Histopathologic examination of the rat nasal cavity

Young, John T.

doi:10.1016/s0272-0590(81)80037-1

Cited by 371 publications

(74 citation statements)

References 6 publications

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“…Whole heads were prepared for immunohistochemical examination as described previously (Banger et al 1994). After decalcification, heads were sectioned transversely into the four levels described by Young (1981) and were embedded in wax. ETs were fixed in Bouin's fixative for 48 h, decalcified in saturated ethylenediaminetetraacetic acid, pH 7.4 for 5 days and embedded in wax.…”

Section: Preparation and Treatment Of Tissuesmentioning

confidence: 99%

Heat shock protein 70 in the rat nasal cavity: localisation and response to hyperthermia

Simpson

Alexander

Reed

2004

Archives of Toxicology

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Heat shock proteins (HSPs) are a group of proteins that are rapidly induced in response to physiological stress, including hyperthermia and exposure to toxicants. Thus they may provide a useful index of toxicity in in vitro systems for screening for toxicity. We have recently developed a rat nasal explant system for investigating upper respiratory tract toxicity, and the aims of this study were to localise HSP70 within the rat nasal cavity and to characterise its response to hyperthermia. Constitutively, HSP70 was found to be predominantly localised to the sustentacular cells, basal cells and Bowman's glands of the olfactory epithelium (OE), with the most intense immunohistochemical staining at levels 3 and 4 of the posterior of the rat nasal cavity. Ethmoturbinates (ETs) and liver slices were exposed to heat shock (37 degrees and 43 degrees C, respectively) for 45 min and then returned to normal culture temperatures (31 degrees and 37 degrees C, respectively) for 24 h. In ETs, HSP72 was maximally induced 4-fold at 4 h after heat shock, and levels then returned to those of control tissue. ATP concentrations were markedly decreased up to 4 h after heat shock and then returned to control levels. In contrast, HSP72 levels in liver slices increased and ATP levels decreased steadily throughout the 24 h culture period. ETs were also able to withstand a 45-min heat shock at 43 degrees C, that is 12 degrees C above normal culture temperature. Incubation of ETs with cycloheximide prior to heat shock reduced the ability of the OE to recover from heat shock at 37 degrees C. Thus the OE of the rat nasal cavity expresses HSP72, and this protein appears to play an important role in the ability of the tissue to withstand hyperthermia.

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Section: Preparation and Treatment Of Tissuesmentioning

confidence: 99%

Heat shock protein 70 in the rat nasal cavity: localisation and response to hyperthermia

Simpson

Alexander

Reed

2004

Archives of Toxicology

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“…Paraffin sections (5 lm) were stained with hematoxylin and eosin or used for immunohistochemistry; methacrylate sections (2 lm) were stained with hematoxylin and periodic acid-Schiff (PAS) or with Toluidine blue. Immunohistochemistry Nasal tissue sections from level 2-4 (Young 1981) were deparaffinized. The sections were then rinsed in phosphate-buffered saline (PBS) and PBS containing 0.3% Triton X-100 (PBT).…”

