic Cells ◽

Cell Lineage ◽

Allergic Inflammation ◽

Cell Types ◽

Lymphoid Cells ◽

Whole Body

AbstractSrc homology 2 domain–containing inositol 5-phosphatase 1 (SHIP-1) regulates the intracellular levels of phosphotidylinositol-3, 4, 5-trisphosphate, a phosphoinositide 3–kinase (PI3K) product. Emerging evidence suggests that the PI3K pathway is involved in allergic inflammation in the lung. Germline or induced whole-body deletion of SHIP-1 in mice led to spontaneous type 2-dominated pulmonary inflammation, demonstrating that SHIP-1 is essential for lung homeostasis. However, the mechanisms by which SHIP-1 regulates lung inflammation and the responsible cell types are still unclear. Deletion of SHIP-1 selectively in B cells, T cells, dendritic cells (DC) or macrophages did not lead to spontaneous allergic inflammation in mice, suggesting that innate immune cells, particularly group 2 innate lymphoid cells (ILC2 cells) may play an important role in this process. We tested this idea using mice with deletion of SHIP-1 in the hematopoietic cell lineage and examined the changes in ILC2 cells. Conditional deletion of SHIP-1 in hematopoietic cells in Tek-Cre/SHIP-1 mice resulted in spontaneous pulmonary inflammation with features of type 2 immune responses and airway remodeling like those seen in mice with global deletion of SHIP-1. Furthermore, when compared to wild-type control mice, Tek-Cre/SHIP-1 mice displayed a significant increase in the number of IL-5/IL-13 producing ILC2 cells in the lung at baseline and after stimulation by allergen Papain. These findings provide some hints that PI3K signaling may play a role in ILC2 cell development at baseline and in response to allergen stimulation. SHIP-1 is required for maintaining lung homeostasis potentially by restraining ILC2 cells and type 2 inflammation.

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