Studies reveal how bacterial pathogens adapt to nutritional stress

Scanning electron micrograph of Staphylococcus aureus. False colors have been added. Credit: CDC

To cause the disease, the human pathogen Staphylococcus aureus must adapt to the changing host environment. Many of these adaptations are mediated via a two-component signaling system (TCS) that regulates gene expression in response to environmental stimuli.In a new study reported in Journal of BacteriologyResearchers in Illinois provide insights into the signaling mechanisms utilized by the staphylococcus TCSArlRS in response to host-imposed manganese and glucose starvation.

“Signal transduction systems such as ArlRS play an important role in enabling pathogens to adapt to the ever-changing environment encountered during infection and are therefore a major contributor to disease,” microbiology and Research leader.

Hosts are isolated to limit the pathogenicity of Staphylococcus aureus Essential nutrients— A process called nutritional immunization of manganese, zinc, iron, etc. during infection. However, successful pathogens can evade the host’s defenses and cause illness. Researchers have focused on one mechanism utilized by Staphylococcus aureus to circumvent this host response, which depends on the ArlRS2 component system, which includes the histidine kinase ArlS and the response-regulating protein ArlR.

“This response regulator is of particular interest to elucidate how ArlR is activated, as it is involved in the ability of S. aureus to overcome nutritional restrictions and regulate responses that attack the host. .. Immune system“Kehl-Fie said.

“One of the concerns of the Kehl-Fie lab is trying to understand how Staphylococcus aureus resists nutritional immunity,” said Dr. Paola Párraga Solórzano. A student at the Kehl-Fie Lab and the lead author of the dissertation. “Since it was suggested that ArlR is activated by other histidine kinases, we wanted to understand whether ArlS is required for ArlR’s response to manganese and glucose limiting conditions.”

Histidine kinases have certain interactions with their cognate response regulators, but crosstalk can occur if histidine kinases can activate non-cologous response regulators. Other studies have shown that non-homogeneous histidine kinase activates ArlR, questioning the role of ArlS in resisting nutritional immunity.

To determine if ArlS is required for ArlR activation, mutants lacking the arlS gene were evaluated for their ability to grow and activate ArlR in a manganese deficient state. These conditions were achieved using calprotectin, an immune effector that isolates manganese. Pathogen Like Staphylococcus aureus. This study revealed that ArlS is required for activation of ArlR under these conditions, says Párraga Solórzano.

Since glucose is the preferred carbon source for Staphylococcus aureus, Párraga Solórzano evaluated the role of ArlS in glucose deficiency. ArlR showed constant levels of activity in the absence of ArlS, but ArlS was required for full activation in response to glucose restriction, Párraga Solórzano said.

“We were able to understand how these signaling mechanisms work and how S. aureus regulates its response to the stressful conditions normally encountered during infection,” Párraga Solórzano said. Says. “We have determined that ArlS is important for S. aureus’s response to both manganese starvation and glucose restriction.”

Preliminary research to facilitate this work was conducted by co-author and former undergraduate student Angela Shupe.

The team discovers how bacteria utilize the gaps in the body’s armor

For more information:
The sensor histidine kinase ArlS is required for Staphylococcus aureus and others to activate ArlR depending on the availability of nutrients, including Paola K. Párraga Solórzano. Journal of Bacteriology (2021). DOI: 10.1128 / JB.00422-21

Quote: Studies have revealed how bacterial pathogens adapt to nutritional stress (December 6, 2021).

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