Detection of Chlamydia pneumoniae but not of Helicobacter pylori in symptomatic atherosclerotic carotids associated with enhanced serum antibodies, inflammation and apoptosis rate.
OBJECTIVE
Numerous seroepidemiological and pathological studies linked Chlamydia pneumoniae and Helicobacter pylori with atherosclerosis. However, analyses of these infectious agents in the pathogenesis of stroke are either lacking or contradictory. Therefore, we evaluated the detection rate of C. pneumoniae and H. pylori in normal carotids vs. atherosclerotic carotids and compared these findings with serology, plaque morphology, inflammatory cell infiltrates and apoptosis rate.


METHODS
The study was performed on 40 morphological normal carotids from autopsy and 20 advanced atherosclerotic carotids from endarterectomy after stroke. Serum IgG antibody titre was measured by enzyme immunoassay (H. pylori) and microimmunofluorescence (MIF) technique (C. pneumoniae). Immunohistochemistry (IHC) and Western blotting were performed to identify C. pneumoniae, H. pylori, to characterize plaque morphology (macrophages and smooth muscle cells) and the inflammatory infiltrate (T- and B cells) and to detect apoptosis (TUNEL staining).


RESULTS
C. pneumoniae was found significantly more frequently in atherosclerotic than in normal carotids (P=0.001), which correlated with elevated C. pneumoniae IgG-antibody titres (P=0.048). Although H. pylori was not detected in carotids, elevated H. pylori antibody titres were significantly associated with the degree of atherosclerosis (P=0.001). The C. pneumoniae infected carotids displayed a slightly enhanced infiltrate of T cells and apoptosis rate, but no morphological changes.


CONCLUSIONS
C. pneumoniae but not H. pylori, was detected by IHC primarily in symptomatic carotids, without specific morphological differences. Correlation of C. pneumoniae in-situ-detection and IgG antibodies suggested a possible connection between respiratory-tract and endovascular infection. The C. pneumoniae associated T-lymphocytes and apoptosis rate indicate an immune-mediated inflammatory process, involving vascular walls.
Neureiter
Daniel
D
Institute of Pathology, University of Erlangen-Nuremberg, Krankenhausstr. 8-10, Germany. daniel.neureiter@patho.imed.uni-erlangen.de
Heuschmann
Peter
P
Stintzing
Sebastian
S
Kolominsky-Rabas
Peter
P
Barbera
Letterio
L
Jung
Andreas
A
Ocker
Matthias
M
Maass
Matthias
M
Faller
Gerhard
G
Kirchner
Thomas
T
D000368:Aged; D000369:Aged, 80 and over; D000907:Antibodies, Bacterial / Q000097:blood* / Q000276:immunology*; D000918:Antibody Specificity / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology / Q000378:metabolism; D017209:Apoptosis / Q000502:physiology*; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000097:blood* / Q000276:immunology / Q000382:microbiology*; D002455:Cell Division / Q000502:physiology; D023521:Chlamydophila Infections / Q000097:blood* / Q000276:immunology / Q000382:microbiology*; D016993:Chlamydophila pneumoniae / Q000276:immunology*; D005260:Female; D005858:Germany; D016481:Helicobacter Infections / Q000097:blood* / Q000276:immunology / Q000382:microbiology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D007150:Immunohistochemistry; D007249:Inflammation / Q000097:blood* / Q000382:microbiology*; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D032389:Myocytes, Smooth Muscle / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D011446:Prospective Studies; D013223:Statistics as Topic
D000907:Antibodies, Bacterial; D000945:Antigens, Differentiation, T-Lymphocyte; D007074:Immunoglobulin G