| First Author | Borjesson DL | Year | 2003 |
| Journal | Blood | Volume | 101 |
| Issue | 8 | Pages | 3257-64 |
| PubMed ID | 12480703 | Mgi Jnum | J:82941 |
| Mgi Id | MGI:2656087 | Doi | 10.1182/blood-2002-04-1019 |
| Citation | Borjesson DL, et al. (2003) Roles of neutrophil beta 2 integrins in kinetics of bacteremia, extravasation, and tick acquisition of Anaplasma phagocytophila in mice. Blood 101(8):3257-64 |
| abstractText | Tick saliva contains anti-inflammatory and immunosuppressive substances that facilitate blood feeding and enhance tick-vectored pathogen transmission, including Anaplasma phagocytophila, an etiologic agent of granulocytic ehrlichiosis. As such, inflammation at a tick-feeding site is strikingly different than that typically observed at other sites of inflammation. Up-regulation of CD11b/CD18 occurs in host granulocytes following interaction or infection with A phagocytophila, and the absence of CD11b/CD18 results in early increases in bacteremia. We hypothesized that beta 2 integrin-dependent infection kinetics and leukocyte extravasation are important determinants of neutrophil trafficking to, and pathogen acquisition at, tick-feeding sites. A phagocytophila infection kinetics were evaluated in CD11a/CD18, CD11b/CD18, and CD18 knock-out mice using quantitative polymerase chain reaction (PCR) of blood, ticks, and skin biopsies in conjunction with histopathology. A marked increase in the rate of A phagocytophila infection of neutrophils and pathogen burden in blood followed tick feeding. Infection kinetics were modified by beta 2 integrin expression and systemic neutrophil counts. Significant neutrophil-pathogen trafficking was observed to both suture and tick sites. Despite the prominent role for beta 2 integrins in neutrophil arrest in flowing blood, successful pathogen acquisition by ticks occurred in the absence of beta 2 integrins. Establishment of feeding pools that rely less on leukocyte trafficking and more on small hemorrhages may explain the ready amplification of A phagocytophila DNA from ticks infested on CD11/CD18-deficient mouse strains. |
