scholarly journals Epithelial invasion bySalmonellaTyphiusingSTIV–Metinteraction

2018 ◽  
pp. e12982 ◽  
Author(s):  
Rimi Chowdhury ◽  
Sayan Das ◽  
Atri Ta ◽  
Santasabuj Das
Keyword(s):  
2008 ◽  
Vol 76 (10) ◽  
pp. 4431-4438 ◽  
Author(s):  
Rogier Louwen ◽  
Astrid Heikema ◽  
Alex van Belkum ◽  
Alewijn Ott ◽  
Michel Gilbert ◽  
...  

ABSTRACT Campylobacter jejuni is a frequent cause of bacterial gastroenteritis worldwide. Lipooligosaccharide (LOS) has been identified as an important virulence factor that may play a role in microbial adhesion and invasion. Here we specifically address the question of whether LOS sialylation affects the interaction of C. jejuni with human epithelial cells. For this purpose, 14 strains associated with Guillain-Barré syndrome (GBS), 34 enteritis-associated strains, the 81-176 reference strain, and 6 Penner serotype strains were tested for invasion of two epithelial cell lines. C. jejuni strains expressing sialylated LOS (classes A, B, and C) invaded cells significantly more frequently than strains expressing nonsialylated LOS (classes D and E) (P < 0.0001). To further explore this observation, we inactivated the LOS sialyltransferase (Cst-II) via knockout mutagenesis in three GBS-associated C. jejuni strains expressing sialylated LOS (GB2, GB11, and GB19). All knockout strains displayed significantly lower levels of invasion than the respective wild types. Complementation of a Δcst-II mutant strain restored LOS sialylation and reset the invasiveness to wild-type levels. Finally, formalin-fixed wild-type strains GB2, GB11 and GB19, but not the isogenic Δcst-II mutants that lack sialic acid, were able to inhibit epithelial invasion by viable GB2, GB11, and GB19 strains. We conclude that sialylation of the LOS outer core contributes significantly to epithelial invasion by C. jejuni and may thus play a role in subsequent postinfectious pathologies.


2013 ◽  
Vol 27 (7) ◽  
pp. 805-817 ◽  
Author(s):  
A. L. Correia ◽  
H. Mori ◽  
E. I. Chen ◽  
F. C. Schmitt ◽  
M. J. Bissell

Cancer ◽  
1967 ◽  
Vol 20 (12) ◽  
pp. 2245-2249 ◽  
Author(s):  
Herbert B. Taylor ◽  
Henry J. Norris

2005 ◽  
Vol 8 (5) ◽  
pp. 717-726 ◽  
Author(s):  
Kenneth N. Wallace ◽  
Amy C. Dolan ◽  
Christoph Seiler ◽  
Erin M. Smith ◽  
Shamila Yusuff ◽  
...  

1988 ◽  
Vol 102 (11) ◽  
pp. 1000-1002 ◽  
Author(s):  
R. Herdman ◽  
J. L. W. Wright

Cholesteatoma in children may be a sequel to chronic exudative otitis media with tympanic membrane retraction but he the role of grommets in the possible facilitation of squamous epithelial invasion into the middle ear is not yet clear. A retrospective study was made of the history and prior treatment in 25 children who underwent mastoidectomy for cholesteatoma at St. Mary's Hospital between 1975 and 1986. Thirteen patients had undergone previous middle ear aeration procedures which included myringotomy, cortical mastoidectomy and grommets. There was no difference in the site or severity of cholesteatoma in the operated and non-operated cases. Of the seven patients with a history of multiple grommets three had primarily attic, and three had primarily mesotympanic disease. The latter had greater ossicular erosion. One patient with an intact tympanic membrane had grommet insertion subsequently developed a cholesteatoma. While cholesteatoma due directly to the presence of grommets is rare, it appears that children who require multiple grommet insertions constitute a high risk group and should be very closely monitored.


1983 ◽  
Vol 92 (6) ◽  
pp. 558-560 ◽  
Author(s):  
Joseph Freeman

Extralabyrinthine fractures of the temporal bone offer the opportunity for squamous epithelial invasion of the middle ear, petrous pyramid and mastoid air-cell system as a late complication. Cholesteatoma, secondary acquired in this situation, can be very aggressive and difficult to manage surgically, particularly where the temporal bone air-cell system is well developed. Polytomography is extremely helpful in determining the sites of fracture and in fashioning the surgical approach. Three cases are presented to illustrate the problems in diagnosis and surgical management.


2004 ◽  
Vol 72 (5) ◽  
pp. 2907-2914 ◽  
Author(s):  
Li Fang ◽  
Bogdan J. Nowicki ◽  
Petri Urvil ◽  
Pawel Goluszko ◽  
Stella Nowicki ◽  
...  

ABSTRACT We previously reported that inhibition of nitric oxide (NO) increases the rate of bacteremia and maternal mortality in pregnant rats with uterine infection by Escherichia coli expressing the Dr fimbria (Dr+). Epithelial binding and invasion by Dr+ E. coli has also been shown to be dependent upon the expression level of the cellular receptor decay-accelerating factor (DAF; CD55). Here, we hypothesize that NO-related severity of infection could be mediated by changes in DAF expression and in the rate of epithelial invasion. The cellular basis of NO effects on epithelial invasion with Dr+ E. coli was studied using Ishikawa endometrial carcinoma cells as an in vitro model of the human endometrial epithelium. Initially, we show that Ishikawa cells produce NO and express both NO synthase enzymes, NOS II and NOS III, and DAF protein. We next tested the abilities of both Dr+ E. coli and a Dr− E. coli mutant to invade Ishikawa cells, and invasion was seen only with Dr+ E. coli. Invasion by Dr+ E. coli was decreased by elevated NO production and increased by NO inhibition. Elevated NO production significantly decreased DAF protein and mRNA expression in Ishikawa cells in a time- and dose-dependent manner. Here, we propose that in vitro invasion of an epithelial cell line is directly related to NO-regulated expression of DAF. The significance of NO-regulated receptor-ligand invasion is that it may represent a novel unrecognized phenomenon of epithelial defense against infection.


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