M. Brittany Johnson, PhD
The Johnson lab investigates host-pathogen interactions and identification of therapeutic points of intervention in meningitis and osteomyelitis.
Biological Sciences, UNC Charlotte
Johnson Lab Projects
Figure 1: Investigation of RIG-I as a therapeutic target for bacterial CNS infection
Immune responses by resident brain cells are initiated when innate immune sensors called pattern recognition receptors (PRRs) recognize pathogen-associated molecular patterns (PAMPs) upon infection. The cytosolic nucleic acid sensor, retinoic-acid inducible gene-I (RIG-I), promotes potentially beneficial interferon production. Our research investigates the hypothesis that RIG-I-dependent identification of bacteria promotes protective brain cell responses during acute or chronic CNS infections. In collaboration with Dr. Kirill Afonin’s laboratory, we have developed novel synthetic RIG-I agonists to enhance these beneficial responses.
Figure 2: Investigation of host cell cytokine-directed changes in Neisseria meningitidis gene expression
N. meningitidis triggers harmful inflammatory responses by brain cells that result in long-term morbidity or mortality. The host-pathogen interactions required for such responses are not well understood. Our research investigates the immune mediators released when resident brain cells identify N. meningitidis PAMPs. Intriguingly, immune mediators can serve as an environmental cue, as N. meningitidis has been reported to bind and import host cytokines that then drive changes in bacterial gene expression. Accordingly, our studies investigate the hypothesis that N. meningitidis PAMPs initiate brain cell immune responses that, in turn, regulate bacterial gene expression to further exacerbate infection.
Figure 3: Investigation of the host-pathogen interactions in osteomyelitis
During osteomyelitis, there is damaging bone resorption due to a disruption in the process of bone remodeling. Bone remodeling is managed by bone-forming osteoblasts that produce bone components and bone-resorbing osteoclasts that release enzymes to degrade bone. Our lab is interested in dissecting the dynamic host-pathogen interactions between Staphylococcus aureus and resident bone cells that occur during osteomyelitis.