Phagocytic defects

Quie, Paul G.; Mills, Elaine L.; McPhail, Linda C.; Johnston, Richard B.

doi:10.1007/bf01857310

Cited by 9 publications

(3 citation statements)

References 86 publications

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“…Very young age has been associated with suboptimal wound healing in many studies. Impaired or immature wound healing and higher risks to develop wound infection explain the increased risk of developing abdominal wound dehiscence in children younger than aged 1 year [6][7][8][9][10]. Necrotizing enterocolitis is highly prevalent in this age group and is without exception combined with poor clinical condition and emergency surgery, which again negatively influence wound healing.…”

Section: Discussionmentioning

confidence: 99%

Risk Factors for Abdominal Wound Dehiscence in Children: A Case‐Control Study

et al. 2009

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Background In the limited literature concerning abdominal wound dehiscence after laparotomy in children, reported incidences range between 0.2-1.2% with associated mortality rates of 8-45%. The goal of this retrospective case-control study was to identify major risk factors for abdominal wound dehiscence in the pediatric population. Methods Patients younger than aged 18 years who developed abdominal wound dehiscence in three pediatric surgical centers during the period 1985-2005 were identified. For each patient with abdominal wound dehiscence, four controls were selected by systematic random sampling. Patients with (a history of) open abdomen treatment or abdominal wound dehiscence were excluded as control subjects. Putative relevant patient-related, operation-related, and postoperative variables for both cases and control subjects were evaluated in univariate analyses and subsequently entered in multivariate stepwise logistic regression models to identify major independent predictors of abdominal wound dehiscence. Results A total number of 63 patients with abdominal wound dehiscence and 252 control subjects were analyzed. Mean presentation of abdominal wound dehiscence was at postoperative day 5 (range, 1-15) and overall mortality was 11%. Hospital stay was significantly longer (p \ 0.001) in the case group (median, 42 vs. 10 days). Major independent risk factors for abdominal wound dehiscence were younger than aged 1 year, wound infection, median incision, and emergency surgery. Incisional hernia was reported in 12% of the patients with abdominal wound dehiscence versus 3% in the control group (p = 0.001). Conclusions Abdominal wound dehiscence is a serious complication with high morbidity and mortality. Median incisions should be avoided whenever possible.

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Section: Discussionmentioning

confidence: 99%

Risk Factors for Abdominal Wound Dehiscence in Children: A Case‐Control Study

et al. 2009

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“…Polymorphonuclear leukocytes (PMN) and monocytes from patients with chronic granulomatous disease (CGD), which serves as the paradigm of such conditions, fail to kill a variety of bacteria and are known to be defective in oxygen metabolism (1)(2)(3)(4)(5)(6)(7). A number of oxygen metabolites produced by phagocytic cells could mediate this cytocidal activity, including°a, OH-, singlet 2, and hypohalide.…”

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confidence: 99%

Reconstitution of a variant macrophage cell line defective in oxygen metabolism with a H2O2-generating system.

Tanaka¹,

Kiyotaki²,

Tanowitz³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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A variant clone, C3C, derived from the cloned macrophage cell line J774. 16 lacks the capacity to produce 02 or H202 after appropriate stimulation. When the parental and variant cell lines were infected with epimastigotes of Trypanosoma cruzi, the parasites were killed or their growth was inhibited by the parental line, but they grew readily in the variant clone C3C. It was possible to reconstitute the variant cell line with an enzyme system targeted to the lysosomal compartment capable of generating a single oxygen metabolite, H202. This was accomplished by allowing the cells to phagocytize zymosan particles covalently coupled with glucose oxidase (GO-Zy particles). Approximately onethird of the H202 theoretically expected to be produced by the ingested GO-Zy particles could be detected outside the cells by the cytochrome c peroxidase assay; this fraction may represent the efficiency of extracellular assays for H202 production. When T. cruzi-infected clone C3C cells were reconstituted with GO-Zy particles, upon addition of glucose, intracellular killing of the parasites occurred. It was possible to estimate the level of H202 production required to kill a single parasite (8.7 x 10' nmol/min) by GO-Zy particles in suspension and to formulate a first approximation of the killing potency ofthe reconstituted cells-i.e., number of parasites expected to be killed-that correlated well with the observed growth of the parasites intracellularly.Appreciation of the importance of oxidative cytocidal mechanisms in intracellular killing of a variety of microorganisms ingested by phagocytic cells derives in part from the study of patients with a variety of genetic deficiency diseases. Polymorphonuclear leukocytes (PMN) and monocytes from patients with chronic granulomatous disease (CGD), which serves as the paradigm of such conditions, fail to kill a variety of bacteria and are known to be defective in oxygen metabolism (1-7). A number of oxygen metabolites produced by phagocytic cells could mediate this cytocidal activity, including°a, OH-, singlet 2, and hypohalide. There are very few instances in which the precise oxygen metabolite responsible for killing a particular organism within cells has been established.For the past several years we and others have developed and studied continuous cloned macrophage-like cell lines as models for understanding mononuclear phagocyte function (8-10). We have previously described a murine cloned macrophage cell line, J774.16 which, upon stimulation with phorbol 12-myristate 13-acetate or aggregated immunoglobulins, oxidizes glucose via the hexose monophosphate shunt and produces°-and

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“…Since the need for substances able to in terfere with neutrophil function has been re cently emphasized by the increasing number of clinical syndromes depending on neutro phil functional abnormalities, mainly chem otaxis [23], we have experimented with MPG on the locomotion of normal human neutrophils. Our results show that MPG is able to enhance random migration and chemotaxis as a result of an increased rate of locomotion.…”

Section: Introductionmentioning

confidence: 99%

Effects of <i>N</i>-(2-Mercaptopropionyl) Glycine on Neutrophil Locomotion

Patrone¹,

Dallegri²,

Lanzi³

et al. 1981

Int Arch Allergy Immunol

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The effects of the sulphydryl group donor N-(2-mercaptopropionyl) glycine on neutrophil locomotion were evaluated in vitro. The drug, when used at a concentration of 10^––³M was found to stimulate the random migration and chemotaxis of normal neutrophils as a result of an enhanced rate of locomotion. The true chemotactic response was unaffected. N-(2-mercaptopropionyl) glycine appeared to exert its effect on the whole moving cell population.

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Phagocytic defects

Cited by 9 publications

References 86 publications

Risk Factors for Abdominal Wound Dehiscence in Children: A Case‐Control Study

Risk Factors for Abdominal Wound Dehiscence in Children: A Case‐Control Study

Reconstitution of a variant macrophage cell line defective in oxygen metabolism with a H2O2-generating system.

Effects of <i>N</i>-(2-Mercaptopropionyl) Glycine on Neutrophil Locomotion

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