A novel mechanism for neutrophil priming in trauma: Potential role of peritoneal fluid

Shah, Shinil K.; Jiménez, Fernando; Walker, Peter A.; Aroom, Kevin R.; Xue, Hasen; Feeley, Teri D.; Uray, Karen; Norbury, Kenneth C.; Stewart, Randolph H.; Laine, Glen A.; Cox, Charles S.

doi:10.1016/j.surg.2010.03.019

Cited by 15 publications

(11 citation statements)

References 28 publications

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“…In contrast, CCL3-deficient neutrophils were slightly more sensitive to cyclophosphamide treatment, as their decay was considerably faster in CCL3 -/-mice (1.9±0.4 days in WT compared with 1.0±0.1 days in CCL3 -/-; P=0.11; Figure 4C). Interestingly, the accelerated decay was associated with higher activation status, as indicated by enhanced surface expression of CD18 28 Figure 4D), which fits with the notion that nonactivated have a half life of 2 to 4 days, whereas activated neutrophils survive for only 1 to 2 days. Next, we assessed if the decreased half life of CCL3 -/-neutrophils was because of enhanced apoptosis of these cells.…”

Section: Resultssupporting

confidence: 80%

Leukocyte-Specific CCL3 Deficiency Inhibits Atherosclerotic Lesion Development by Affecting Neutrophil Accumulation

Jager

Bot

Kraaijeveld

et al. 2013

ATVB

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Objective-Despite common disbelief that neutrophils are involved in atherosclerosis, evidence is accumulating for a causal role of neutrophils in atherosclerosis. CC chemokine ligand (CCL)3 is an inflammatory chemokine and its expression is significantly increased during atherosclerotic lesion formation in mice. It has recently been shown that under conditions of inflammation neutrophils can migrate along a CCL3 gradient. In this study, we aimed to elucidate the role of leukocytederived CCL3 in atherogenesis. Methods and Results-Irradiated low density lipoprotein receptor -/-mice, reconstituted with CCL3 -/-or littermate bone marrow showed markedly reduced CCL3 response to lipopolysaccharide treatment, establishing the critical relevance of leukocytes as source of CCL3. Hematopoietic deficiency of CCL3 significantly reduced aortic sinus lesion formation by 31% after 12 weeks of western-type diet. Interestingly, whereas plaque macrophage, collagen, and vascular smooth muscle cell content were unchanged, neutrophil adhesion to and presence in plaques was significantly attenuated in CCL3 -/-chimeras. These mice had reduced circulating neutrophil numbers, which could be ascribed to an increased neutrophil turnover and CCL3 -/-neutrophils were shown to be less responsive toward the neutrophil chemoattractant CXC chemokine ligand 1. Conclusion-Our

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Section: Resultssupporting

confidence: 80%

Leukocyte-Specific CCL3 Deficiency Inhibits Atherosclerotic Lesion Development by Affecting Neutrophil Accumulation

Jager

Bot

Kraaijeveld

et al. 2013

ATVB

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“…Decompressive laparotomy after development of abdominal compartment syndrome in pigs has been shown not to decrease the ability of peritoneal fluid to prime naïve neutrophils when measured at up to 12 hours post decompression. 3 More detailed time course studies are required to determine the exact role of peritoneal fluid in propagation of the inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

“…2 More recently, our group has demonstrated that peritoneal fluid from a non-infectious model of abdominal compartment syndrome may contribute to the inflammatory response by serving as a primer of naïve neutrophils. 3 …”

Section: Introductionmentioning

confidence: 99%

Peritoneal fluid: a potential mechanism of systemic neutrophil priming in experimental intra-abdominal sepsis

Shah

Jiménez²,

Walker³

et al. 2012

The American Journal of Surgery

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Background Recent studies suggest that peritoneal fluid (PF) may be an important mediator of inflammation. We hypothesize that PF may drive systemic inflammation in intra-abdominal sepsis by representing a priming agent for neutrophils. Methods PF was collected 12 hours after initiation of intra-abdominal sepsis in swine. Naïve human neutrophils were primed with PF prior to treatment with N-formyl-met-leu-phe or phorbol 12-myristate 13-acetate to elucidate receptor dependent and independent mechanisms of neutrophil activation. Flow cytometry was used to quantify neutrophil surface adhesion marker expression of integrins and selectins and superoxide anion production. Additionally, pro-inflammatory cytokines were quantified in PF. Results PF primed neutrophils via receptor dependent and independent mechanisms. There were significant increases in the pro-inflammatory cytokines IL-6 and TNF-alpha in PF correlating with the development of intra-abdominal sepsis. Conclusions PF represents a priming agent for naïve PMN's in intra-abdominal sepsis. This may be secondary to increased levels of pro-inflammatory cytokines. Strategies to reduce the amount of PF may decrease the systemic inflammatory response by reducing a priming agent for neutrophils.

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“…We have recently demonstrated that peritoneal fluid from ACS serves as a primer of naïve neutrophils and monocytes [10]. It is well documented that peritoneal fluid can be reabsorbed into the systemic circulation, primarily via lymphatic conduits [18,19].…”

Section: Discussionmentioning

confidence: 99%

“…New organ dysfunction was manifested by changes in the CVP, PAP, PCWP, MAP, peak airway pressures, P:F ratios, lactate, anion gap, and base excess. The specific values are presented in Table 2 [10].…”

Section: Development Of New Organ Dysfunctionmentioning

confidence: 99%

Evaluating the effects of immediate application of negative pressure therapy after decompression from abdominal compartment syndrome in an experimental porcine model

Shah

Jiménez²,

Walker³

et al. 2011

Eur J Trauma Emerg Surg

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Early application of NPT in this porcine ACS model is safe and does not appear to be associated with an increased risk of recurrent intra-abdominal hypertension. The results of this animal study suggest that the application of NPT following decompression from ACS results in greater peritoneal fluid removal and may translate into augmented intestinal edema resolution secondary to more favorable fluid flux profiles.

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A novel mechanism for neutrophil priming in trauma: Potential role of peritoneal fluid

Cited by 15 publications

References 28 publications

Leukocyte-Specific CCL3 Deficiency Inhibits Atherosclerotic Lesion Development by Affecting Neutrophil Accumulation

Leukocyte-Specific CCL3 Deficiency Inhibits Atherosclerotic Lesion Development by Affecting Neutrophil Accumulation

Peritoneal fluid: a potential mechanism of systemic neutrophil priming in experimental intra-abdominal sepsis

Evaluating the effects of immediate application of negative pressure therapy after decompression from abdominal compartment syndrome in an experimental porcine model

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