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Mucosal Epithelia (mucosal + epithelia)
Selected AbstractsChlamydiae and polymorphonuclear leukocytes: unlikely allies in the spread of chlamydial infectionFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2008Roger G. Rank Abstract While much is known about the attachment of the chlamydiae to the host cell and intracellular events during the developmental cycle, little is known about the mechanism(s) by which elementary bodies exit the cell. In this report, we use the guinea-pig conjunctival model of Chlamydia caviae infection to present in vivo ultrastructural evidence supporting two mechanisms for release of chlamydiae from the mucosal epithelia. Four days after infection, histopathologic observation shows an intense infiltration of polymorphonuclear leukocytes (PMN) in the conjunctival epithelium. Using transmission electron microscopy, a gradient-directed PMN response to chlamydiae-infected epithelial cells was observed. As PMN infiltration intensifies, epithelial hemidesmosome/integrin/focal adhesion adherence with the basal lamina is disconnected and PMNs literally lift off and release infected superficial epithelia from the mucosa. Many of these infected cells appear to be healthy with intact microvilli, nuclei, and mitochondria. While lysis of some infected cells occurs with release of chlamydiae into the extracellular surface milieu, the majority of infected cells are pushed off the epithelium. We propose that PMNs play an active role in detaching infected cells from the epithelium and that these infected cells eventually die releasing organisms but, in the process, move to new tissue sites via fluid dynamics. [source] Preliminary study of chemical bile duct embolization to treat hepatolithiasis in rabbitsJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2006Fu Yu Li Abstract Background:, The high recurrence rate of hepatolithiasis is still a problem to be solved. The purpose of the present study was therefore to carry out a preliminary study of the practical value of chemical bile duct embolization (CBDE) to treat hepatolithiasis in rabbits. Methods:, Chemical bile duct embolization was performed with phenol or absolute ethanol along with N -butyl-cyanoacrylate. The feasibility and effectiveness of CBDE for chemical hepatectomy was assessed by investigating histological changes, biochemistry for hydroxyproline and in situ hybridization for collagen I. Results:, Histologically, the mucosal epithelia of the embolized bile ducts were entirely replaced by collagen fibers, thus effectively eradicating chronic proliferative cholangitis. Also of note, the diseased biliary duct lumens were completely filled with N -butyl-cyanoacrylate, thus effectively preventing calculus formation. The hepatocytes also disappeared completely in the periphery of the embolized lobe, demonstrating that the desired effects of chemical hepatectomy were achieved through CBDE. In a further comparison of embolizing agents, the phenol-cyanoacrylate embolized livers and bile ducts had a higher level of hydroxyproline and collagen I than those embolized with ethanol plus cyanoacrylate. Conclusion:, Chemical bile duct embolization is a promising approach to prevent the recurrence of hepatolithiasis and to achieve the effect of chemical hepatectomy. [source] Dysplasia and carcinoma development in a repeated dextran sulfate sodium-induced colitis modelJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2002Isao Okayasu Abstract Background: As an important mechanism underlying the increased risk of colorectal carcinoma development in patients with long-standing ulcerative colitis, promotion as a result of the regenerative process has been proposed. In the present study, a dysplasia-carcinoma sequence in a novel repeated colitis model in mice is documented. Methods: Repeated colitis was induced by nine administration cycles of 3% dextran sulfate sodium (DSS; molecular weight, 54 000): each administration cycle comprised 3% DSS for 7 days followed by distilled water for the subsequent 14 days, to give conditions similar to the clinically observed active and remission phases in humans. Results: Multiple colorectal tumors (nine low- and four high-grade dysplasias and two carcinomas) developed in 25 mice. These neoplastic lesions consisted of tubular structures, presenting as various types of elevated, flat and depressed tumor, similar to those in ulcerative colitis patients. A time-course study with assessment of the severity of colitis and in vivo bromodeoxyuridine uptake during a single 3% DSS administration cycle revealed a high level of regenerative activity in the colitis-affected mucosal epithelia. Conclusion: Thus, with the present repeated colitis model, regeneration and neoplastic lesions were apparent, the biological features of which provide evidence of a colorectal dysplasia,invasive carcinoma sequence in ulcerative colitis. [source] Influences of Helicobacter pylori on gastric angiogenesis and ulcer healing in miceJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2002Edhi Gunawan Abstract Background and Aims:Helicobacter pylori infection is associated with peptic ulcers; however, it is unclear whether the bacterium delays ulcer healing. We investigated the influence of H. pylori on ulcer healing in mice. We also examined the influence of H. pylori infection on angiogenesis. Methods: An acetic acid ulcer was made in male BALB/c mice. Three days later (day 0), the animals were inoculated with H. pylori SS1 strain. The healing process of the ulcer was examined macroscopically and microscopically on days 0, 6 and 9. The index of angiogenesis was also determined using carmine dye injection. Results: On day 0, angiogenesis began at the ulcer margin while the mucosal epithelia had not yet regenerated. On days 6 and 9, angiogenesis and epithelial regeneration developed and ulcer size reduced. These phenomena were significantly suppressed in mice infected with H. pylori. Conclusion:Helicobacter pylori infection significantly suppressed angiogenesis and delayed ulcer healing. These results indicate that H. pylori plays an important role in ulcer healing. © 2002 Blackwell Publishing Asia Pty Ltd [source] Histopathological varieties of oral carcinoma in situ: Diagnosis aided by immunohistochemistry dealing with the second basal cell layer as the proliferating center of oral mucosal epitheliaPATHOLOGY INTERNATIONAL, Issue 3 2010Takanori Kobayashi To make reproducible diagnoses