Leukocytic Mechanisms in Inflammation

Hersh, E.; Bodey, G P

doi:10.1146/annurev.me.21.020170.000541

Cited by 40 publications

(8 citation statements)

References 133 publications

(193 reference statements)

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“…PMN's were obtained by the technique of intraperitoneal injection of 1% glycogen and paracentesis 8 h later (27). PAIN's so obtained were washed in isotonic saline, disrupted by sonication and suspended in isotonic saline.…”

Section: Additional Studiesmentioning

confidence: 99%

Pathogenesis of Salmonellosis STUDIES OF FLUID SECRETION, MUCOSAL INVASION, AND MORPHOLOGIC REACTION IN THE RABBIT ILEUM

Giannella¹,

Formal²,

Dammin³

et al. 1973

J. Clin. Invest.

191

111

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A B S T R A C T Strains of Salmonela typhimurium were studied in the ligated rabbit ileal loop model to gain insight into the mechanisms whereby bacteria which invade the gastrointestinal mucosa evoke fluid exsorption. The organisms employed differed in various biologic attributes including the ability to invade the ileal epithelium, multiply within the mucosa, elicit an acute inflammatory reaction, and disseminate across the intestinal wall. Some strains provoked small intestinal fluid exsorption although these did not elaborate enterotoxin. Only those strains which invaded the mucosa were accompanied by either mucosal inflammation or fluid exsorption. Noninvasive strains produced neither histologic abnormalities nor fluid secretion. While strains which invaded the mucosa caused an acute inflammatory reaction, not all such strains evoked flnid secretion. Furthermore, there was no correlation in ability of invasive organisms to evoke fluid secretion or in the intensity of mucosal inflammation, number of intramucosal salmonellae, or in ability to disseminate from the rabbit ileum.These observations suggest that, as is the case in shigellosis, mucosal invasion may be a necessary factor for the intestinal fluid loss in salmonellosis. A bacterial property or factor, in addition to invasion of the gastrointestinal mucosa, seems to be responsible for fluid exsorption. However, it is unlikely that a salmonella enterotoxin comparable to that elaborated by Vibrio cholerae, toxigenic Escherichia coli, or Shigella dysenteriae 1 is related to fluid secretion in salmonellosis.A preliminary report has been published in abstract form. 1972. Gastroenterology. 62: 752.

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Section: Additional Studiesmentioning

confidence: 99%

Pathogenesis of Salmonellosis STUDIES OF FLUID SECRETION, MUCOSAL INVASION, AND MORPHOLOGIC REACTION IN THE RABBIT ILEUM

Giannella¹,

Formal²,

Dammin³

et al. 1973

J. Clin. Invest.

191

111

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“…Many types of cells have the ability to sense chemicals and migrate toward a gradient of chemoattractant, an important biological process in many areas, such as the immune response (Harris 1954; Hersh and Bodey 1970), embryonic development (Behar et al 1994), and cancer metastasis (Muller et al 2001; Payne and Cornelius 2002). Neutrophils are an essential component of the innate immune system and an early line of defense against bacterial infections, trauma, infarction, and other stimuli.…”

Section: Introductionmentioning

confidence: 99%

Microfluidic switching system for analyzing chemotaxis responses of wortmannin-inhibited HL-60 cells

Liu

Sai

Richmond

et al. 2008

Biomed Microdevices

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The chemotaxis of phosphoinositide kinase-3 (PI3K)-inhibited differentiated HL-60 cells stably expressing CXCR2 was studied in a microfluidic switching gradient device that can generate stable and well-defined forward and reverse gradients. Wortmannin, a widely used PI3K inhibitor, was added during cell preparation and the experiment process. The studies quantify the chemotaxis gradient and the effects of a change in the direction of a CXCL-8 gradient on cell migration. PI3K-inhibited HL-60 cells migrated more efficiently toward the gradient before gradient switching than after, as measured by the effective chemotactic index. The inhibited HL-60 cells also showed that inadequate polarization, slower response time, and reduced cell populations can follow the gradient change. We observed that the role of PI3K in directing cellular response to gradient reversal was important in cell polarization and directional sensing associated with gradient switching.

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“…At day 3, lymphocytes and leukocytes were seen near the PCL struts in treated CTO. Leukocytes are the cell type present during acute inflammation (Hersh and Bodey, 1970). At day 10, leukocytes resided in the adventitia of both control and treated CTOs.…”

Section: Resultsmentioning

confidence: 99%

Development of a total atherosclerotic occlusion with cell-mediated calcium deposits in a rabbit femoral artery using tissue-engineering scaffolds

Zhu

Bailey

Elliott

et al. 2011

J Tissue Eng Regen Med

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This study sought to establish a chronic total occlusion (CTO) model with cell-mediated calcium deposits in rabbit femoral arteries. CTO is the most severe case in atherosclerosis and contains calcium deposits. Previous animal models of CTO do not mimic the gradual occlusion of arteries or have calcium in physiological form. In the present study we tested the strategy of placing tissue-engineering scaffolds preloaded with cells in arteries to develop a novel CTO model. Primary human osteoblasts (HOBs) were first cultured in vitro on polycaprolactone (PCL) scaffolds with 5 ng TGFβ1 loading for 28 days for precalcification. The HOB-PCL construct was then implanted into a rabbit femoral artery for an additional 3, 10 or 28 days. At the time of sacrifice, angiograms and gross histology of arteries were captured to examine the occlusion of arteries. Fluorescent staining of calcium and EDS detection of calcium were used to evaluate the presence and distribution of calcium inside arteries. Rabbit femoral arteries were totally occluded over 28 days. Calcium was presented at CTO sites at 3, 10 and 28 days, with the day 10 specimens showing the maximum calcium. Chronic inflammatory response and recanalization were observed in day 28 CTO sites. A novel CTO model with cell-mediated calcium has been successfully established in a rabbit femoral artery. This model can be used to develop new devices and therapies to treat severe atherosclerotic occlusion.

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Leukocytic Mechanisms in Inflammation

Cited by 40 publications

References 133 publications

Pathogenesis of Salmonellosis STUDIES OF FLUID SECRETION, MUCOSAL INVASION, AND MORPHOLOGIC REACTION IN THE RABBIT ILEUM

Pathogenesis of Salmonellosis STUDIES OF FLUID SECRETION, MUCOSAL INVASION, AND MORPHOLOGIC REACTION IN THE RABBIT ILEUM

Microfluidic switching system for analyzing chemotaxis responses of wortmannin-inhibited HL-60 cells

Development of a total atherosclerotic occlusion with cell-mediated calcium deposits in a rabbit femoral artery using tissue-engineering scaffolds

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