1.Nasal mucosa remodeling in guinea pig model of allergic rhinitis.
Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2006;41(1):48-53
OBJECTIVETo explore the feature of nasal mucosa remodeling in experimental allergic rhinitis.
METHODSTwenty-four male Hartley guinea pigs (4 weeks, 250 -300 g) were randomly divided into four groups (control group and allergen exposure groups 1 - 3), each group had 6 guinea pigs. Allergen exposure animals were sensitized by intraperitoneal (ip) injection of ovalbumin (OVA). Sensitized guinea pigs were subjected to either brief or prolonged exposure to allergen. Both brief exposure group (allergen exposure groups) and prolonged exposure group (allergen exposure group 2 and 3) received a daily intranasal challenge with 5% OVA in 0.9% saline from Day 22 to Day 28, the prolonged exposure group (allergen exposure group 2 and 3) followed by twice weekly exposure to 5% OVA intranasal for an additional 8 and 12 weeks respectively. Control animals were given saline only. At 24 h after the last intranasal challenge, the guinea pigs were killed and the heads of the animals were removed and fixed in 10% neutral buffered formalin for 24 hours, then decalcified in 5% trichloroacetic acid for 10 days. The tissue blocks were embedded in paraffin. The paraffin sections 3 microm thick were stained with hematoxylin and eosin (HE), alcian blue (pH, 2. 6)-periodic acid-Schiff (AB-PAS), and Masson's Trichrome (MT). The infiltrating eosinophils in nasal mucosa were examined, AB-PAS-positive cells in the surface epithelium in nasal septal mucosa were counted. The percentage area of MT stained extracellular matrix in septal mucosa and conchae and damage of epithelium were determined by an image analyzer.
RESULTSThe control group only presented a few eosinophils. Significant eosinophil infiltration was observed in the sensitized groups. Compared with control group (intact epithelium 87.7% +/- 11.1%), there was no significant epithelial damage in 1 week exposure group. Significant epithelial damage were observed in 8 and 12 weeks groups (intact epithelium 36.7% +/- 16.9%, 37.9% +/- 12.9%, respectively). An increase in AB-PAS-positive cells was observed in the mucosa of nasal septum in the prolonged allergen exposure groups, but not in the brief allergic inflammation group in comparison with the control. The brief OVA exposure group did not show increased collagen fibrils within the mucosa of nasal septum and conchae. In contrast, after prolonged OVA exposure an increase in matrix was observed. Furthermore, in both the nasal septum and conchae, significant increasing of ECM deposition was found in a further prolonged exposure for 12 weeks compared to 8 weeks.
CONCLUSIONSEpithelial damage, goblet cells hyperplasia and extracellular matrix deposition were observed as the features of remodeling in this guinea pig model of allergic rhinitis.
Animals ; Disease Models, Animal ; Eosinophils ; immunology ; Epithelial Cells ; pathology ; Extracellular Matrix ; pathology ; Goblet Cells ; pathology ; Guinea Pigs ; Male ; Mice ; Nasal Mucosa ; cytology ; pathology ; Rhinitis, Allergic, Perennial ; immunology ; pathology
2.STAT6 Expression and IL-13 Production in Association with Goblet Cell Hyperplasia and Worm Expulsion of Gymnophalloides seoi from C57BL/6 Mice.
Jin Joo LEE ; Donghee KIM ; Kyoung Ho PYO ; Min Ki KIM ; Hyo Jin KIM ; Jong Yil CHAI ; Eun Hee SHIN
The Korean Journal of Parasitology 2013;51(5):589-594
In intestinal helminth infections, Th2 immune respones are generally associated with mucin secretion for worm expulsion from the host intestine. In particular, IL-4 and IL-13 are the important cytokines related with intestinal mucus production via STAT6 signalling in nematode infections. However, this perspective has never been studied in Gymnophalloides seoi infection. The present study aimed to observe the STAT6 signalling and cytokine responses in C57BL/6 mice, a mouse strain resistant to infection with this trematode. The results showed that worm expulsion occurred actively during days 1-2 post-infection (PI), when goblet cells began to proliferate in the small intestine. The STAT6 gene expression in the mouse spleen became remarkable from day 2 PI. Moreover, G. seoi infection induced a significant increase of IL-13 from day 4 PI in the spleen of infected mice. Our results suggested that goblet cell hyperplasia and worm expulsion in G. seoi-infected mice should be induced by STAT6 signalling, in which IL-13 may be involved as a dominant triggering cytokine.
