African Journal of
Microbiology Research

  • Abbreviation: Afr. J. Microbiol. Res.
  • Language: English
  • ISSN: 1996-0808
  • DOI: 10.5897/AJMR
  • Start Year: 2007
  • Published Articles: 5211

Full Length Research Paper

NFκB is differentially activated in macrophages from J774A.1 cell line infected with vaccine or virulent strains of Brucella abortus

Maribel Cervantes-Flores1, Aurora Martínez-Romero2, Eda Guadalupe Ramírez-Valles1, Leticia Saucedo Mendiola1,  Martha C. Moreno-Lafont3,  Rubén López-Moreno3,  Iris Estrada-García3 and Virgilio Mojica-Marín1*
  1Facultad de Ciencias Químicas. Universidad Juárez Del Estado de Durango (UJED). Av. Veterinária s/n, Circuito Universitário, Col. Valle del Sur. CP. 34200. Durango, Dgo., México. 2Facultad de Ciencias Químicas unidad Gómez-Palacio. Universidad Juárez Del Estado de Durango (UJED). Av. Artículo 123 s/n Colonia Filadelfia CP 35010; AP. No. 51 Gómez Palacio, Dgo., México. 3Escuela Nacional de Ciencias Biológicas-IPN. Prol. de Carpio y Plan de Ayala s/n. Col. Santo Tomás. 11340 México, D.F., México.
Email: [email protected]

  •  Accepted: 01 March 2011
  •  Published: 18 April 2011



The activation and nuclear translocation of NF-kB and the expression of the pro-inflammatory cytokine genes by macrophages infected with the attenuated Brucella abortus RB51 and virulent 2308 strains were evaluated. pIkBα and NF-kB were determined by immunoblot, and cytokines IFN-g and IL12 mRNA were determined by reverse transcriptase polymerase chain reaction (qPCR) and translocation of NF-kB protein to the nucleus was determined by electrophoretic mobility shift assay (EMSA). We demonstrate that the attenuated B. abortus RB51 strain stimulates cells resulting in NF-kB activation and nuclear translocation, during experimental infection in macrophages J774A.1 which induced a pro-inflammatory response producing IL-6, 12 TNF-s INF-g and iNOS. The virulent strain B. abortus 2308 also stimulated the cells but induced a p50 homodimer of NF-kB which is inactive. The p50 homodimer of NF-kB binds to DNA, and thus blocked the activation of pro-inflammatory cytokines genes. Therefore, an evasion mechanism of the strain 2308 is to produce an inactive homodimer of NF-kB which does not give rise to pro-inflammatory response to eliminate the bacteria.


Key words: Brucella abortus, RB51, 2308, NF-kB, transduction signals.