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Search: WFRF:(Nettelbladt Carl Gustaf)

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1.
  • Katouli, Mohammad, et al. (author)
  • Selective translocation of coliform bacteria adhering to caecal epithelium of rats during catabolic stress
  • 1997
  • In: Journal of Medical Microbiology. - : The Microbiology Society. - 0022-2615 .- 1473-5644. ; 46:7, s. 571-578
  • Journal article (peer-reviewed)abstract
    • Adult conventional rats were starved for 48 h with or without haemorrhage at 24 h, and translocation of caecal coliforms to mesenteric lymph nodes (MLNs) was measured. Translocation was detected in three of 11 rats without haemorrhage, in 6 of 11 starved and sham-operated rats and in 12 of 22 rats after haemorrhage. In contrast, only one of 13 non-instrumented and fed control rats showed translocation. Translocation was associated with more coliforms adhering to caecal epithelium in rats. Coliform isolates from caecum, caecal epithelium and MLNs were characterised and grouped into different biochemical phenotypes (BPTs) by a biochemical fingerprinting method. Of 291 BPTs detected in the caecum of all rats, 108 were also found on caecal epithelium; 36 BPTs were detected in MLNs, of which 17 were not detected either in the caecum or on the caecal epithelium of the corresponding rats. One isolate from each of these 36 BPTs was selected and compared to the others. Four common (C) BPTs (i.e., C1-C4) were identified among them. Strains of C1 formed the majority of isolates from the caecum (79%), caecal epithelium(71%) and MLNs (91%). In contrast, C2-C4 had a significantly lower incidence both in the caecum and on the caecal epithelium, but not in the MLNs. These findings indicate that not all caecal coliforms adhere to the epithelium during catabolic stress and that for translocation to occur, other bacterial properties besides adhesion are needed. It is also concluded that coliforms with a low incidence in the caecum can translocate with the same efficiency as those with a high incidence.
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2.
  • Nettelbladt, Carl Gustaf, et al. (author)
  • Bulking fibre prevents translocation of an efficiently translocating Escherichia coli strain in rats
  • 1998
  • In: Clinical Nutrition. - : Elsevier. - 0261-5614 .- 1532-1983. ; 17:4, s. 185-190
  • Journal article (peer-reviewed)abstract
    • Background: starvation for 24 h prior to experimental haemorrhage increases bacterial translocation in rats. Forty-eight hours starvation alone causes pronounced microbiological changes in caecal contents and a marked increase in bacterial adherence to caecal epithelium. The aim of the present study was to examine whether bulking fibre prevents these microbiological changes induced by starvation, i.e. mucosal adherence and/or bacterial translocationwith and without haemorrhage in rats. Methods: 32 rats were inoculated with the translocating Escherichia cell strain KI-C1. Groups of these rats were then starved for 48 h with or without access to bulking fibre. An additional group of rats was given bulking fibre and subjected to haemorrhage. A control group was untreated and given regular food. Samples were taken from caecal contents, caecal epithelium, mesenteric lymph nodes and blood. A biochemical fingerprinting method was used to characterize and compare E. coil strains in all samples. Results: ingestion of bulking fibre alone for 48 h significantly reduced the frequency of KI-C1 both in caecal contents and on caecal epithelium and completely prevented translocation of the strain, compared to starvation without bulking fibre for 48 h. Enforced stress (haemorrhage) increased bacterial translocation to the same level as starvation for 48 h. E. coli phenotypes found in mesenteric lymph nodes were also found adhering to the caecal epithelium. Conclusions: the presence of bulking fibre in gut lumen, by unknown mechanisms, reduces the frequency of an inoculated translocating strain of E. coil in caecal contents and on caecal epithelium and prevents its translocationto mesenteric lymph nodes.
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3.
  • Nettelbladt, Carl-Gustaf (author)
  • Effects of starvation and haemorrhage on the large bowel coliform flora with special reference to bacterial mucosal adherence and translocation
  • 1998
  • Doctoral thesis (other academic/artistic)abstract
    • Intestinal bacteria translocating to extra-intestinal sites have been suggested to play a role in the etiology of posttraumatic infections and multiple organ failure. In the present study, effects of haemorrhagic stress and /or starvation on the gut flora and bacterial translocation were studied in the rat. Hyperosmotic glucose infusion during haemorrhage in starved rats improved plasma refill but did not reduce bacterial translocation. In this experiment four groups of rats were subjected to haemorrhage. Two groups were given an i.v. infusion of hyperosmotic glucose during moderate (38% blood loss; n=12) or severe (43% blood loss; n=19) haemorrhage without reinfusion. Control groups received an i.v. infusion of saline during moderate (n=12) or severe (n=18) haemorrhage. No difference in bacterial translocation was observed between groups infused with glucose or saline. Starvation increased the number of coliform bacteria in caecal contents and induced adherence of coliform bacteria to caecal epithelium. Rats in a control group (n=19) were given their regular food. Six rats were starved for 24 hours and another 15 for 48 hours, with free access to water. Six rats underwent non-lethal haemorrhage (mean arterial pressure=55 mm Hg). These animals were only allowed water until sampling 24 hours later. Twenty-four hours starvation increased the number of bacteria in caecal contents 25-fold (p<0.05). 