Acute Lung Injury
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Acute Lung Injury : IL-17A-Mediated Inflammatory Pathway and Its Regulation by Curcumin. / Gouda, Mahesh Manjunath; Bhandary, Yashodhar Prabhakar.
in: INFLAMMATION, Jahrgang 42, Nr. 4, 08.2019, S. 1160-1169.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - Acute Lung Injury
T2 - IL-17A-Mediated Inflammatory Pathway and Its Regulation by Curcumin
AU - Gouda, Mahesh Manjunath
AU - Bhandary, Yashodhar Prabhakar
PY - 2019/8
Y1 - 2019/8
N2 - Acute lung injury (ALI) is characterized by acute inflammation and tissue injury results in dysfunction of the alveolar epithelial membrane. If the epithelial injury is severe, a fibroproliferative phase of ALI can develop. During this phase, the activated fibroblast and myofibroblasts synthesize excessive collagenous extracellular matrix that leads to a condition called pulmonary fibrosis. Lung injury can be caused by several ways; however, the present review focus on bleomycin (BLM)-mediated changes in the pathology of lungs. BLM is a chemotherapeutic agent and has toxic effects on lungs, which leads to oxidative damage and elaboration of inflammatory cytokines. In response to the injury, the inflammatory cytokines will be activated to defend the system from injury. These cytokines along with growth factors stimulate the proliferation of myofibroblasts and secretion of pathologic extracellular matrix. During BLM injury, the pro-inflammatory cytokine such as IL-17A will be up-regulated and mediates the inflammation in the alveolar epithelial cell and also brings about recruitment of certain inflammatory cells in the alveolar surface. These cytokines probably help in up-regulating the expression of p53 and fibrinolytic system molecules during the alveolar epithelial cells apoptosis. Here, our key concern is to provide the adequate knowledge about IL-17A-mediated p53 fibrinolytic system and their pathogenic progression to pulmonary fibrosis. The present review focuses mainly on IL-17A-mediated p53-fibrinolytic aspects and how curcumin is involved in the regulation of pathogenic progression of ALI and pulmonary fibrosis.
AB - Acute lung injury (ALI) is characterized by acute inflammation and tissue injury results in dysfunction of the alveolar epithelial membrane. If the epithelial injury is severe, a fibroproliferative phase of ALI can develop. During this phase, the activated fibroblast and myofibroblasts synthesize excessive collagenous extracellular matrix that leads to a condition called pulmonary fibrosis. Lung injury can be caused by several ways; however, the present review focus on bleomycin (BLM)-mediated changes in the pathology of lungs. BLM is a chemotherapeutic agent and has toxic effects on lungs, which leads to oxidative damage and elaboration of inflammatory cytokines. In response to the injury, the inflammatory cytokines will be activated to defend the system from injury. These cytokines along with growth factors stimulate the proliferation of myofibroblasts and secretion of pathologic extracellular matrix. During BLM injury, the pro-inflammatory cytokine such as IL-17A will be up-regulated and mediates the inflammation in the alveolar epithelial cell and also brings about recruitment of certain inflammatory cells in the alveolar surface. These cytokines probably help in up-regulating the expression of p53 and fibrinolytic system molecules during the alveolar epithelial cells apoptosis. Here, our key concern is to provide the adequate knowledge about IL-17A-mediated p53 fibrinolytic system and their pathogenic progression to pulmonary fibrosis. The present review focuses mainly on IL-17A-mediated p53-fibrinolytic aspects and how curcumin is involved in the regulation of pathogenic progression of ALI and pulmonary fibrosis.
KW - Acute Lung Injury/chemically induced
KW - Alveolar Epithelial Cells/pathology
KW - Animals
KW - Bleomycin/pharmacology
KW - Curcumin/pharmacology
KW - Humans
KW - Inflammation/metabolism
KW - Interleukin-17/metabolism
KW - Pulmonary Fibrosis/etiology
KW - Tumor Suppressor Protein p53/metabolism
U2 - 10.1007/s10753-019-01010-4
DO - 10.1007/s10753-019-01010-4
M3 - SCORING: Review article
C2 - 31011925
VL - 42
SP - 1160
EP - 1169
JO - INFLAMMATION
JF - INFLAMMATION
SN - 0360-3997
IS - 4
ER -