scholarly journals Chlamydia Pneumoniae in Asymptomatic Carotid Atherosclerosis

2006 ◽  
Vol 19 (1) ◽  
pp. 205873920601900 ◽  
Author(s):  
R. Sessa ◽  
M. DI Pietro ◽  
G. Schiavoni ◽  
M. Galdiero ◽  
P. Cipriani ◽  
...  

We evaluated, in 415 patients with asymptomatic carotid atherosclerosis: (i) the prevalence of C. pneumoniae DNA in atherosclerotic carotid plaques and peripheral blood mononuclear cells (PBMC); (ii) the distribution of C. pneumoniae in atherosclerotic carotid plaques and PBMC from the same patients; (iii) the correlation between circulating anti-chlamydial antibodies and the presence of C. pneumoniae DNA. Overall, 160 atherosclerotic carotid plaques and 174 PBMC specimens from patients with asymptomatic carotid atherosclerosis were examined by ompA nested touchdown PCR for presence of C. pneumoniae. In addition, C. pneumoniae DNA was detected in 81 specimens of atherosclerotic carotid plaque and PBMC obtained from the same patients. C. pneumoniae DNA was found in 36.9% of atherosclerotic carotid plaques and in 40.2% of PBMC specimens examined (P=NS). With regard to 81 patients, C. pneumoniae DNA was detected in 27.2% of atherosclerotic carotid plaques and in 44.4% of PBMC specimens (P=0.05). In 18 patients, the presence of C. pneumoniae DNA in PBMC specimens and atherosclerotic carotid plaques coincided (P=0.005). No statistically significant association was found between anti-C pneumoniae antibodies (IgG and IgA) and positive PCR results. In conclusion, our results suggest that the detection of C. pneumoniae DNA in PBMC specimens seems to be a first-choice method to identify the patients at risk for endovascular chlamydial infection.

1993 ◽  
Vol 95 (5) ◽  
pp. 499-504 ◽  
Author(s):  
Sandra L. Melnick ◽  
Eyal Shahar ◽  
Aaron R. Folsom ◽  
J.Thomas Grayston ◽  
Paul D. Sorlie ◽  
...  

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S758-S758
Author(s):  
Aviva Szigeti ◽  
Margaret Hammerschlag ◽  
Diana Weaver ◽  
Tamar Smith-Norowitz ◽  
Stephan Kohlhoff

Abstract Background Chlamydia pneumoniae (Cpn) is unique in its ability to cause chronic infections, potentially triggering asthma exacerbations as well as subsequent asthma development. Th1-mediated immunity and IFN-γ are critical for clearing chlamydial infections. Persistent or recent Cpn infection may be identified in vitro by detecting T-helper cytokine IFN-γ produced by peripheral blood mononuclear cells (PBMC) stimulated by Cpn. Inhaled corticosteroids (ICS) may have an inhibitory effect on IFN-γ. Prior studies have shown increased Th2 responses upon in vitro Cpn stimulation with increased age. Our aim was to determine whether age and inhaled corticosteroid (ICS) use affect Cpn-induced PBMC produced IFN-γ levels. Methods Pediatric and adult subjects with (n = 23) and without (n = 10) asthma were enrolled. PBMC obtained from all subjects were stimulated with Cpn (MOI = 0.1 x48h) in vitro. IFN-γ levels in culture supernatants were determined by ELISA and reported as pg/mL. Nasopharyngeal (NP) swabs were tested for Cpn using Real-Time PCR. Statistical analysis for continuous variables was performed using the Mann–Whitney U test. Results None of the subjects were positive for Cpn by PCR on NP swab. Levels of IFN-γ produced by PBMC stimulated by Cpn were similar between asthmatic vs. control subjects (41.7 vs. 68.8, respectively; P = 0.72) and between pediatric and adult subjects with asthma (IFN-γ 54 vs. 20.1 respectively, P = 0.95). Pediatric subjects with asthma who received ICS had lower IFN-γ levels than those who did not (median IFN-γ 25.5 vs. 209; P = 0.003). Conclusion Our finding of lower IFN-γ levels among asthma patients on ICS compared with those not on ICS suggests that ICS use may dampen the systemic inflammatory response. While we did not find a statistically significant difference between pediatric and adult age groups in this pilot study, there was a trend to higher Cpn-induced IFN-γ levels among younger pediatric subjects. Future prospective studies should further define predictors of diminished IFN-γ responses in patients with asthma. Disclosures All authors: No reported disclosures.