48 hours starvation further increased the number (p<0.001)and induced a marked increase in bacteria adherent to caecal epithelium (p<0.001). In the haemorrhaged group similar changes were observed and bacterial translocation increased (p<0.05) as compared to control rats. In order to characterise and compare coliform bacteria in caecal contents, on caecal epithelium and in mesenteric Iymph nodes of 57 rats subjected to different degrees of stress a biochemical finger printing method was used. A total of 291 biochemical phenotypes were found in caecal contents of all rats. Out of these, 108 were detected on caecal epithelium and only 19 of these appeared in mesenteric Iymph nodes of the corresponding rat. A total of 36 biochemical phenotypes were found in mesenteric Iymph nodes of all rats. Twenty-one of these belonged to four common phenotypes. The prevalence of these four phenotypes in mesenteric Iymph nodes did not differ significantly, while some of them had a low and some a high prevalence in caecal contents and on caecal epithelium. The phenotypes found in mesenteric Iymph nodes were also, mostly, found adherent to the caecal epithelium of the corresponding rat. Orally inoculated translocating strains of E. coli were able to colonise the gut. Thus, inoculation increased bacterial translocation in rats lacking these strains in their indigenous gut flora. Two groups of rats were inoculated with two translocating strains of E. coli. One group (n=l l ) was starved for 24 hours and the other (n=20)underwent non-lethal haemorrhage (mean arterial pressure=50 mm Hg) and was starved for 24 hours thereafter. Two non-inoculated groups of similar size, subjected to the same treatments served as controls. In the inoculated groups, bacterial translocation increased both after 24 hours starvation (p<0.05) and haemorrhage (p<0.01)as compared to non-inoculated control rats. Ingestion of bulking fibre prevented mucosal adherence and translocation of a translocating strain of E. coli. Four groups of rats were inoculated with a translocating strain of E coli. Animals in a control group (n=8) were given their regular food. Eight rats were starved for 48 hours and eight given only bulking fibre for 48 hours. An additional group (n=8) ingested bulking fibre only for 24 hours before and after haemorrhage (mean arterial pressure=50 mm Hg). Bulking fibre for 48 hours reduced both mucosal adherence (p<0.05) and translocation (p<0.001) of the inoculated bacteria as compared to starved rats. It is concluded that haemorrhagic stress and starvation have marked effects on the gut flora. Glucose infusion given during haemorrhage, previously shown to protect the animal during circulatory shock, cannot prevent bacterial translocation. Brief starvation increases the number of coliform bacteria in caecum and induces bacterial mucosal adherence. Only a limited number of strains of coliform bacteria translocate after stress. Adherence to caecal epithelium was associated with bacterial translocation. Inoculation with translocating strains of E. coli increases bacterial translocation. Bulking fibre prevents bacterial mucosal adherence and translocation. Detailed knowledge of the gut E. coli flora is of great importance when interpreting results of studies on bacterial translocation.
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4.
  • Nettelbladt, Carl Gustaf, et al. (author)
  • Hyperosmotic glucose infusion during hemorrhage does not reduce bacterial translocation in 24 hour-starved rats
  • 1995
  • In: Shock. - : Lippincott Williams & Wilkins. - 1073-2322 .- 1540-0514. ; 4:2, s. 113-116
  • Journal article (peer-reviewed)abstract
    • Food deprivation 24 h before stress increases bacterial translocation in hemorrhage. Presently it tested whether hyperosmolality, induced by exogenous glucose infusion to improve plasma refill, prevents or reduces bacterial translocation after experimental hemorrhage in 24 h food-deprived rats. Rats were given an i.v. infusion of either 2 mL of 30% glucose (G) or the same volume of .9% NaCl (C) while simultaneously being submitted to a standardized 60 min hemorrhage period, of moderate or more severe hemorrhage. Blood was not reinfused. Despite development of marked hyperglycemia (p < .001, G vs. C) resulting in significantly greater reductions in packed cell volume (p < .001, G vs. C), bacterial translocation was detected similarly in both groups regardless of whether moderate (10/12-G, 9/12-C) or severe (15/19-G, 15/18-C) hemorrhage was inflicted. It was concluded that hyperglycemic hyperosmolality did not prevent bacterial translocation in these models of hemorrhagic stress in 24 h-starved rats.
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5.
  • Nettelbladt, Carl-Gustaf, et al. (author)
  • Orally inoculated Escherichia coli strains colonize the gut and increase bacterial translocation after stress in rats
  • 2003
  • In: Shock. - Philadelphia, USA : Lippincott Williams & Wilkins. - 1073-2322 .- 1540-0514. ; 20:3, s. 251-6
  • Journal article (peer-reviewed)abstract
    • Coliforms are the members of the indigenous gut flora that most often translocate to mesenteric lymph nodes. Very few strains of Escherichia coli found in cecal contents of rats are able to translocate. The present study investigated the role of the composition of the gut flora for the occurrence of bacterial translocation. Two strains of E. coli (KI-C1 and KI-C2), previously shown to translocate in rats subjected to stress, were given by oral inoculation to rats lacking these strains. A biochemical fingerprinting method was used to identify bacteria in cecal contents, on cecal epithelium, and in mesenteric lymph nodes. In a challenge study, the inoculated E. coli strains were shown to colonize the rats and persist for up to 75 days in cecum. Subsequently, one group was starved for 24 h and a second group was subjected to experimental hemorrhage and then starved for 24 h before sampling for bacteriological analyses from blood, cecum, and mesenteric lymph nodes. Two parallel groups of rats served as controls and were not inoculated but otherwise received the same treatment before sampling. In the inoculated group, starved for 24 h, seven out of 11 rats showed translocation, whereas in the noninoculated group one of 11 rats showed translocation (P < 0.05). In groups subjected to hemorrhage and then starved for 24 h, 15/22 rats in the inoculated and 5/20 rats in the noninoculated group showed translocation (P < 0.01). These findings show that orally inoculated KI-C1 and KI-C2 strains can colonize the gut and can substantially increase bacterial translocation in rats subjected to mild and severe stress. The composition of the gut flora seems to be an underestimated factor in the pathophysiology of bacterial translocation.
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