Role of arginase 1 in lung protective immunity against Streptococcus pneumoniae infection in mice

Knippenberg, Sarah; Brumshagen, Christina; Aschenbrenner, Franziska; Welte, Tobias; Maus, UA

doi:10.1055/s-0035-1548634

Cited by 3 publications

(5 citation statements)

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“…It has been demonstrated that increased arginase activity may contribute to allergen-induced airway remodeling, inflammation and hyperresponsiveness in asthma (41). The expression of arginase was strongly induced by Th2 cytokines (37,41,42). Associated with the enhanced Th2 response in OVA-immunized mice in this study, the Arg1 expression was significantly elevated in the lung, which was consistent with previous findings (41,43).…”

Section: Discussionsupporting

confidence: 91%

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Pidotimod exacerbates allergic pulmonary infection in an OVA mouse model of asthma

et al. 2017

Molecular Medicine Reports

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Pidotimod is a synthetic dipeptide with biological and immuno‑modulatory properties. It has been widely used for treatment and prevention of recurrent respiratory infections. However, its impact on the regulation of allergic pulmonary inflammation is still not clear. In the current study, an ovalbumin (OVA)‑induced allergic asthma model was used to investigate the immune‑modulating effects of pidotimod on airway eosinophilia, mucus metaplasia and inflammatory factor expression compared with dexamethasone (positive control). The authors determined that treatment with pidotimod exacerbated pulmonary inflammation as demonstrated by significantly increased eosinophil infiltration, dramatically elevated immunoglobulin E production, and enhanced T helper 2 response. Moreover, treatment failed to attenuate mucus production in lung tissue, and did not reduce OVA‑induced high levels of FIZZ1 and Arg1 expression in asthmatic mice. In contrast, administration of dexamethasone was efficient in alleviating allergic airway inflammation in OVA‑induced asthmatic mice. These data indicated that pidotimod as an immunotherapeutic agent should be used cautiously and the effectiveness for controlling allergic asthma needs further evaluation and research.

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Section: Discussionsupporting

confidence: 91%

“…Arg1, which hydrolyses L-arginine into ornithine and urea, has been identified as a key player in the pathophysiology of asthma (37,38). An enhanced level of arginase has been observed in airways and lung tissue obtained from animal models of allergic asthma (39) and from patients (40).…”

Section: Discussionmentioning

confidence: 99%

Pidotimod exacerbates allergic pulmonary infection in an OVA mouse model of asthma

et al. 2017

Molecular Medicine Reports

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“…Moreover, arginase I expression, more than arginase II, was induced in Th2 cytokine-mediated lung inflammation and allergen-challenged lungs in mice [82][83][84]. It has also been demonstrated that, in bronchoalveolar lavage from asthmatics and in airway epithelium obtained from bronchial biopsies, inflammatory cells show increased mRNA and protein expression of arginase I [83][84][85]. Therefore, it seems particularly interesting that the extracts from L. sibiricus roots in the present study significantly reduced the expression of arginase increased by HRV16.…”

Section: Discussionmentioning

confidence: 99%

“…It has recently been reported that arginine metabolism controls neutrophilic and eosinophilic pathways which regulate inflammation severity [81]. Moreover, arginase I expression, more than arginase II, was induced in Th2 cytokine‐mediated lung inflammation and allergen‐challenged lungs in mice [82–84]. It has also been demonstrated that, in bronchoalveolar lavage from asthmatics and in airway epithelium obtained from bronchial biopsies, inflammatory cells show increased mRNA and protein expression of arginase I [83–85].…”

Section: Discussionmentioning

confidence: 99%

Leonurus sibiricus root extracts decrease airway remodeling markers expression in fibroblasts

Wieczfińska

Sitarek

Kowalczyk

et al. 2020

Clinical and Experimental Immunology

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Airway remodeling is a complex process, and controlling it appears to be a key for halting the progression of asthma and other obstructive lung diseases. The aim of this study was to evaluate the anti‐remodeling properties of extracts from transformed and transgenic L. sibiricus roots with overexpression of AtPAP1 transcriptional factor. Our study shows for the first time that transformed AtPAP1 TR extract from L. sibiricus root may affect the remodeling process.

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“…, upper right), and depletion of ILCs has been shown to result in loss of airway epithelial integrity and diminished lung function in mice . Similarly, ILC2s in the lung produce arginase‐1 which stimulates M2 macrophages and is thought to have a regulatory role during allergic inflammation . Taken together, improving our understanding of the links between ILC2s, virus‐induced epithelial injury, and virus‐induced asthma exacerbations may provide novel therapeutic approaches for the treatment of lung inflammation associated with viral infection.…”

Section: Ilc2s In Lung Inflammation Associated With Viral Infectionsmentioning

confidence: 99%

Innate lymphoid cells in asthma: Will they take your breath away?

Kim

Umetsu²

2016

Eur J Immunol

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Asthma is a complex and heterogeneous disease that is characterized by airway hyperreactivity (AHR) and airway inflammation. Although asthma was long thought to be driven by allergen-reactive Th2 cells, it has recently become clear that the pathogenesis of asthma is more complicated and associated with multiple pathways and cell types. A very exciting recent development was the discovery of innate lymphoid cells (ILCs) as key players in the pathogenesis of asthma. ILCs do not express antigen receptors but react promptly to “danger signals” from inflamed tissue and produce an array of cytokines that direct the ensuing immune response. The roles of ILCs may differ in distinct asthma phenotypes. ILC2s may be critical for initiation of adaptive immune responses in inhaled allergen-driven AHR, but may also function independently of adaptive immunity, mediating influenza-induced AHR. ILC2s also contribute to resolution of lung inflammation through their production of amphiregulin. Obesity-induced asthma, is associated with expansion of IL-17A-producing ILC3s in the lungs. Furthermore, ILCs may also contribute to steroid-resistant asthma. Although the precise roles of ILCs in different types of asthma are still under investigation, it is clear that inhibition of ILC function represents a potential target that could provide novel treatments for asthma.

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Role of arginase 1 in lung protective immunity against Streptococcus pneumoniae infection in mice

Cited by 3 publications

References 0 publications

Pidotimod exacerbates allergic pulmonary infection in an OVA mouse model of asthma

Pidotimod exacerbates allergic pulmonary infection in an OVA mouse model of asthma

Leonurus sibiricus root extracts decrease airway remodeling markers expression in fibroblasts

Innate lymphoid cells in asthma: Will they take your breath away?

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