The Effects of G-CSF Treatment and Starvation on Bacterial Translocation in Hemorrhagic Shock

Agalar, Fatih; İskit, Alper B.; Ağalar, Canan; Hamaloğlu, Erhan; Güç, M. Oğuz

doi:10.1006/jsre.1998.5386

Cited by 14 publications

(8 citation statements)

References 26 publications

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“…Additionally, it was previously demonstrated that EPCs are mobilized by G-CSF to damaged tissues and significantly promote angiogenesis by increasing the secretion of angiogenic cytokines in full-thickness incision, burned, and focal cerebral ischemia rats and myocardial infarcted rabbits [28–30]. Thus, G-CSF administration would be expected to play important roles in wound repair, partly by ameliorating inflammation and enhancing angiogenesis [31,32]. …”

Section: Discussionmentioning

confidence: 99%

Granulocyte-Colony Stimulating Factor (G-CSF) Accelerates Wound Healing in Hemorrhagic Shock Rats by Enhancing Angiogenesis and Attenuating Apoptosis

et al. 2017

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BackgroundFollowing severe trauma, treatment of cutaneous injuries is often delayed by inadequate blood supply. The aim of the present study was to determine whether granulocyte-colony stimulating factor (G-CSF) protects endothelial cells (ECs) and enhances angiogenesis in a rat model of hemorrhagic shock (HS) combined with cutaneous injury after resuscitation.Material/MethodsThe HS rats with full-thickness defects were resuscitated and randomly divided into a G-CSF group (200 μg/kg body weight), a normal saline group, and a blank control group. Histological staining was to used estimate the recovery and apoptosis of skin. Apoptosis- and angiogenesis-related factors were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot (WB). Scratch assay, tube formation, and WB experiments were performed to verify the functional effects of G-CSF on HUVECs in vitro.ResultsH&E staining and Masson trichrome staining showed earlier inflammation resolution and collagen synthesis in the G-CSF-treated group. Angiogenesis-related factors were elevated at mRNA and protein levels. TUNEL staining suggested fewer apoptotic cells in the G-CSF group. The apoptotic-related factors were down-regulated and anti-apoptotic factors were up-regulated in the G-CSF-treated group. Scratch assay and tube formation experiments revealed that G-CSF facilitated migration ability and angiogenic potential of HUVECs. The angiogenic and anti-apoptotic effects were also enhanced in vitro.ConclusionsOur results suggest that G-CSF after resuscitation attenuates local apoptosis and accelerates angiogenesis. These findings hold great promise for improving therapy for cutaneous injury in severe trauma and ischemia diseases.

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Section: Discussionmentioning

confidence: 99%

Granulocyte-Colony Stimulating Factor (G-CSF) Accelerates Wound Healing in Hemorrhagic Shock Rats by Enhancing Angiogenesis and Attenuating Apoptosis

et al. 2017

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“…OK-432, which activates cell-mediated immunity, is a hemolytic streptococcus preparation and has been used for immunotherapy of cancer patients [45]. Gm-csf, g-csf, IFN-Á, and heparan sulfate have also been shown to improve host defence, and to reduce the bacterial translocation in mice and rats [46][47][48][49]. Hyperbaric oxygen treatment is another modality that prevented BT by destruction of translocated bacteria via increased bactericidal or phagocytic activity [50].…”

Section: Discussionmentioning

confidence: 99%

Effect of Different Enteral Nutrients on Bacterial Translocation in Experimental Obstructive Jaundice

Kuru¹,

Dinç²,

Altınok

et al. 2004

Eur Surg Res

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Obstructive jaundice leads to bacterial translocation (BT) by disruption of the gut barrier, intestinal microecology, and impaired host immune defence. The objective of the present study is to investigate the effects of different enteral nutrients on BT that is induced by obstructive jaundice in rats. Eighty male Wistar-Albino rats were randomly assigned into 4 groups. Group 1: 20 rats underwent laparotomy, common bile duct (CBD) was not actually ligated and transected, but sham ligation of CBD was performed. Groups 2–4: 60 rats underwent laparotomy, CBD ligation and transection. Group 1 and 2 rats were given rat chow, group 3 rats were fed a glutamine and arginine supplemented enteral diet, and group 4 rats were fed an arginine, m-RNA and ω-3 supplemented enteral diet, an immunonutrient. Rats in groups 3 and 4 had significantly less BT to mesenteric lymph nodes compared to rats in group 2 (p = 0.001). These findings suggest that oral administration of an arginine and glutamine supplemented diet and immunonutrition reduce BT in rats with obstructive jaundice.

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“…Even a brief period of starvation has been found to increase the number of coliform bacteria in the cecal content, and it increased bacterial adherence to cecal epithelium [21]. The additional traumatic stress of hemorrhagic hypotension may cause damage to the gut mucosal barrier functions, which may be necessary for BT to occur [22].…”

Section: Discussionmentioning

confidence: 99%

“…Short-term food deprivation, such as overnight fasting, has been shown to increase the rate of BT in experimental models, and this effect is more prominent when the animals are subjected to secondary insults such as nonlethal hemorrhagic shock or burn injury [13,[19][20][21][22][23]. Even a brief period of starvation has been found to increase the number of coliform bacteria in the cecal content, and it increased bacterial adherence to cecal epithelium [21].…”

Section: Discussionmentioning

confidence: 99%

Oral Carbohydrate Solution Ameliorates Endotoxemia-Induced Splanchnic Ischemia

et al. 2006

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The purpose of this study was to investigate the effect of oral administration of a simple carbohydrate solution on splanchnic circulation and bacterial translocation in endotoxemia. Group 1 was sham control; group 2 was starved for 24 hours; in group 3, endotoxin was administrated at the end of starvation; in group 4, carbohydrate solution was administrated via orogastric route for 24 hours; and in group 5, carbohydrate solution was given and endotoxin was administrated at the end of 24 hours. Splanchnic blood flows were recorded and tissue samples were collected for microbiological analyses. There was a significant increase (P<.05) in the incidence of bacterial translocation in starvation. Endotoxemia decreased distal (P=.021) and midmesenteric (P=.046) flow in starved animals. Oral carbohydrate significantly increased ileal blood flow in starvation (P=.036) and endotoxemia (P=.008). In conclusion, oral carbohydrate solution prevents bacterial translocation during starvation and endotoxemia. The possible mechanism is the improvement in the mesenteric blood flow.

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The Effects of G-CSF Treatment and Starvation on Bacterial Translocation in Hemorrhagic Shock

Cited by 14 publications

References 26 publications

Granulocyte-Colony Stimulating Factor (G-CSF) Accelerates Wound Healing in Hemorrhagic Shock Rats by Enhancing Angiogenesis and Attenuating Apoptosis

Granulocyte-Colony Stimulating Factor (G-CSF) Accelerates Wound Healing in Hemorrhagic Shock Rats by Enhancing Angiogenesis and Attenuating Apoptosis

Effect of Different Enteral Nutrients on Bacterial Translocation in Experimental Obstructive Jaundice

Oral Carbohydrate Solution Ameliorates Endotoxemia-Induced Splanchnic Ischemia

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