Over millions of year's co-evolution between host and pathogen have resulted in strategies to survive in the host and cause disease presumably without eliminating the host entirely. Recent studies reveal that bacteria exploit the host TLR pathway, resulting either in enhanced virulence or immune suppression (Arpaia et al., 2011; Round et al., 2011) . Our previous study has shown that Brucella can use TLR4 to gain entry into the host cells (Pei et al., 2008) . It is possible that Brucella inhibit IgA class switch recombination or secretion via MyD88 by an unknown mechanism in order to initiate infection through mucosal surfaces.