Immunophenotypic characterization and depletion 
of pulmonary intravascular macrophages of horses

Parbhakar, Om P.; Duke, Tanya; Townsend, H. G. G.; Singh, Baljit

doi:10.1051/vetres:2003041

Cited by 25 publications

(32 citation statements)

References 32 publications

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“…The procedure used for the measurement of pulmonary pressures has been described previously [23]. Briefly, the right jugular vein of all horses was aseptically catheterized with an 8 Fr catheter introducer sheath PIM depletion and lung inflammation in horses 559 following sedation with xylazine (0.5 mg/kg iv; Rompun, Bayer Inc. Etobicoke, Canada).…”

Section: Pressure Measurementsmentioning

confidence: 99%

“…Horses were euthanized and tissues collected as described previously [23]. Briefly, the lungs were fixed in situ for 30 min by pouring 5 L of 2% paraformaldehyde and 0.5% glutaraldehyde in 0.1 M sodium cacodylate buffer (pH 7.2) into the trachea.…”

Section: Tissue Fixationmentioning

confidence: 99%

“…The immunohistology protocols have been described previously [23]. Briefly, sections from paraffin blocks were dewaxed, rehydrated and treated with pepsin (2 mg/mL 0.01N HCl; Sigma Co.) for 90 min to unmask the antigen sites.…”

Section: Immunohistology With E Coli Lps Tnf-α and Il-1β Antibodiesmentioning

confidence: 99%

“…The color was developed with a commercial kit (Vector Laboratories, Burlington, Canada). Selected lung sections from each group were stained with MAC-387 (1:75; Serotec Ltd. Raleigh, USA), which we had previously used to identify equine PIMs, in order to assess depletion of PIMs [23]. Immunohistochemical controls included incubation with isotypematched immunoglobulins, staining of lung vasculature with anti-von Willebrand Factor antibody and omission of primary or both primary and secondary antibodies.…”

Section: Immunohistology With E Coli Lps Tnf-α and Il-1β Antibodiesmentioning

confidence: 99%

“…The data show a reduction in PIM numbers in GCtreated horses compared to the controls (Figs. 6A and 6B) as demonstrated previously [23]. In order to determine the effects of PIM depletion on the LPS-induced accumulation of cytokine-positive cells, we counted the numbers of cells stained for TNF-α and IL-β.…”

Section: Quantification Of Cells Positivementioning

confidence: 99%

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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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Section: Pressure Measurementsmentioning

confidence: 99%

Section: Tissue Fixationmentioning

confidence: 99%

Section: Immunohistology With E Coli Lps Tnf-α and Il-1β Antibodiesmentioning

confidence: 99%

Section: Immunohistology With E Coli Lps Tnf-α and Il-1β Antibodiesmentioning

confidence: 99%

Section: Quantification Of Cells Positivementioning

confidence: 99%

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

et al. 2005

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Pharmacoengineering of Lipid Nanoarchitectonics in Modulating Particle Uptake by Lung Macrophages

Thalla¹,

Banerjee²

2021

Nanoengineering of Biomaterials

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Expression of Toll‐Like Receptor 9 in Horse Lungs

Schneberger

Caldwell

Suri

et al. 2009

The Anatomical Record

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Toll-like receptor 9 (TLR9) has been found to be the main receptor to respond to bacterial DNA in a wide variety of species. Recent work has shown that TLR9 is expressed in a diverse set of cells within the lung. However, much of this data has been centered on human and mouse cell culture lines or primary cultures and very little is known of TLR9 expression in intact lung, especially that of the horse. Here we show that TLR9 is expressed in the lungs of horses in a wide variety of cells. In particular, we note expression in pulmonary intravascular macrophages (PIMs), alveolar macrophages, bronchial epithelial cells, and type-II cells amongst others. Immunogold electron microscopy localized TLR9 in nuclei, cytoplasm, and plasma membrane of various lung cells. The data also show that E. coli lipopolysaccharide significantly increased expression of TLR9 mRNA in lungs and the number of cells in the lung septa that were positive for TLR9 protein. Protein expression was seen in airway epithelium, vascular endothelium, and inflammatory cells in blood vessels. Intravenous administration of gadolinium chloride, which depletes macrophages, before the lipopolysaccharide treatment significantly inhibited the LPSinduced increase in TLR9 mRNA in the lungs of the horses. We conclude that TLR9 is expressed in lung cells including PIMs and that the lipopolysaccharide treatment increases TLR9 mRNA expression. The increase in TLR9 mRNA is eliminated by depletion of PIMs, implicating these cells as a major source of TLR9 in the equine lung.

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Immunophenotypic characterization and depletion of pulmonary intravascular macrophages of horses

Cited by 25 publications

References 32 publications

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

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

Pharmacoengineering of Lipid Nanoarchitectonics in Modulating Particle Uptake by Lung Macrophages

Expression of Toll‐Like Receptor 9 in Horse Lungs

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