Down-Regulation of Tumor Necrosis Factor-Associated Factor 6 Is Associated with Progression of Acute Pancreatitis Complicating Lung Injury in Mice

Zhou, Xiangyu; Li, Yuan; Ding, Jiong; Wang, Rong; Zhou, Bing; Gu, Jun; Sun, Xiaodong; Zhou, Zong-Guang

doi:10.1620/tjem.217.279

Cited by 11 publications

(12 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The acute pancreatitis mouse model was induced as previously described [18]. In brief, the acute pancreatitis was induced by an intra-peritoneal injection of cerulein (Sigma, MO) at a dose of 50 µg/kg body weight at hourly intervals for 7 times; timing was made after the last injection, and sampling was made at the 0, 8th, 16th, and 24th hour.…”

Section: Methodsmentioning

confidence: 99%

Autocrine Sonic Hedgehog Attenuates Inflammation in Cerulein-Induced Acute Pancreatitis in Mice via Upregulation of IL-10

et al. 2012

Self Cite

View full text Add to dashboard Cite

Hedgehog signaling plays critical roles in pancreatic oncogenesis and chronic pancreatitis, but its roles in acute pancreatitis (AP) are largely ambiguous. In this study, we provide evidence that Sonic hedgehog (Shh), but neither Desert hedgehog (Dhh) nor Indian hedgehog (Ihh), is the main protein whose expression is activated during the development of cerulein-induced acute pancreatitis in mice, and the Shh serves as an anti-inflammation factor in an autocrine manner. Blocking autocrine Shh signaling with anti-Shh neutralizing antibody aggravates the progression of acute pancreatitis. Mechanistic insight into Shh signaling activation in acute pancreatitis indicates that inflammatory stimulation activates Shh expression and secretion, and subsequently upregulates the expression and secretion of interleukin-10 (IL-10). Moreover, inhibition of Shh signaling with neutralizing antibody abolishes IL-10 production in vivo and in vitro. Molecular biological studies show that autocrine Shh signaling activates the key transcriptional factor Gli1 so that the target gene IL-10 is upregulated, leading to the protective and anti-inflammatory functions in the mouse model of acute pancreatitis. Thus, this study suggests autocrine Shh signaling functions as a protective signaling in the progression of acute pancreatitis.

show abstract

Section: Methodsmentioning

confidence: 99%

Autocrine Sonic Hedgehog Attenuates Inflammation in Cerulein-Induced Acute Pancreatitis in Mice via Upregulation of IL-10

et al. 2012

Self Cite

View full text Add to dashboard Cite

show abstract

“…TNF-α activates neutrophils that cause lung inflammation and dysfunction to other distal organs [43]. Down-regulation of TNF-associated factor 6 (TRAF-6) is associated with progression of acute pancreatitis complicating lung injury in mice [13]. IL-1β is also believed to play a role in the pathogenesis of pancreatitis associated lung inflammation.…”

Section: Cytokines and Chemokinesmentioning

confidence: 99%

“…Phase (II) is a fibroproliferative phase that is mainly characterized by repair of lung, type II pneumocyte hyperplasia, and proliferation of lung fibroblasts [2,11,12]. The molecular mechanisms of ALI and ARDS is still not well explored, but available reports indicate the involvement of several pro-inflammatory mediators including cytokines (TNF-α, IL-1β, IL-6) [2,13,14] and chemokines [like interleukin-8 (IL-8) and macrophage inhibitory factor (MIF)] [2,15]as well as macrophage polarization regulating the migration and pulmonary infiltration of neutrophils into the pulmonary interstitial tissue, causing injury to the pulmonary parenchyma [16]. A summarized mechanistic possible pathway involved in ALI is shown as a diagrammatic representation in Figure 1.…”

Section: Introductionmentioning

confidence: 99%

Chronic Pancreatitis Associated Acute Respiratory Failure

Anil¹

2017

MOJI

View full text Add to dashboard Cite

“…Phase (II) is a fibro-proliferative phase that is mainly characterized by repair of lung, type II pneumocyte hyperplasia, and proliferation of lung fibroblasts [2,11,12]. The molecular mechanisms of ALI and ARDS is still not well explored, but available reports indicate the involvement of several pro-inflammatory mediators including cytokines (TNF-α, IL-1β, IL-6) [2,13,14] and chemokines [like interleukin-8 (IL-8) and macrophage inhibitory factor (MIF)] [2,15]as well as macrophage polarization regulating the migration and pulmonary infiltration of neutrophils into the pulmonary interstitial tissue, causing injury to the pulmonary parenchyma [16]. A summarized mechanistic possible pathway involved in ALI is shown as a diagrammatic representation in Figure 1.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic Pancreatitis Associated Acute Respiratory Failure

Manohar

Verma

Venkateshaiah

et al. 2017

MOJI

View full text Add to dashboard Cite

Pancreatitis is a condition characterized by parenchymal inflammation of the pancreas, which is often associated with lung injury due to low level of oxygen and the condition is termed as acute pancreatitis-associated lung injury (APALI). Clinical reports indicated that ~ 20% to 50% of patients from low oxygen levels in blood with acute respiratory distress syndrome (ARDS). ARDS is a severe form of acute lung injury (ALI), a pulmonary disease with impaired airflow making patients difficult to breathe. ALI is frequently observed in patients with severe acute pancreatitis. Approximately one third of severe pancreatitis patients develop acute lung injury and acute respiratory distress syndrome that account for 60% of all deaths within the first week. The major causes of ALI and ARDS are sepsis, trauma, aspiration, multiple blood transfusion, and most importantly acute pancreatitis. The molecular mechanisms of ALI and ARDS are still not well explored, but available reports indicate the involvement of several pro-inflammatory mediators including cytokines (TNF-α, IL-1β, IL-6) and chemokines [like interleukin-8 (IL-8) and macrophage inhibitory factor (MIF)], as well as macrophage polarization regulating the migration and pulmonary infiltration of neutrophils into the pulmonary interstitial tissue, causing injury to the pulmonary parenchyma. Acute lung injury and acute respiratory distress syndrome in acute pancreatitis remains an unsolved issue and needs more research and resources to develop effective treatments and therapies. However, recent efforts have tested several molecules in an experimental model and showed promising results as a treatment option. The current review summarized the mechanism that is operational in pancreatitis-associated acute respiratory failure and respiratory distress syndrome in patients and current treatment options.

show abstract

Down-Regulation of Tumor Necrosis Factor-Associated Factor 6 Is Associated with Progression of Acute Pancreatitis Complicating Lung Injury in Mice

Cited by 11 publications

References 28 publications

Autocrine Sonic Hedgehog Attenuates Inflammation in Cerulein-Induced Acute Pancreatitis in Mice via Upregulation of IL-10

Autocrine Sonic Hedgehog Attenuates Inflammation in Cerulein-Induced Acute Pancreatitis in Mice via Upregulation of IL-10

Chronic Pancreatitis Associated Acute Respiratory Failure

Chronic Pancreatitis Associated Acute Respiratory Failure

Contact Info

Product

Resources

About