The Manganese-Responsive Transcriptional Regulator MumR Protects Acinetobacter baumannii from Oxidative Stress
Acinetobacter baumannii is an emerging pathogen and a leading cause of hospital-acquired infections. However, many of the mechanisms utilized by this pathogen to cause disease remain poorly understood. In this issue, Green et al. (e00762-19) characterize a mechanism by which A. baumannii coordinates a response to manganese (Mn) starvation and reactive oxygen species (ROS), two stressors encountered by pathogens during infection. They find that A. baumannii Mn utilization facilitates resistance to ROS and uncover a relationship between Mn homeostasis, metabolism, and oxidative stress in this organism, highlighting the interconnectedness of these processes and exposing a promising target for antimicrobial development.
Major Histocompatibility Complex Class II-Restricted, CD4+ T Cell-Dependent and -Independent Mechanisms Are Required For Vaccine-Induced Protective Immunity against Coxiella burnetii
Coxiella burnetii is an obligate intracellular Gram-negative bacterium that causes Q fever in humans. The mechanism of vaccine-induced protective immunity against Coxiella burnetii infection remains unclear. This study (e00824-19) provides novel evidence to support that major histocompatibility complex class II (MHC-II)-restricted, CD4+ T cell-dependent and -independent mechanisms are required for vaccine-induced protective immunity against C. burnetii infection and that the MHC-II-dependent mechanism of protection partially depends on Tbet, CD4+ T cells, and interferon gamma. Additionally, this study highlights differences in the primary and secondary immune response, which should be considered when designing future vaccines against Q fever.
Poor B Cell Memory May Contribute to Recurrent Clostridioides difficile Infection
In this study, Amadou Amani and colleagues (e00829-19) use a murine model of recurrent Clostridioides difficile disease to demonstrate that initial and repeat infections are equally severe and associated with poor establishment of toxin- or bacteria-specific antibody and B cell memory. In contrast, subcutaneous immunization established protective antibody and B cell memory. However, infection was unable to restimulate the immunization-induced B cell memory compartment. These results may have implications for understanding C. difficile disease recurrence and potential limitations of vaccination.
The Twin-Arginine Translocation System of Citrobacter rodentium Plays an Important Role in Gut Infection
Enteric bacterial pathogens elicit gut inflammatory responses and colonize the gut lumen. Otake et al. (e00892-19) show that the twin-arginine translocation (Tat) system is involved in the gut infection with Citrobacter rodentium, a murine enteric pathogen. Mouse infection experiments demonstrate that the Tat mutant of C. rodentium displays reduced inflammatory responses, resulting in prolonged gut colonization. This mutant also becomes hypersensitive to bile acids. Furthermore, increased fecal levels of bile acids foster C. rodentium clearance from the gut lumen. These data indicate that the Tat system and luminal bile acids might be promising therapeutic targets for infections with enteric pathogens.
- Copyright © 2020 American Society for Microbiology.
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- The Manganese-Responsive Transcriptional Regulator MumR Protects Acinetobacter baumannii from Oxidative Stress
- Major Histocompatibility Complex Class II-Restricted, CD4+ T Cell-Dependent and -Independent Mechanisms Are Required For Vaccine-Induced Protective Immunity against Coxiella burnetii
- Poor B Cell Memory May Contribute to Recurrent Clostridioides difficile Infection
- The Twin-Arginine Translocation System of Citrobacter rodentium Plays an Important Role in Gut Infection
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