International Journal of Diseases and Disorders

ISSN 2329-9835

International Journal of Diseases and Disorders ISSN 2329-9835 Vol. 11 (4), pp. 001-009, April, 2023. © International Scholars Journals

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.

Accepted 1 March, 2023

Abstract

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.