Animals
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Crassostrea
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Female
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Goblet Cells/*pathology
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Hyperplasia/pathology
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Interleukin-13/*metabolism
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Interleukin-4/*metabolism
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Intestine, Small/immunology
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Metacercariae
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Mice
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Mice, Inbred C57BL
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STAT6 Transcription Factor/*metabolism
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Signal Transduction
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Specific Pathogen-Free Organisms
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Spleen/immunology
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Trematoda/*immunology
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Trichinellosis/*immunology/parasitology
3.Establishment and evaluation of the SD rat allergic rhinitis model.
Journal of Clinical Otorhinolaryngology Head and Neck Surgery 2015;29(15):1372-1374
OBJECTIVE:
To investigate method established and system evaluated in the model of SD rat with AR.
METHOD:
To establish AR model of SD rats by ovalbumin (OVA), 20 cases of SD rats were randomly divided into two groups, namely control group (10 cases) and AR group (10 cases). AR models were sensitized and challenged by OVA. Control group were used with normal saline instead of OVA. The score of pathology and praxiology were observed when the SD rats in AR group appeared typical symptom of allergic rhinitis, and levels of IL-4, IFN-γ, IgE in the serum were examined by ELISA. According to the behavioral score, nasal histology and content of IL-4, IFN-γ, IgE of serum, Rat allergic rhinitis model were judged successfully established or not.
RESULT:
Behavioral scores were significantly increased in OVA-challenged rats compared with the control group, P<0.05. Nasal epithelial goblet cells, eosinophils and lymphocytes in nasal mucosa in the AR rats exhibited obvious increase relative to the control group. IL-4, IgE levels in the AR rat exhibited obvious increase relative to control group while INF-γ levels exhibited obvious reduction (P<0.05).
CONCLUSION
The allergic rhinitis models in SD rat by OVA were successfully established. The levels of IgE, INF-γ and IL-4 in Serum can be used as objective evaluation of animal models of allergic rhinitis established successfully or not.
Animals
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Disease Models, Animal
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Enzyme-Linked Immunosorbent Assay
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Eosinophils
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immunology
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Goblet Cells
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immunology
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Immunoglobulin E
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blood
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Interferon-gamma
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blood
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Interleukin-4
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blood
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Nasal Mucosa
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cytology
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pathology
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Ovalbumin
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Rats
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Rats, Sprague-Dawley
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Rhinitis, Allergic
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physiopathology
4.Mucosal Immune Responses of Mice Experimentally Infected with Pygidiopsis summa (Trematoda: Heterophyidae).
Jong Yil CHAI ; Young Jin PARK ; Jae Hwan PARK ; Bong Kwang JUNG ; Eun Hee SHIN
The Korean Journal of Parasitology 2014;52(1):27-33
Mucosal immune responses against Pygidiopsis summa (Trematoda: Heterophyidae) infection were studied in ICR mice. Experimental groups consisted of group 1 (uninfected controls), group 2 (infection with 200 metacercariae), and group 3 (immunosuppression with Depo-Medrol and infection with 200 metacercariae). Worms were recovered in the small intestine at days 1, 3, 5, and 7 post-infection (PI). Intestinal intraepithelial lymphocytes (IEL), mast cells, and goblet cells were counted in intestinal tissue sections stained with Giemsa, astra-blue, and periodic acid-Schiff, respectively. Mucosal IgA levels were measured by ELISA. Expulsion of P. summa from the mouse intestine began to occur from days 3-5 PI which sustained until day 7 PI. The worm expulsion was positively correlated with proliferation of IEL, mast cells, goblet cells, and increase of IgA, although in the case of mast cells significant increase was seen only at day 7 PI. Immunosuppression suppressed all these immune effectors and inhibited worm reduction in the intestine until day 7 PI. The results suggested that various immune effectors which include IEL, goblet cells, mast cells, and IgA play roles in regulating the intestinal mucosal immunity of ICR mice against P. summa infection.
Animals
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Disease Models, Animal
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Enzyme-Linked Immunosorbent Assay
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Goblet Cells/immunology
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Heterophyidae/*immunology
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*Immunity, Mucosal
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Immunoglobulin A/analysis
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Intestine, Small/parasitology/pathology
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Leukocyte Count
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Lymphocytes/immunology
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Male
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Mast Cells/immunology
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Mice
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Mice, Inbred ICR
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Parasite Load
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Time Factors
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Trematode Infections/*immunology/parasitology