Dr David Bruce (1855–1931) first identified the causative agent of brucellosis as a small Gram-negative α-Proteobacterium, which was later on called Brucella melitensis in his honor by Meyer and Shaw. Nowadays, four strains exhibit pathogenicity in humans with B. melitensis being the least host specific and also the most infectious for humans. The other strains are Brucella suis and Brucella abortus and more recently human cases being infected with Brucella cetaceae have been reported. Why such a reemerging disease is so difficult to fight, evidence shows that the pathogenic bacterium has developed strategies to hide from immune recognition.

Research into intracellular sensing of microbial products is an up and coming field in innate immunity. Toll-like receptors (TLRs) recognize Brucella spp. and bacterial components and initiate mononuclear phagocyte responses that influence both innate and adaptive immunity. Recent studies have revealed the intracellular signaling cascades involved in the TLR-initiated immune response to Brucella infection. TLR2, TLR4 and TLR9 have been implicated in host interactions with Brucella; however, TLR9 has the most prominent role. Further, the relationship between specific Brucella molecules and various signal transduction pathways needs to be better understood. MyD88-dependent and TRIF-independent signaling pathways are involved in Brucella activation of innate immune cells through TLRs. We have recently reported the critical role of MyD88 molecule in dendritic cell maturation and interleukin-12 production during B. abortus infection. This article discusses recent studies on TLR signaling and also highlights the contribution of NOD and type I IFN receptors during Brucella infection. The better understanding of the role by such innate immune receptors in bacterial infection is critical in host–pathogen interactions.

Research into intracellular sensing of microbial products is an up and coming field in innate immunity. Toll-like receptors (TLRs) recognize Brucella spp. and bacterial components and initiate mononuclear phagocyte responses that influence both innate and adaptive immunity. Recent studies have revealed the intracellular signaling cascades involved in the TLR-initiated immune response to Brucella infection. TLR2, TLR4 and TLR9 have been implicated in host interactions with Brucella; however, TLR9 has the most prominent role. Further, the relationship between specific Brucella molecules and various signal transduction pathways needs to be better understood. MyD88-dependent and TRIF-independent signaling pathways are involved in Brucella activation of innate immune cells through TLRs. We have recently reported the critical role of MyD88 molecule in dendritic cell maturation and interleukin-12 production during B. abortus infection. This article discusses recent studies on TLR signaling and also highlights the contribution of NOD and type I IFN receptors during Brucella infection. The better understanding of the role by such innate immune receptors in bacterial infection is critical in host-pathogen interactions.

A record number of bison foraging outside Yellowstone National Park have been captured and killed this winter as part of a US plan to try to keep the animals from spreading the disease brucellosis to livestock. The bacterium Brucella abortus can cause spontaneous abortion in cattle.

More than 900 people working in 254 labs around the United States and Canada might have been exposed to modified Brucella abortus last autumn, because of their failure to follow proper handling procedures for the bacterium, the Atlanta Journal-Constitution has reported.

One of the most thoroughly studied and virulent kinds of bacteria has just revealed a surprising and potentially useful new trait. Brucella, which causes the sometimes fatal disease brucellosis in humans and farm animals, seems to depend on blue wavelengths of light--like those found in the sun's rays--for its survival. The finding should open up new ways of fighting the organism and its ilk.

Histidine kinases, used for environmental sensing by bacterial two-component systems, are involved in regulation of bacterial gene expression, chemotaxis, phototaxis, and virulence. Flavin-containing domains function as light-sensory modules in plant and algal phototropins and in fungal blue-light receptors. We have discovered that the prokaryotes Brucella melitensis, Brucella abortus, Erythrobacter litoralis, and Pseudomonas syringae contain light-activated histidine kinases that bind a flavin chromophore and undergo photochemistry indicative of cysteinyl-flavin adduct formation. Infection of macrophages by B. abortus was stimulated by light in the wild type but was limited in photochemically inactive and null mutants, indicating that the flavin-containing histidine kinase functions as a photoreceptor regulating B. abortus virulence.

Light, a nearly ubiquitous environmental signal, regulates myriad developmental and behavioral responses in plant, fungal, bacterial, and animal cells. Photosensitive proteins abound in the bacterial kingdom, but their cellular functions often remain a mystery. On page 1090 in this issue, Swartz et al. (1) identify a functional role for a new type of light sensor in bacteria--light, oxygen, or voltage (LOV) histidine kinase. In the notorious pathogen Brucella abortus, light increases the enzymatic activity of this kinase, which, remarkably, increases virulence of the bacterium. Related LOV histidine kinases are conserved across a range of bacterial taxa, suggesting that this virulence pathway could be one of many new photosensory pathways regulating bacterial physiology.