title: Co-infection ratios versus inflammation, growth factors and progression of early atheromas.
abstract: Mycoplasma pneumoniae (MP) and Chlamydophila pneumoniae (CP) antigens are encountered in complicated atheromas and may be implicated in the diversity of atherosclerotic lesions. Mycoplasma can downregulate the immune system, altering levels of inflammation, which may favor the proliferation of other co-infectious agents. In the present study we analyze whether initially stable human atheromas exhibit different ratios of MP/CP antigens compared to ongoing atheromatous lesions. Two groups were examined for the presence of inflammatory cells, macrophages, growth factors and infectious agents: Group I (GI), n=16, early stable atheromas, <4 CD68(+) macrophages/400 x field, showing a normal distribution and a fibrous cap; Group II (GII), n=14, growing atheromas, > or =4 CD68+ cells/400 x field, lacking a fibrous cap, showing a non-normal macrophage distribution. The amounts of CP (but not MP) antigens and lymphocytes in GI were significantly lower than in GII. MP/CP ratios were higher in GI. MP correlated with CP and PDGFB in GI (r=0.79 and r=0.83, p<0.001), but not in GII (r=-0.4 and r=-0.08, p=0.81). MP and CP antigens are already present in early atheromas, and a higher MP/CP ratio correlates with increased growth factors, lower inflammation and plaque stability.
authors.affiliation: Heart Institute of Clinical Hospital, Medical School, University of São Paulo, Brazil.
authors.forename: Maria L
authors.initials: ML
authors.lastname: Higuchi
authors.forename: José M
authors.initials: JM
authors.lastname: Góis
authors.forename: Marcia M
authors.initials: MM
authors.lastname: Reis
authors.forename: Marilia H
authors.initials: MH
authors.lastname: Higuchi-Dos-Santos
authors.forename: Jayme
authors.initials: J
authors.lastname: Diament
authors.forename: Januário M
authors.initials: JM
authors.lastname: Sousa
authors.forename: José A F
authors.initials: JA
authors.lastname: Ramires
authors.forename: Sérgio A
authors.initials: SA
authors.lastname: Oliveira
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000942:Antigens, Bacterial / Q000032:analysis; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D002452:Cell Count; D023521:Chlamydophila Infections / Q000150:complications*; D016993:Chlamydophila pneumoniae / Q000276:immunology / Q000302:isolation & purification*; D003324:Coronary Artery Disease / Q000175:diagnosis* / Q000382:microbiology* / Q000473:pathology; D003331:Coronary Vessels / Q000382:microbiology / Q000473:pathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology; D008264:Macrophages / Q000166:cytology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009177:Mycoplasma pneumoniae / Q000276:immunology / Q000302:isolation & purification*; D010982:Platelet-Derived Growth Factor / Q000378:metabolism; D011019:Pneumonia, Mycoplasma / Q000150:complications*; D000097382:CD68 Molecule
chemical_list: D000942:Antigens, Bacterial; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D010982:Platelet-Derived Growth Factor; C067980:CD68 antigen, human; D000097382:CD68 Molecule