Uptake, distribution and fate of bacterial lipopolysaccharides in monocytes and macrophages: An ultrastructural and functional correlation

Kang, Yong-Cheol; Lee, Che-Hung; Monroy, Rod; Dwivedi, R. S.; Odeyale, Charles O.; Newball, Harold H.

doi:10.1016/0892-0354(92)90016-j

Cited by 30 publications

(26 citation statements)

References 147 publications

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“…At the electron microscopic level, LPS micelles are identified on the basis of lamellar structure and use of immunocytochemistry (Kang et al, 1992;Risco and da Silva, 1995). The failure to depict the LPS with their typical lamellar arrangement in our micrographs could be a consequence of in vivo study or the limitation of our tissue-processing technique.…”

Section: Discussionmentioning

confidence: 99%

“…Lipopolysaccharide is believed to be an important cause of acute respiratory distress syndrome in humans and animals (Frevert and Warner, 1992). Mononuclear phagocytes including Kupffer cells and alveolar macrophages play a central role in the removal and processing of LPS and in mediating LPS-induced organ pathobiology by secreting various inflammatory mediators (Kang et al, 1992). Pulmonary intravascular macrophages (PIMs) are a recently identified population of mononuclear phagocytes in different animal species including sheep (Warner and Brain, 1990;Staub, 1994).…”

mentioning

confidence: 99%

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Ultrastructural and immunocytochemical study of the pulmonary intravascular macrophages ofEscherichia coli lipopolysaccharide-treated sheep

Singh

Atwal

1997

Anat. Rec.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Ultrastructural and immunocytochemical study of the pulmonary intravascular macrophages ofEscherichia coli lipopolysaccharide-treated sheep

Singh

Atwal

1997

Anat. Rec.

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“…In the mammalian system, lipopolysaccharides are internalized by the endocytic uptake into macrophages (Kang et al, 1992). Up to now, various LPS-receptors have been described in the mammalian system, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…This implies the involvement of a specific LPS-receptor in plant cells. Up to now, no LPS-receptor could be identified and nothing is known about the fate of the LPS molecules after the perception by the plant (Kang et al ., 1992;Kriegsmann et al ., 1993). Therefore we decided to monitor the fate of the LPS X.c.c.…”

Section: Introductionmentioning

confidence: 99%

Endocytosis of Xanthomonas campestris pathovar campestris lipopolysaccharides in non‐host plant cells of Nicotiana tabacum

et al. 2004

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Summary• The specific recognition of phytopathogenic bacteria by plant cells is generally mediated by a number of signal molecules. The elicitor-active lipopolysaccharides (LPS) of the phytopathogenic bacterium Xanthomonas campestris pv. campestris ( X.c.c ) are recognized by its non-host plant Nicotiana tabacum ( N.t .).• This LPS was purified and labelled with fluorescein isothiocyanate (FITC) for monitoring the fate of these signal molecules in intact plant cells of tobacco.• In this study we were able to show that the so-labelled LPS rapidly bound to the cell wall and was then internalized into the cells in a temperature-and energydependent way. This uptake of LPS could be outcompeted by the addition of an excess of unlabelled LPS. Furthermore, it was blocked by amantadine, an inhibitor of receptor-mediated endocytosis of mammalian cells. Immunolocalization experiments showed for the first time a significant co-localization of the LPS-elicitor with endosomal structures using an anti-Ara6 antibody.• These observations suggest specific endocytosis of LPS X.c.c. into tobacco cells. The possibility for a receptor-mediated endocytosis comparable to the mammalian system will be discussed.

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“…Monocytes and macrophages use their CD14 and Toll-like receptor-4 to bind and endocytose LPS, and to initiate cell signaling [1]. The internalized LPS escapes from endosomes, interacts with mitochondria and Golgi complexes, and enters the nuclei of monocytes and macrophages to activate proinflammatory gene transcription [12,22,35]. Therefore, macrophages play a central role in the host response to endotoxins.…”

Section: Introductionmentioning

confidence: 99%

Depletion of pulmonary intravascular macrophages partially inhibits lipopolysaccharide-induced lung inflammation in horses

et al. 2005

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-Horses are unique in their extreme sensitivity to endotoxin-induced cardio-pulmonary shock and mortality. The mechanisms behind increased sensitivity of the horse to endotoxin remain unknown. Pulmonary intravascular macrophages (PIMs) are pro-inflammatory cells occurring in horses. Because the functions of equine PIMs in endotoxemia remain unknown, we studied the role played by equine PIMs in endotoxin-induced pulmonary pathophysiology. We achieved this by using a recently developed protocol to deplete PIMs in order to compare lipopolysaccharide (LPS)-induced pulmonary responses in horses with or without PIMs. Horses treated with gadolinium chloride (GC; 10 mg/kg intravenous) to deplete PIMs or endotoxin-free saline (n = 4) were injected with Escherichia coli LPS (E. coli LPS; 50 ng/kg intravenously) 48 h after GC or saline. Control horses (n = 5) received two injections of endotoxin-free saline at 48 h intervals. All the horses were euthanized 2 h after LPS or saline challenge. Immunohistology for the PIMs showed their reduced numbers in GC-treated horses. The LPS treatment of normal and GC-treated horses increased diastolic and systolic pulmonary arterial pressures at 30 min compared to the saline-treated horses (P < 0.05). However, horses pre-treated with GC did not have an LPS-induced increase in mean pulmonary arterial pressure compared to the LPS-treated horses (P < 0.05). Light and electron microscopic immunocytochemistry detected extensive labeling for LPS in PIMs of LPS-treated horses. Both the LPS-treated groups had more alveolar septal cells positive for TNF-α and IL-1β compared to control horses, which did not receive LPS (P < 0.05). However, GC-treated horses challenged with the LPS showed less IL-1β-positive cells (P < 0.05). Immuno-electron microscopy localized TNF-α and IL-1β in PIMs. These new data show that PIMs endocytose LPS and contain TNF-α and IL-1β and their depletion partially inhibits LPS-induced pulmonary inflammatory responses. PIMs

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Uptake, distribution and fate of bacterial lipopolysaccharides in monocytes and macrophages: An ultrastructural and functional correlation

Cited by 30 publications

References 147 publications

Ultrastructural and immunocytochemical study of the pulmonary intravascular macrophages ofEscherichia coli lipopolysaccharide-treated sheep

Ultrastructural and immunocytochemical study of the pulmonary intravascular macrophages ofEscherichia coli lipopolysaccharide-treated sheep

Endocytosis of Xanthomonas campestris pathovar campestris lipopolysaccharides in non‐host plant cells of Nicotiana tabacum

Depletion of pulmonary intravascular macrophages partially inhibits lipopolysaccharide-induced lung inflammation in horses

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