Phagocytotic Activity of Monocytes from Diabetic Patients

Katz, S; Klein, Barbara E.K.; Elian, I.; Fishman, Pnina; Djaldetti, M

doi:10.2337/diacare.6.5.479

Cited by 76 publications

(34 citation statements)

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“…with diabetes is altered, resulting in a decreased bactericidal capacity of the cells and an increased susceptibility to infections. It has been shown that the number of phagocytes from these patients is significantly reduced in comparison with that from healthy individuals (Katz et al, 1983). However, the number of bacteria phagocytosed per each individual cell was similar in individuals of both groups.…”

Section: Certain Conditions Affectingmentioning

confidence: 90%

Phagocytosis—The mighty weapon of the silent warriors

Djaldetti

Salman

Bergman

et al. 2002

Microscopy Res & Technique

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Professional phagocytes, comprising polymorphonuclear neutrophils and monocyte/macrophage cells, play an important role in the host defense. Any defect in their function exposes the organism to microbial intruders terminating in fatal diseases. The functional responses of the phagocytes to bacterial and fungal infections include chemotaxis, actin assembly, migration, adhesion, aggregation, phagocytosis, degranulation, and reactive oxygen species production. Superoxide generation by phagocytic NADPH oxidase is an imperative step toward bacterial killing. Phagocytes participate in inflammatory reactions and exert tumoricidal activity. They are supported by serum factors such as immunoglobulins, cytokines, complement, the acute phase reactant C-reactive protein, production of antibacterial proteins, and others. In addition to their principal task to eliminate bacteria, they are engaged in removing damaged, senescent, and apoptotic cells. Engulfed cell debris, large particles such as latex beads, fat, and oil droplets, are examples of phagocytic activity illustrated in the present review with transmission and scanning electron microscope micrographs. Numerous factors, such as diseases and stressful conditions, affect the engulfing activity of the professional phagocytes. Our experience regarding the impaired phagocytic capacity of cells in patients with diabetes and chronic renal failure is discussed. The results obtained in our laboratory from experiments detecting the effect of strenuous physical exercise, hypothermia, fasting, and abdominal photon irradiation on the phagocytic capacity of human polymorphonuclear neutrophils and rat peritoneal macrophages are hereby summarized and the reports on those subjects in the recent literature are reviewed. A variety of assays are applied for quantifying phagocytosis. Flow cytometry based on incubation of phagocytic cells with fluorescent conjugated particles and measuring the amount of fluorescence as an indicator of the engulfing capacity of the cells is a useful method. A direct visualization of the ingested particles using light or electron microscopy is a valuable tool for estimation of phagocytic function. In our hands, the use of semithin sections of embedded phagocytes following their incubation with latex particles provided satisfactory results for measuring the total number of phagocytic cells, as well as the internalizing capacity of each individual cell. Microbiological assays, the nitroblue tetrazolium test, quantitation of antibody- and antigen-mediated phagocytosis, as well as methods reviewed in detail in other reports are additional applications for determination of this intricate process.

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Section: Certain Conditions Affectingmentioning

confidence: 90%

Phagocytosis—The mighty weapon of the silent warriors

Djaldetti

Salman

Bergman

et al. 2002

Microscopy Res & Technique

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“…A likely common denominator in all these abnormalities is the dysfunction of the macrophage system. Numerous phenotypic abnormalities, including altered metabolism (9-13), aberrations in chemotactic response (12)(13)(14), phagocytosis (12,15,16), antigen presentation (17)(18)(19), receptor functions (20,21), and cytokine release (18,(22)(23)(24)(25)(26)(27) have indeed been found in peripheral blood mononuclear cells from both type 1 and type 2 diabetic patients. On the other hand, data on the function of tissue macrophages in human diabetes are not available.…”

Section: Discussionmentioning

confidence: 99%

Altered cytokine and nitric oxide secretion in vitro by macrophages from diabetic type II-like db/db mice.

et al. 2000

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Macrophage dysfunction is a likely mechanism underlying common diabetic complications such as increased susceptibility to infection, accelerated atherosclerosis, and disturbed wound healing. There are no available studies on the function of tissue macrophages in diabetes in humans. We have therefore studied peritoneal macrophages from diabetic type 2-like db/db mice. We found that the release of tumor necrosis factor-␣ and interleukin-1␤ from lipopolysaccharide plus interferon-␥-stimulated macrophages and vascular endothelial growth factor from both stimulated and nonstimulated macrophages was significantly reduced in diabetic animals compared with nondiabetic controls. Nitric oxide production from the stimulated db/db macrophages was significantly higher than that in the db/+ cultures, whereas there was no difference in their ability to generate reactive oxygen species. When studied both at light and electron microscopic levels, macrophages in diabetic animals had an altered morphological appearance compared with those of normal controls. We conclude that the function and morphology of the macrophages are disturbed in db/db mice and that this disturbance is related to the mechanisms underlying common inflammatory and degenerative manifestations in diabetes.

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“…Moreover, monocytes with impaired chemotaxis 24 and phagocytosis 25 are also found in diabetic patients. We found an increased subpopulation of mononuclear cells and neutrophils both in adipose tissue and in systemic circulation.…”

Section: Foreign Body-induced Insulin Resistance H-t Wu Et Almentioning

confidence: 99%

Insulin resistance without obesity induced by cotton pellet granuloma in mice

Chang

Tsao

et al. 2009

Laboratory Investigation

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Obesity leads to insulin resistance because the larger adipocytes in obese persons secrete proinflammatory cytokines that cause chronic inflammation in adipose tissue. This, in turn, leads to the alteration of adipokine secretion, which can induce insulin resistance. However, the development of insulin resistance without obesity is still obscure. We aimed to use an animal inflammation model with cotton pellet granuloma (CPG) in adipose tissue to characterize insulin resistance formation. We found that CPG in epididymal white adipose tissue (WAT), rather than in interscapular brown adipose tissue, impaired insulin sensitivity, and glucose utilization, and that it decreased levels of phosphoinsulin receptor and phospho-Akt in both muscle and liver tissue, but that it did not modify the body weight or food intake in mice. Macrophage infiltration in adipose tissue, leukocyte counts, monocyte chemoattractant protein-1, and interleukin-6 were elevated in CPG-treated mice. However, we found a marked decrease of plasma adiponectin only in the WAT group, which might have been because of the lower level of peroxisome proliferator-activated receptor-g in WAT. These results show that granuloma formation in WAT by implantation of a cotton pellet may induce insulin resistance under nonobese condition through circulating inflammatory mediators, especially the low level of adiponectin.

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Phagocytotic Activity of Monocytes from Diabetic Patients

Cited by 76 publications

References 0 publications

Phagocytosis—The mighty weapon of the silent warriors

Phagocytosis—The mighty weapon of the silent warriors

Altered cytokine and nitric oxide secretion in vitro by macrophages from diabetic type II-like db/db mice.

Insulin resistance without obesity induced by cotton pellet granuloma in mice

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