title: Differential expression of chemokines and chemokine receptors in inflammatory periapical diseases.
abstract: BACKGROUND
  Periapical lesions are thought to be the result of a local inflammatory response mediated by inflammatory cell infiltration and production of inflammatory mediators. Although chemokines are strongly implicated in the migration and activation of leukocytes in different inflammatory diseases and experimental models, little is known regarding the expression of chemokines and their receptors in human apical periodontitis.
  
  
  OBJECTIVE
  The objective of this study was to determine the expression of chemokines and their receptors by real-time polymerase chain reaction in samples obtained from healthy gingiva, periapical granulomas, and inflammatory periradicular cysts. The inflammatory infiltrate was characterized by immunohistochemistry.
  
  
  RESULTS
  Comparing cysts and granulomas, an increase in CD4+ and CD8+ cells was observed in granulomas, despite the similar numbers of CD45RO-positive cells detected in both lesions. The analysis of mRNA expression revealed increased levels of CCR1, CCR2, CCR3, CCR5, CXCR1, and CXCR3 in both types of lesion compared with controls. Cysts exhibited a higher expression of CCR3, CCR5, CXCR1, and CXCR3 compared to granulomas. A significantly higher expression of RANTES, IP-10, and MCP-1 was detected in cysts compared with controls or granulomas. The expression of interleukin-8, MIP-1alpha, and MIP-1beta was not different in the three experimental groups.
  
  
  CONCLUSIONS
  The increase in Th1 type (CCR1, CCR5, and CXCR3) and Th2 type (CCR2 and CCR3) receptors in both periapical lesions suggests the concomitant occurrence of Th1 and Th2 responses. Furthermore, the prevalent expression of the receptors CCR3, CCR5, CXCR1, and CXCR3 and of the chemokines RANTES, IP-10, and MCP-1 in cysts may point to a role in the progression of granulomas to cysts.
authors.affiliation: Department of Pharmacology, School of Medicine of Ribeirao Preto, Brazil. tarcilia@unb.br
authors.forename: T A
authors.initials: TA
authors.lastname: Silva
authors.forename: G P
authors.initials: GP
authors.lastname: Garlet
authors.forename: V S
authors.initials: VS
authors.lastname: Lara
authors.forename: W
authors.initials: W
authors.lastname: Martins
authors.forename: J S
authors.initials: JS
authors.lastname: Silva
authors.forename: F Q
authors.initials: FQ
authors.lastname: Cunha
mesh_terms: D000328:Adult; D000368:Aged; D018932:Chemokine CCL2 / Q000032:analysis; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5 / Q000032:analysis; D054357:Chemokine CXCL10; D018925:Chemokines / Q000032:analysis*; D019742:Chemokines, CC / Q000032:analysis; D019743:Chemokines, CXC / Q000032:analysis; D002634:Chemotaxis, Leukocyte / Q000276:immunology; D005881:Gingiva / Q000276:immunology; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis; D007962:Leukocytes / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000032:analysis; D008875:Middle Aged; D010484:Periapical Granuloma / Q000276:immunology; D010485:Periapical Periodontitis / Q000276:immunology*; D011842:Radicular Cyst / Q000276:immunology; D019713:Receptors, CCR5 / Q000032:analysis; D019707:Receptors, Chemokine / Q000032:analysis*; D015728:Receptors, HIV / Q000032:analysis; D023062:Receptors, Interleukin-8A / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054357:Chemokine CXCL10; D018925:Chemokines; D019742:Chemokines, CC; D019743:Chemokines, CXC; D016209:Interleukin-8; D019402:Macrophage Inflammatory Proteins; D019713:Receptors, CCR5; D019707:Receptors, Chemokine; D015728:Receptors, HIV; D023062:Receptors, Interleukin-8A