2.Development of the mucociliary system in the eustachian tube and middle ear: murine model.
Yonsei Medical Journal 1992;33(1):64-71
In order to describe the developmental anatomy of the murine eustachian tube and its related structures, seventy six mice of ages ranging from gestational day 11 to postnatal day 21 were investigated through the light and electron microscopic observations. Development of the ciliated cells was seen concurrently in both the eustachian tube and middle ear on the 16 th gestation day, one day earlier than the epithelial secretory cells appeared in both the eustachian tube and middle ear. The number of ciliated cells and secretory cells increased rapidly after birth. Tubal glands were well identified with evidence of secretory activity around the time of birth. Thus, the findings of this study indicate that the mucociliary defense system starts to develop during the fetal stage and is well established immediately after birth.
Animal
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Animals, Newborn
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Cilia/physiology/ultrastructure
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Epithelium/ultrastructure
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Eustachian Tube/*cytology/embryology/ultrastructure
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Female
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Male
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Mice
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Mice, Inbred BALB C
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Mucous Membrane/physiology/ultrastructure
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Pregnancy
3.The staphylococcal enterotoxin burden determines the ultrastructure of ciliated epithelia and inflammatory changes in maxillary sinus mucosa of rabbits.
Hongqi WEI ; Zhengwen ZHU ; Zhongsheng CAO ; Zhiyong LIU ; Xiaofan WU ; Hui YUAN
Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2014;49(12):1006-1012
OBJECTIVETo investigate the ultrastructure of ciliated epithelia and inflammatory changes upon repeated exposure to staphylococcal enterotoxin A (SEA) of different concentrations in the maxillary sinus mucosa of rabbits.
METHODSThe rabbits were randomly divided into 2 groups (24 rabbits per group): low-dose SEA group and high-dose SEA group. The low-dose SEA group and high-dose SEA group received daily injections of 0.6 ng of SEA (2 ml) and 60 ng of SEA (2 ml) into the left maxillary sinus of rabbits for 28 days, respectively. Concurrent treatment of the right maxillary sinus with normal saline was used as control. Six rabbits chosen randomly in two groups were examined by computed tomography (CT) scans and then sacrificed to obtain the sinus mucosa from the two-side of maxillary sinuses for histological assessment on days 3, 7, 14 and 28. To characterize the inflammatory changes of the sinus mucosa examined using light microscope, hematoxylin and eosin (HE) and toluidine blue staining was performed. Scanning and transmission electron microscopy were performed to observe ultrastructure of ciliated epithelia in the maxillary sinus mucosa. SPSS 13.0 software was used to analyze the data.
RESULTSOn days 14 and 28, CT images showed opacification of the left maxillary sinus in the high-dose SEA group. The percentage of epithelial disruption was (22.73 ± 5.72) % and (30.79 ± 4.30)% in the high-dose SEA group respectively, and were significantly greater than those in the low-dose SEA group (5.12% ± 1.98% and 5.38% ± 1.64%, q value was 10.079 and 19.132) and control group (4.08% ± 1.29% and 4.81% ± 1.62%, q value was 11.016 and 19.592, respectively, all P < 0.01). The subepithelial thickness in the high-dose SEA group was (113.34 ± 14.81)µm and (120.86 ± 12.35) µm respectively, and were significantly different from those of the low-dose SEA group [(71.08 ± 10.39)µm and (81.63 ± 9.32)µm, q value was 8.090 and 8.782] and control group [(37.45 ± 7.67)µm and (38.79 ± 7.68)µm, q value was 15.759 and 19.541, all P < 0.01]. Viewed under the electron microscope, loss of cilia was observed, a few compound cilia and cytoplasmic protrusion were found, an obvious stretching of the endoplasmic reticulum and an obvious turgescence of the mitochondria was also observed. However, in the low-dose SEA group on days 14 and 28, CT scan of the left maxillary sinus showed transparency; light microscopy observations of the maxillary sinus mucosa showed the number of eosinophils was markedly increased as compared with the high-dose SEA and control groups, the differences were significant (q value was 5.871 and 6.766 on day 14, and q value was 7.572 and 8.970 on day 28, respectively, all P < 0.05). But no significant differences were observed in epithelial disruption between the low-dose SEA and the control groups on days 14 and 28 (q value was 1.512 and 0.859 respectively, all P > 0.05); inordinate array and adhesion of cilia was observed, but cilia loss, compound cilia, cytoplasmic protrusions, mitochondrial swelling and endoplasmic reticulum stretching were not found.