for oral carcinoma in situ (CIS), combined immunohistochemistry directed at the positioning of squamous cell proliferation (Ki-67) and differentiation (keratin (K) 13 and K19) was used, both of which support histological evaluations by providing biological evidence. Normal/hyperplastic epithelia was defined by K19+ cells only in the first basal layer, K13+ cells in the third basal and upper layers, and sporadic Ki-67+ cells in the second basal layer. These profiles indicated that a proliferating center of the oral epithelium is located in the parabasal cell layer, and K19 and K13 can be regarded as markers for basal and prickle cells, respectively. Epithelial dysplasia was characterized by irregular stratification of Ki-67+ cells and the absence of K19/K13 in proliferating cells. Irregular emerging of K19+ and K13+ cells in proliferating foci with unique stratification of atypical Ki-67+ cells indicated CIS. When the definition was applied, surgical margins in 172 recurrent cases were shown to contain CIS (39.4%) and squamous cell carcinoma (55.8%), indicating that the new diagnostic criteria for CIS reflected clinical behaviors of the cases. The results indicate that oral CIS contain more histological variations, especially those with definite keratinization, than what had been previously defined. [source] Identification of MUC5B Mucin Gene in Human Middle Ear With Chronic Otitis Media,THE LARYNGOSCOPE, Issue 4 2000Hirokazu Kawano MD Objectives To identify the mucin gene and its expressing cells in the middle ear mucosa with chronic otitis media (COM), and to study the correlation between infiltration of inflammatory cells in the submucosa and expression of the mucin gene in the mucosal epithelium with COM. Study Design Middle ear mucosal specimens removed from the inferior promontory area of 19 patients undergoing middle ear surgery for COM were studied. Methods Sections were stained with H&E, Alcian blue-periodic acid Schiff (AB-PAS), polyclonal MUC5B antibody, and specific MUC5B riboprobe for histological, histochemical, immunohistochemical, and mucin mRNA analyses. Results H&E staining revealed pseudostratified epithelia in 18 of the middle ear specimens with COM and cuboidal secretory epithelia in one. AB-PAS staining of epithelia revealed abundant secretory cells and their products (glycoconjugates). In situ hybridization and immunohistochemistry studies demonstrated that the secretory cells of the middle ear mucosa with COM expressed MUC5B mucin mRNA and its product MUC5B mucin. Conclusions The MUC5B mucin gene and its product were identified in the middle ear secretory cells of patients with COM. Its e-pression was e-tensive in pseudostratified mucosal epithelia and related to infiltration of inflammatory cells in the submucosa of the middle ear cleft with COM, suggestive that inflammatory cell products are involved in the production of MUC5B. [source] The natural history of human papillomavirus infections of the mucosal epitheliaAPMIS, Issue 6-7 2010LOUISE T. CHOW Chow LT, Broker TR, Steinberg BM. The natural history of human papillomavirus infections of the mucosal epithelia. APMIS 2010; 118: 422,449. Human papillomaviruses (HPVs), members of a very large family of small DNA viruses, cause both benign papillomas and malignant tumors. While most research on these viruses over the past 30 years has focused on their oncogenic properties in the genital tract, they also play an important role in diseases of the upper aerodigestive tract. Rapidly accelerating advances in knowledge have increased our understanding of the biology of these viruses and this knowledge, in turn, is being applied to new approaches to prevent, diagnose, and treat HPV-induced diseases. In this introductory article, we provide an overview of the structure and life cycle of the mucosal HPVs and their interactions with their target tissues and cells. Finally, we provide our thoughts about treatments for HPV-induced diseases, present and future. [source] Interaction of viral oncoproteins with cellular target molecules: infection with high-risk vs low-risk human papillomavirusesAPMIS, Issue 6-7 2010DAVID PIM Pim D, Banks L. Interaction of viral oncoproteins with cellular target molecules: infection with high-risk vs low-risk human papillomaviruses. APMIS 2010; 118: 471,493. Persistent infection by a subgroup of so-called high-risk human papillomaviruses (HPVs) that have a tropism for mucosal epithelia has been defined as the cause of more than 98% of cervical carcinomas as well as a high proportion of other cancers of the anogenital region. Infection of squamous epithelial tissues in the head and neck region by these same high-risk HPVs is also associated with a subset of cancers. Despite the general conservation of genetic structure amongst all HPV types, infection by the low-risk types, whether in genital or head and neck sites, carries a negligible risk of malignant progression, and infections have a markedly different pathology. In this review, we will examine and discuss the interactions that the principal viral oncoproteins of the high-risk mucosotrophic HPVs and their counterparts from the low-risk group make with cellular target proteins, with a view to explaining the differences in their respective pathology. [source] Neonatal pemphigus vulgaris with extensive mucocutaneous lesions from a mother with oral pemphigus vulgarisBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2002A. Campo-Voegeli Summary The clinical phenotype of pemphigus is well explained by the combination of desmoglein (Dsg) 1 and Dsg3 distribution pattern and antiDsg autoantibody profile (Dsg compensation theory). It has been reported that neonatal skin has a similar Dsg distribution pattern to adult mucosal epithelia. We describe a newborn girl with mucocutaneous pemphigus vulgaris (PV) from a mother with mucosal dominant PV. The mother had had painful oral erosions for at least 7 months. Histopathological examination and direct and indirect immunofluorescence studies confirmed the diagnosis of PV and neonatal PV in the mother and daughter, respectively. The mother had a high titre of anti-Dsg3 IgG and a low titre of antiDsg1 IgG, while the neonate had only a high titre of anti-Dsg3 IgG, but no detectable antiDsg1 IgG. AntiDsg3 IgG, which caused the oral dominant phenotype in the mother, induced extensive oral as well as cutaneous lesions in the neonate. Our case provides clinical evidence for the Dsg compensation theory in neonatal PV. [source] | ||||||||||