Section: Histopathologymentioning

confidence: 99%

Differential effects of olfactory toxicants on olfactory regeneration

Bergman

Östergren²,

Gustafson

et al. 2002

Archives of Toxicology

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The aim was to study the long-term response in the olfactory mucosa of NMRI mice after exposure to the olfactory toxicants dichlobenil (a herbicide) or methimazole (an antithyroid drug). Three and six months after exposure to dichlobenil (2x or 1 x 25 mg/kg i.p.), the dorsomedial part of the olfactory region showed a respiratory metaplasia with abundant invaginations and a fibrotic lamina propria. In contrast, 3 months after exposure to a toxic dose of methimazole (2 x 50 mg/kg i.p.), the olfactory neuroepithelium and lamina propria had been restored. To study the regenerative events, we used an antibody derived against growth-associated protein 43 (GAP-43), which stains immature neurons. To study epithelial differentiation and horizontal basal cells (HBCs) we used an antibody derived against some cytokeratins. Two weeks after methimazole treatment, there was a marked increase of GAP-43-stained cells in the whole olfactory region, which correlated with the observed regeneration at that time. Two weeks after dichlobenil treatment, the damaged atypical epithelium in the olfactory region showed a distinct keratin staining of basal and columnar cells whereas GAP-43-stained cells were not found. Despite a transient increase of GAP-43-stained cells in the border zone between damaged and undamaged olfactory mucosa, an expansion of a normal neuroepithelium into the damaged olfactory region was not detected in the dichlobenil-treated mice. An intact lamina propria is suggested as a prerequisite for repopulation of the neuroepithelium after toxicant-induced injury.

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“…The head was fixed with 10% buffered formalin solution for at least 7 days and then decalcified with formic acid for at least 10 days. In accordance with the methods of Young [18], blocks of the transverse section of the nasal cavity at the second palatal ridge (level 3) were cut and embedded in paraffin blocks. Tissue sections (4 µm) were placed on microscope slides, deparaffinized and stained with Eosinostain ® (Torii Pharmaceutical Co., Ltd., Tokyo, Japan) or hematoxylin and eosin.…”

Section: Methodsmentioning

confidence: 99%

Involvement of Eosinophils in the Early-Phase Allergic Reaction in a Guinea Pig Rhinitis Model

Imai¹,

Miyahara²,

Yamazaki³

et al. 2000

Int Arch Allergy Immunol

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Background: Eosinophils are found in the nasal lavage fluid (NLF) and nasal biopsies of patients with allergic rhinitis after a nasal antigen challenge, and associated not only with a late-phase allergic reaction (LPR) but also an early phase allergic reaction (EPR). Numerous studies have been carried out to clarify the participation of eosinophils in LPR or airway hyperresponsiveness. However, there has been no published report describing in detail the role of eosinophils during EPR. To better understand the involvement of eosinophils in EPR, we studied the effects of repeated antigen challenges on nasal airway responsiveness and eosinophilic inflammation in EPR using a guinea pig rhinitis model. Methods: Nasal airway responsiveness was measured as the nasal airway resistance (NAR) after nasal antigen provocation. Eosinophilic inflammation during EPR was assessed by nasal lavage and histopathological examination using two groups of animals: those in group 1 were subjected to a sensitization pretreatment only, and those in group 2 were subjected to a pretreatment of sensitization followed by repeated nasal challenges. Results: Repeated antigen challenges induced nasal hyperresponsiveness as indicated by a decrease in the antigen provocation dose and a significant increase in NAR. Furthermore, significant increases in eosinophil counts, eosinophil peroxidase (EPO) activity and protein content in NLF during EPR were observed following antigen provocation in group 2. There were significant correlations between the levels of these parameters, and albumin was the most prevalent of the proteins in NLF. Histopathological examination showed that the degree of eosinophil infiltration into the lamina propria of the nasal mucosa of the animals in group 2 was significantly and apparently higher than in group 1. Particularly, epithelial disruption and mucosal edema were significantly elevated after antigen provocation in group 2. Conclusions: These results suggest that chronic eosinophil accumulation is induced by repeated antigen challenges in the nasal tissue, and that once antigen provocation occurs, eosinophils in the tissue are activated and responsible for the amplification of EPR such as vascular permeability and mucosal edema.

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Histopathologic examination of the rat nasal cavity

Cited by 371 publications

References 6 publications

Heat shock protein 70 in the rat nasal cavity: localisation and response to hyperthermia

Heat shock protein 70 in the rat nasal cavity: localisation and response to hyperthermia

Differential effects of olfactory toxicants on olfactory regeneration

Involvement of Eosinophils in the Early-Phase Allergic Reaction in a Guinea Pig Rhinitis Model

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