Effects of anti-IL17 on acute lung injury induced by LPS in mice

Righetti, Renato Fraga; Santos, Tabata Maruyama Dos; Camargo, Leandro do Nascimento; Aristóteles, Luciana Ritha de Cássia Rolim Barbosa; Fukuzaki, Silvia; Souza, Flávia Castro Ribas de; Cruz, Maysa Mariana; Alonso-Vale, Maria Isabel Cardoso; Saraiva-Romanholo, Beatriz Mangueira; Leick, Edna Aparecida; Martins, Mílton de Arruda; Prado, Carla M.; Tibério, Iolanda de Fátima Lopes Calvo

doi:10.1183/1393003.congress-2017.pa346

Cited by 2 publications

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“…As discussed earlier, the crucial role of IL-17A is to trigger the inflammatory response against the cellular damage [6,20]. The elevated expression of IL-17A also indicates the severe progression of injury to the fibro-proliferative phase of the disease [6].…”

Section: Il-17a Mediated Changes During Acute Lung Injury and Progres...mentioning

confidence: 89%

IL-17A Mediated Downstream Changes During Acute Lung Injury

Gouda¹,

Bhandary²

2018

Biochem Mol biol J

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Acute lung injury is the severe health issue characterized by inflammation in the airways results in the alteration of alveolar architecture. The inflammatory phase usually mediated by the neutrophil accumulation, migration of macrophages, alveolar infiltration and cytokines activation. IL-17A is a class of pro-inflammatory cytokines elevated during the initial phase of injury. IL-17A mediation could alter various pathways such as, alveolar epithelial cells (AECs) apoptosis, chemokines enhancement and excitation as well as other proliferatory pathways. IL-17A mediated activation of chemokines expression is one of the key phenomenon promotes the inflammatory process. IL-17A mediated downstream modulation leads to the severe form of injury, which causes the significant loss of AECs. The severe loss of AECs stimulates the conversion of fibroblasts to myofibroblasts and deposition of extracellular matrix (ECM). The excess deposition of ECM at the alveolar epithelial barrier causes the thickening of alveolar epithelium and results in the progression of lethal, irreversible disease called pulmonary fibrosis.

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Section: Il-17a Mediated Changes During Acute Lung Injury and Progres...mentioning

confidence: 89%

IL-17A Mediated Downstream Changes During Acute Lung Injury

Gouda¹,

Bhandary²

2018

Biochem Mol biol J

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“…In the mouse model of myocardial ischemiareperfusion injury, IL-17A was mainly produced by gd T cells, and blockade of IL-17A significantly reduced neutrophil infiltration in the heart and alleviated cardiac injury (11,12). Moreover, anti-IL-17A could protect the lungs in lipopolysaccharide (LPS)-induced acute lung injury and improve survival in polymicrobial sepsis induced by cecal ligation and puncture (CLP) (13)(14)(15). However, the role of IL-17A in sepsis-induced cardiac dysfunction is not clear.…”

Section: Introductionmentioning

confidence: 99%

γδ T/Interleukin-17A Contributes to the Effect of Maresin Conjugates in Tissue Regeneration 1 on Lipopolysaccharide-Induced Cardiac Injury

Yang¹,

Li²,

Li³

et al. 2021

Front. Immunol.

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The mechanisms underlying sepsis-induced cardiomyopathy (SIC) remain poorly understood, and there are no specific therapeutics for SIC. We investigated the effects of maresin conjugates in tissue regeneration 1 (MCTR1) on SIC and explored its potential mechanisms. The experiments were conducted using an endotoxemia model induced by lipopolysaccharide (LPS). Mice were given MCTR1 intravenously 6 h after LPS stimulation. Echocardiography was performed to assess cardiac function 12 h after LPS administration. Treatment with MCTR1 significantly enhanced cardiac function and reduced LPS-induced increase of mRNA expression levels of inflammation cytokines. Transcriptomic analysis indicated that MCTR1 inhibited neutrophil chemotaxis via the IL-17 signaling pathway. We confirmed that MCTR1 reduced the expressions of neutrophil chemoattractants and neutrophil infiltration in the LPS-stimulated hearts. MCTR1 also resulted in a considerable reduction in IL-17A production mainly derived from γδ T cells. Moreover, our results provided the first evidence that neutralizing IL-17A or depletion of γδ T cells markedly decreased neutrophil recruitment and enhanced cardiac function in LPS-induced cardiac injury. These results suggest that MCTR1 alleviates neutrophil infiltration thereby improves cardiac function in LPS-induced cardiac injury via the IL-17 signaling pathway. Thus, MCTR1 represented a novel therapeutic strategy for patients with SIC.

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Effects of anti-IL17 on acute lung injury induced by LPS in mice

Cited by 2 publications

References 0 publications

IL-17A Mediated Downstream Changes During Acute Lung Injury

IL-17A Mediated Downstream Changes During Acute Lung Injury

γδ T/Interleukin-17A Contributes to the Effect of Maresin Conjugates in Tissue Regeneration 1 on Lipopolysaccharide-Induced Cardiac Injury

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