2016 ◽  
Vol 77 (5) ◽  
pp. 382-388 ◽  
Author(s):  
Tamar A. Smith-Norowitz ◽  
Kobkul Chotikanatis ◽  
David P. Erstein ◽  
Jason Perlman ◽  
Yitzchok M. Norowitz ◽  
...  

2020 ◽  
Vol 88 (7) ◽  
Author(s):  
Mads Lausen ◽  
Mathilde Selmar Pedersen ◽  
Nareen Sherzad Kader Rahman ◽  
Liv Therese Holm-Nielsen ◽  
Faduma Yahya Mohamed Farah ◽  
...  

ABSTRACT The human respiratory tract pathogen Chlamydia pneumoniae, which causes mild to severe infections, has been associated with the development of chronic inflammatory diseases. To understand the biology of C. pneumoniae infections, several studies have investigated the interaction between C. pneumoniae and professional phagocytes. However, these studies have been conducted under nonopsonizing conditions, making the role of opsonization in C. pneumoniae infections elusive. Thus, we analyzed complement and antibody opsonization of C. pneumoniae and evaluated how opsonization affects chlamydial infectivity and phagocytosis in human monocytes and neutrophils. We demonstrated that IgG antibodies and activation products of complement C3 and C4 are deposited on the surface of C. pneumoniae elementary bodies when incubated in human serum. Complement activation limits C. pneumoniae infectivity in vitro and has the potential to induce bacterial lysis by the formation of the membrane attack complex. Coculture of C. pneumoniae and freshly isolated human leukocytes showed that complement opsonization is superior to IgG opsonization for efficient opsonophagocytosis of C. pneumoniae in monocytes and neutrophils. Neutrophil-mediated phagocytosis of C. pneumoniae was crucially dependent on opsonization, while monocytes retained minor phagocytic potential under nonopsonizing conditions. Complement opsonization significantly enhanced the intracellular neutralization of C. pneumoniae in peripheral blood mononuclear cells and neutrophils and almost abrogated the infectious potential of C. pneumoniae. In conclusion, we demonstrated that complements limit C. pneumoniae infection in vitro by interfering with C. pneumoniae entry into permissive cells by direct complement-induced lysis and by tagging bacteria for efficient phagocytosis in both monocytes and neutrophils.


2002 ◽  
Vol 126 (4) ◽  
pp. 415-416 ◽  
Author(s):  
Anne Pitkäranta ◽  
Antti Vaheri ◽  
Tuula Penttilä ◽  
Mirja Puolakkainen

The cause of Bell's palsy remains unknown even though available evidence suggests that infection could be a factor. In recent studies, Chlamydia pneumoniae has been associated with neurologic diseases such as multiple sclerosis. In the present study, the association of C pneumoniae with Bell's palsy was studied with the use of serology and polymerase chain reaction to test tear fluid and peripheral blood mononuclear cells from 21 patients with Bell's palsy and 21 control subjects. C pneumoniae DNA was detected from tear fluid samples in 1 patient with Bell's palsy and in 2 healthy control subjects. Whether this indicates earlier disease or subclinical infection remains to be studied. However, an association between Bell's palsy and acute C pneumoniae infection could not be shown.


Transfusion ◽  
2004 ◽  
Vol 44 (7) ◽  
pp. 1072-1078 ◽  
Author(s):  
Hiroyuki Yamaguchi ◽  
Masako Yamada ◽  
Tomonori Uruma ◽  
Masato Kanamori ◽  
Hajime Goto ◽  
...  

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