Pseudomonas aeruginosa is an opportunistic pathogen that synthesizes and secretes a wide range of virulence factors. P. aeruginosa poses a potential threat to human health worldwide due to its omnipresent nature, robust host accumulation, high virulence, and significant resistance to multiple antibiotics. The pathogenicity of P. aeruginosa, which is associated with acute and chronic infections, is linked with multiple virulence factors and associated secretion systems, such as the ability to form and utilize a biofilm, pili, flagella, alginate, pyocyanin, proteases, and toxins. Two-component systems (TCSs) of P. aeruginosa perform an essential role in controlling virulence factors in response to internal and external stimuli. Therefore, understanding the mechanism of TCSs to perceive and respond to signals from the environment and control the production of virulence factors during infection is essential to understanding the diseases caused by P. aeruginosa infection and further develop new antibiotics to treat this pathogen. This review discusses the important virulence factors of P. aeruginosa and the understanding of their regulation through TCSs by focusing on biofilm, motility, pyocyanin, and cytotoxins.

Pseudomonas aeruginosa is a multidrug-resistant opportunistic human pathogen that utilizes two-component systems (TCSs) to sense pathophysiological signals and coordinate virulence. P. aeruginosa contains 64 sensor histidine kinases (HKs) and 72 response regulators (RRs) that play important roles in metabolism, bacterial physiology, and virulence. However, the role of some TCSs in virulence remains uncharacterized. In this study, we evaluated the virulence potential of some uncharacterized sensor HK and RR knockouts in P. aeruginosa using a Galleria mellonella infection model. Furthermore, we demonstrated that KdpD and AauS HKs regulate virulence by affecting P. aeruginosa biofilm formation and motility. Both ΔkdpD and ΔaauS showed reduced biofilm and motility which were confirmed by restored phenotypes upon complementation. Moreover, ΔkdpD and ΔaauS exhibited increased survival of HeLa cells and G. mellonella during in vivo infection. Altered expression of the transcriptional regulators anR and lasR, along with the virulence genes lasA, pelA, cupA, pqsA, pqsB, pqsC, and pqsD in the mutant strains elucidated the mechanism by which ΔkdpD and ΔaauS affect virulence. These findings confirm that kdpD and aauS play important roles in P. aeruginosa pathogenesis by regulating biofilm formation and motility.

Corrigendum: Sensor histidine kinases kdpD and aauS regulate biofilm and virulence in Pseudomonas aeruginosa PA14DOI: [doi: 10.3389/fcimb.2023.1270667]Journal: [Front. Cell. Infect. Microbiol. (2023) 13:1270667]Authors: [Maria Sultan, Rekha Arya*, Akhilesh Kumar Chaurasia*, Kyeong Kyu Kim*]Affiliation[Department of Precision Medicine, Graduate School of Basic Medical Science, Institute for Antimicrobial Resistance Research and Therapeutics, Sungkyunkwan University School of Medicine, Suwon 16319, Republic of Korea.] *Corresponding authors: Rekha Arya (rekhuarya@gmail.com)Akhilesh K. Chaurasia (chaurasia.ak@gmail.comKyeong Kyu Kim (kyeongkyu@skku.edu) Tel.: +82-31-299-6152 Fax: +82-31-299-6159A corrigendum onSensor histidine kinases kdpD and aauS regulate biofilm and virulence in Pseudomonas aeruginosa PA14 by Sultan et. al. (2023) Front. Cell. Infect. Microbiol. 13:1270667; doi: 10.3389/fcimb.2023.1270667In the originally published article, a part of Figure 6 has duplication of waxworm image (Figure 6C) and editing errors in the strain names (Figure 6D) while making the final high-resolution images. Specifically, the worm image in two panels of Figure 6C (PBS control-WT pUCP18 and delta kdpD::pUCP18-delta kdpD::pUCP18kdpD) are duplicated. The names of two strains (delta kdpD::pUCP18kdpD and delta aauS::pUCP18) in Figure 6D are interchanged. These errors have been corrected as shown in Figure 6C&D below. There is no change in the figure legends. We apologize for any inconvenience this error may have caused. It is noteworthy that these modifications do not change the scientific conclusions of the paper in any way.Conflict of Interest Statement: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.CORRECTED FIGURE 6 C & D