scholarly journals The Role of Chlamydia pneumoniae Infection in Children With Chronic Sinusitis

2003 ◽  
Vol 129 (10) ◽  
pp. 1094 ◽  
Author(s):  
Anthony Cultrara ◽  
Nira A. Goldstein ◽  
Alexander Ovchinsky ◽  
Tamara Reznik ◽  
Patricia M. Roblin ◽  
...  
1999 ◽  
Vol 5 (5) ◽  
pp. 724-726 ◽  
Author(s):  
Jerome L. Sullivan ◽  
Eugene D. Weinberg

2014 ◽  
Vol 63 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Junxia Zhang ◽  
Haiwei Wang ◽  
Lijun Zhang ◽  
Tengteng Zhang ◽  
Beibei Wang ◽  
...  

Chlamydia pneumoniae infection has been shown to be associated with the development of atherosclerosis by promoting the migration of vascular smooth muscle cells (VSMCs). However, how C. pneumoniae infection induces VSMC migration is not fully understood. A primary role of Ras-related C3 botulinum toxin substrate 1 (Rac1) is to generate a protrusive force at the leading edge that contributes to cell migration. Whether Rac1 activation plays a role in C. pneumoniae infection-induced VSMC migration is not well defined. In the present study, we therefore examined Rac1 activation in C. pneumoniae-infected rat primary VSMCs and the role of Rac1 activation in C. pneumoniae infection-induced VSMC migration. Glutathione S-transferase pull-down assay results showed that Rac1 was activated in C. pneumoniae-infected rat primary VSMCs. A Rac1 inhibitor, NSC23766 (50 µM,) suppressed Rac1 activation stimulated by C. pneumoniae infection, and thereby inhibited C. pneumoniae infection-induced VSMC migration. In addition, C. pneumoniae infection-induced Rac1 activation in the VSMCs was blocked by LY294002 (25 µM), an inhibitor of phosphatidylinositol 3-kinase (PI3K). Taken together, these data suggest that C. pneumoniae infection promotes VSMC migration, possibly through activating Rac1 via PI3K.


Cardiology ◽  
1998 ◽  
Vol 90 (2) ◽  
pp. 83-88 ◽  
Author(s):  
Heiner Daus ◽  
Cem Özbek ◽  
Dagmar Saage ◽  
Bruno Scheller ◽  
Hermann Schieffer ◽  
...  

2003 ◽  
Vol 23 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Satoshi Kuroda ◽  
Tohru Kobayashi ◽  
Nobuaki Ishii ◽  
Jun Ikeda ◽  
Yumiko Shinohe ◽  
...  

Nature ◽  
2008 ◽  
Vol 456 (7218) ◽  
pp. 112-115 ◽  
Author(s):  
Jin Huang ◽  
Cammie F. Lesser ◽  
Stephen Lory

1994 ◽  
Vol 108 (2) ◽  
pp. 135-137 ◽  
Author(s):  
S. W. Hone ◽  
J. Moore ◽  
J. Fenton ◽  
P. K. Gormley ◽  
R. Hone

AbstractChlamydia pneumoniae has been implicated as a cause of tonsillitis and pharyngitis, but the incidence has varied from one to 19 per cent in various studies. We investigated 51 patients admitted to University College Hospital, Galway, with severe tonsillitis. Throat swabs were examined for evidence of Chlamydia pneumoniae using a direct monoclonal antibody test. Blood was taken for serology from 45 patients. A further specimen was taken at six weeks. A control group of 32 blood bank sera was used. Mean hospital stay was three days (one to eight). Five patients (10 per cent) were monospot positive. Chlamydia pneumoniae was identified by direct immunofluorescence on a tonsillar swab from one patient who did not seroconvert. IgG antibody was identified in 13 cases (29 per cent) and in seven of the control group (22 per cent). No serological evidence of recent infection was found. Chlamydia pneumoniae was not found to be a cause of severe acute tonsillitis in our study group.


2016 ◽  
Vol 70 (2) ◽  
Author(s):  
Eduardo Bossone ◽  
Santi Trimarchi ◽  
Gloria Esposito ◽  
Stefano Aliberti ◽  
Rodolfo Citro ◽  
...  

Chlamydia Pneumoniae (CP) infection is strongly associated with coronary artery disease, as well as with atherosclerosis of the carotid and peripheral arteries. However, the role of CP in the pathogenesis of aortic disease remains controversial. Our present experience suggests no correlation between a current infection with C. pneumoniae and acute aortic dissection. Well-designed large prospective studies are needed in order to clarify the pathophysiologic role of CP infection in acute and chronic aortic disease.


2009 ◽  
Vol 2009 ◽  
pp. 1-5 ◽  
Author(s):  
Hem Chandra Jha ◽  
Pragya Srivastava ◽  
Rakesh Sarkar ◽  
Jagdish Prasad ◽  
Aruna Singh Mittal

Plasma inflammatory markers have been shown to be predictors for cardiovascular risk, however, there is no study where the levels of plasma circulatory markers have been evaluated in coronary artery disease patients (CAD pts) positive forC. pneumoniaeIgA and high sensitive C-reactive protein (hsCRP) which may help in better understanding of disease pathogenesis. A total of 192 patients and 192 controls attending the Cardiology Outpatient Department of Safdarjung Hospital were enrolled. The levels of plasma circulatory inflammatory markers were evaluated by ELISA. The levels of circulatory plasma markers (IL-4, IL-8, IL-13, ICAM-1, and VCAM-1) were significantly higher, whereas, levels of IL-10 and IFN-γwere significantly lower in CAD pts compared to healthy controls. The levels of IL-4, IL-8, and ICAM-1 (P=.007, .015, and .048) were significantly higher, however, IL-10 and IFN-γwere significantly lower (P<.001,<.001) inC. pneumoniaeIgA positive CAD pts. The levels of IL-4, IL-8, IL-13, ICAM-1, and VCAM-1 were higher but not significant and levels of IL-10 and IFN-γwere significantly (P<.001,<.001) lower in hsCRP positive CAD pts. Our study suggested that circulatory cytokines, namely, IL-4, IL-8, and adhesive molecules like ICAM-1 were enhanced after infection withC. pneumoniaewhereas in contrast to this IL-10 and IFN-λwere lowered. Suggesting the important role of these cytokines in progression of CAD.


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