Coxiella burnetii antibody seropositivity is not a risk factor for AIDS-related non-Hodgkin lymphoma

Miller, Halie K.; Santo, Loredana; Camargo, M. Constanza; Winkler, Cheryl A.; Goedert, James J.; Kersh, Gilbert J.; Rabkin, Charles S.

doi:10.1182/blood-2016-12-756569

Cited by 4 publications

(2 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…burnetii- associated NHL, supporting possible involvement of the corresponding proteins in lymphomagenesis. However, these results remain controversial since other studies have not confirmed the link between Q fever and NHL [ 31 – 33 , 61 ].…”

Section: Discussionmentioning

confidence: 99%

“…In more recent investigations [29] and working on Q fever patient samples, we found that specific genes involved in anti-apoptotic processes (e.g., BCL-2) were highly expressed, whereas proapoptotic genes were repressed in PBMCs from patients with C. burnetii-associated NHL, supporting possible involvement of the corresponding proteins in lymphomagenesis. However, these results remain controversial since other studies have not confirmed the link between Q fever and NHL [31][32][33]61].…”

Section: Plos Onementioning

confidence: 99%

See 1 more Smart Citation

Modulation of the E-cadherin in human cells infected in vitro with Coxiella burnetii

et al. 2023

View full text Add to dashboard Cite

High concentration of soluble E-cadherin (E-cad) was previously found in sera from Q fever patients. Here, BeWo cells which express a high concentration of E-cad were used as an in vitro model to investigate the expression and function of E-cad in response to infection by Coxiella burnetii, the etiological agent of Q fever. Infection of BeWo cells with C. burnetii leads to a decrease in the number of BeWo cells expressing E-cad at their membrane. A shedding of soluble E-cad was associated with the post-infection decrease of membrane-bound E-cad. The modulation of E-cad expression requires bacterial viability and was not found with heat-inactivated C. burnetii. Moreover, the intracytoplasmic cell concentration of β-catenin (β-cat), a ligand of E-cad, was reduced after bacterial infection, suggesting that the bacterium induces modulation of the E-cad/β-cat signaling pathway and CDH1 and CTNNB1 genes transcription. Finally, several genes operating the canonical Wnt-Frizzled/β-cat pathway were overexpressed in cells infected with C. burnetii. This was particularly evident with the highly virulent strain of C. burnetii, Guiana. Our data demonstrate that infection of BeWo cells by live C. burnetii modulates the E-cad/β-cat signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%