Increased expression of the intercellular adhesion molecule-1 (ICAM-1) on peripheral blood neutrophils in acute pancreatitis

Dâbrowski, A; Osada, Joanna; Dąbrowska, Milena; Wereszczyńska-Siemiątkowska, Urszula; Siemiątkowski, Andrzej

doi:10.1016/j.advms.2014.01.001

Cited by 16 publications

(13 citation statements)

References 30 publications

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“…L-selectin was equally elevated in MAP and SAP in a recent study and is thus not a useful marker in this respect 66 . Two different authors drew the same conclusion from similar studies 73,74 .…”

Section: Selectinsmentioning

confidence: 84%

“…A recent study revealed an early and significant increase of peripheral blood neutrophil ICAM-1 expression. It was specific for severe AP on the first day and between the 5th and 10th day after symptom onset, but not between the second and fourth day 66 . Another study in 2012 showed a sensitivity of serum ICAM-1 measurement to separate severe from mild AP of 61%, specificity of 71.42%, PPV of 61% and NPV of 71% within the first 24 h after onset of pain or on admission 67 .…”

Section: Icam-1 and Soluble Icam-1mentioning

confidence: 87%

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Laboratory markers predicting severity of acute pancreatitis

Staubli¹,

Oertli²,

Nebiker³

2015

Critical Reviews in Clinical Laboratory Sciences

190

122

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Acute pancreatitis (AP) is an inflammatory disease of highly variable severity, ranging from mild cases with low mortality to severe cases with high mortality. Numerous biomarkers have been studied as potential early predictors of the severity of this disease so that treatment can be optimally tailored to prevent complications. We aim to present and discuss the most relevant biomarkers for early severity assessment in AP that have been studied to date. We review the current literature on biomarkers that have been used to predict the severity in AP. C-reactive protein (CRP) is still considered to be the gold standard, with a cut-off value of 150 mg/ml 48 h after disease onset. Other markers, including procalcitonin (PCT) and interleukin 6 (IL-6) have been implemented in some hospitals, but are not used on a routine basis. Most other markers, including acute phase proteins (LBP, SAA, PTX3), cytokines (Il-8, TNF-a, MIF), activation peptides of pancreatic proteases (TAP, CAPAP, PLAP), antiproteases (AAT, a2M), adhesion molecules (ICAM-1, selectins, E-cadherin) and leukocyte-derived enzymes (PA2, PMN-E) have shown some promising results but have not been routinely implemented. Furthermore, new and interesting biomarkers (Copeptin, TRX-1, Ang-2, E-2) have shown good results, but more research is needed to determine if they could play a role in the future. Various reasons why new markers for disease severity have not been adopted in daily routine include low accuracy, cumbersome laboratory techniques and high cost. Despite these difficulties, research is still very active in finding new markers to predict the severity of AP.

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Section: Selectinsmentioning

confidence: 84%

Section: Icam-1 and Soluble Icam-1mentioning

confidence: 87%

Laboratory markers predicting severity of acute pancreatitis

Staubli¹,

Oertli²,

Nebiker³

2015

Critical Reviews in Clinical Laboratory Sciences

190

122

View full text Add to dashboard Cite

show abstract

“…3A,B), whereas WT mice exhibit robust NF-κB-mediated pro-inflammatory signaling that results in pancreatitis and consequent histological changes. NF-κB is known to regulate ICAM-1 22,23 , a proinflammatory mediator that recruits macrophages 22,24,25 . Our data show significant elevation (p ≤ 0.001) of ICAM-1 following infection with CVB3 in wildtype animals (Fig.…”

Section: Resultsmentioning

confidence: 99%

Mucin-1 is required for Coxsackie Virus B3-induced inflammation in pancreatitis

Liu

Clemens

Grunkemeyer

et al. 2019

Sci Rep

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The Muc-1 oncoprotein is a tumor-associated mucin often overexpressed in pancreatic cancer. We report that knockout of Muc-1 reduced the degree of pancreatic inflammation that resulted from infection with Coxsackievirus B3 (CVB3) in a mouse model. CVB3-infected Muc-1-deficient (Muc-1 KO ) mice had significantly reduced infiltration of macrophages into the murine pancreas. We found that Muc-1 signaling through NF-κB increased expression of ICAM-1, a pro-inflammatory mediator that recruits macrophages. Further investigation revealed that bone marrow derived macrophages (BMDM) from the Muc-1 KO mice exhibited defective migration properties, in part due to low expression of the C-C motif chemokine receptor (CCR2) and the integrin Very Late Antigen 4 (VLA-4). The results presented here provide novel insight into the role of Muc-1 in regulating the inflammatory response and the cellular microenvironment in pancreatitis.

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“…20,21 The degree of microcirculation derangement is related with concentration of adhesion molecules and the peripheral blood neutrophil ICAM-1 expression is significant increase at early stage in severe AP but not in mild AP. 17,22 In addition, the inhibition of ICAM-1 or VCAM-1 by monoclonal antibody and use of antineutrophil antibody can attenuates the severity of AP and lung injury. [23][24][25] The early measurement of serum ICAM-1 levels within 24 hours can distinguish severe AP from mild AP.…”

Section: The Role Of Leukocytementioning

confidence: 99%

Mechanism of Severe Acute Pancreatitis: Focusing on Development and Progression

Hyuk¹

2015

Korean J Pancreas Biliary Tract

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Increased expression of the intercellular adhesion molecule-1 (ICAM-1) on peripheral blood neutrophils in acute pancreatitis

Cited by 16 publications

References 30 publications

Laboratory markers predicting severity of acute pancreatitis

Laboratory markers predicting severity of acute pancreatitis

Mucin-1 is required for Coxsackie Virus B3-induced inflammation in pancreatitis

Mechanism of Severe Acute Pancreatitis: Focusing on Development and Progression

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