CONCLUSIONSSEA may induce allergic inflammation of the sinus mucosa without damaging the structure of ciliated epithelia at low concentration. Whereas SEA impairs the structure of mitochondria and endoplasmic reticulum in ciliated epithelial cells at high concentration, and results in cilia loss and epithelial disruption, which may be one of the main reasons to induce acute sinusitis.
Animals ; Cilia ; drug effects ; physiology ; ultrastructure ; Cost of Illness ; Enterotoxins ; toxicity ; Eosinophils ; Epithelial Cells ; drug effects ; physiology ; ultrastructure ; Leukocyte Count ; Maxillary Sinus ; drug effects ; metabolism ; ultrastructure ; Mucous Membrane ; drug effects ; physiology ; ultrastructure ; Rabbits ; Sinusitis
4.Chemotaxis of Blood Neutrophils from Patients with Primary Ciliary Dyskinesia.
Young Yull KOH ; Yong Han SUN ; Yang Gi MIN ; Je G CHI ; Chang Keun KIM
Journal of Korean Medical Science 2003;18(1):36-41
Primary ciliary dyskinesia is characterized by chronic upper and lower respiratory infections which are caused by the grossly impaired ciliary transport. Since the cilia and neutrophils both utilize microtubular system for their movement, it has been speculated that neutrophil motility such as chemotaxis might be impaired in patients with primary ciliary dyskinesia. Neutrophils were purified from whole blood from 16 patients with primary ciliary dyskinesia and from 15 healthy controls. Chemotactic responses of neutrophils to leukotriene B4 (LTB4), complement 5a (C5a), and formylmethion-ylleucylphenylalanine (fMLP) were examined using the under agarose method. The chemotactic differentials in response to LTB4, C5a, and fMLP in neutrophils from the patient group were significantly lower than the corresponding values in neutrophils from the control group (p<0.05 for all comparisons). The difference in chemotactic index between the two groups was statistically significant for LTB4 and fMLP (p<0.05 for both comparisons), but not for C5a (p=0.20). Neutrophils from patients with primary ciliary dyskinesia showed a decreased chemotactic response as compared with those from normal subjects. It is concluded that the increased frequency of respiratory tract infection in patients with primary ciliary dyskinesia is possibly due to the defective directional migration of neutrophils, as well as to the defective mucociliary clearance of the airways.
Adolescent
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Chemotactic Factors/pharmacology
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Chemotaxis*
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Child
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Cilia/ultrastructure
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Comparative Study
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Complement 5a/pharmacology
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Dose-Response Relationship, Drug
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Dynein ATPase/chemistry
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Human
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Kartagener Syndrome/blood*
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Kartagener Syndrome/classification
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Leukotriene B4/pharmacology
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Male
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N-Formylmethionine Leucyl-Phenylalanine/pharmacology
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Neutrophils/physiology*
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Neutrophils/ultrastructure
5.Cilia in cell signaling and human disorders.
Neil A DULDULAO ; Jade LI ; Zhaoxia SUN
Protein & Cell 2010;1(8):726-736
One of the most widespread cellular organelles in nature is cilium, which is found in many unicellular and multicellular organisms. Formerly thought to be a mostly vestigial organelle, the cilium has been discovered in the past several decades to play critical motile and sensory roles involved in normal organogenesis during development. The role of cilia has also been implicated in an ever increasing array of seemingly unrelated human diseases, including blindness, kidney cysts, neural tube defects and obesity. In this article we review some of the recent developments in research on cilia, and how defects in ciliogenesis and function can give rise to developmental disorders and disease.
Abnormalities, Multiple
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pathology
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Animals
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Cerebellar Diseases
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genetics
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pathology
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Cilia
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physiology
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ultrastructure
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Flagella
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physiology
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Hedgehog Proteins
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metabolism
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Humans
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Models, Animal
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Polycystic Kidney Diseases
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pathology
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Protein Transport
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Signal Transduction
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Wnt Proteins
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metabolism