Chlamydia LPS and MOMP seropositivity are associated with different cytokine profiles in patients with coronary heart disease.
BACKGROUND
Persistent Chlamydia pneumoniae infection within atherosclerotic plaques are possible stimulators of inflammation in atherosclerosis. Why the microbe develops persistency in some individuals is unknown, but experimental studies in cell cultures and animals have demonstrated the levels of gamma interferon (IFNgamma) and interleukin 10 (IL-10) to be of crucial importance.


METHODS
We wanted to evaluate whether Chlamydia seropositivity in patients with coronary heart disease (CHD) (n = 193) was associated with elevated IFNgamma and IL-10. Two methods for detection of Chlamydia antibodies were included as well as analysis of tumour necrosis factor alpha (TNFalpha), soluble vascular cell adhesion molecule 1 (sVCAM-1) and soluble E-selectin for the evaluation of vascular inflammation.


RESULTS
We found that patients with IgA antibodies towards Chlamydia lipopolysaccharide (LPS) had elevated levels of IFNgamma (P = 0.048), IL-10 (P = 0.029), TNFalpha (P = 0.009) and sE-selectin (P = 0.045), while Chlamydia LPS IgG seropositivity predicted elevated levels of IL-10 (P = 0.013). Patients with IgA antibodies towards C. pneumoniae major outer membrane protein (MOMP) without simultaneous LPS IgA seropositivity had lower levels of IFNgamma and sVCAM-1 when compared to patients with Chlamydia LPS IgA alone (P = 0.005 for IFNgamma, P = 0.016 for VCAM-1) and patients with combined Chlamydia MOMP and LPS IgA seropositivity (P = 0.046 and P = 0.013, respectively).


CONCLUSIONS
In summary, we demonstrated an association between Chlamydia LPS IgA seropositivity and elevated levels of IFNgamma, IL-10, TNFalpha, sVCAM-1 and sE-selectin in CHD patients that might indicate persistent Chlamydia infection and a proinflammatory state. On the other hand, C. pneumoniae MOMP antibodies were not associated with elevated inflammatory markers and might merely be indicative of past infection, possibly with successful microbe clearance.
Schumacher
A
A
Department of Microbiolgy and Division of Cardiology, Hospital of Vestfold, Tønsberg, Norway. anita.schumacher@siv.vo
Seljeflot
I
I
Lerkerød
A B
AB
Sommervoll
L
L
Otterstad
J E
JE
Arnesen
H
H
D000328:Adult; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000276:immunology*; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology*; D002689:Chlamydia / Q000276:immunology*; D002690:Chlamydia Infections / Q000150:complications / Q000276:immunology; D003327:Coronary Disease / Q000276:immunology / Q000382:microbiology*; D016207:Cytokines / Q000097:blood*; D019040:E-Selectin / Q000097:blood; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; D016207:Cytokines; D019040:E-Selectin; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D016753:Interleukin-10; D007371:Interferon-gamma