PMID- 37155716
OWN - NLM
STAT- MEDLINE
DCOM- 20230613
LR  - 20230720
IS  - 2373-9878 (Electronic)
IS  - 2373-9878 (Linking)
VI  - 9
IP  - 6
DP  - 2023 Jun 12
TI  - Nucleotide Messenger Signaling of Staphylococci in Responding to Nitric Oxide - 
      Releasing Biomaterials.
PG  - 3285-3296
LID - 10.1021/acsbiomaterials.2c01536 [doi]
AB  - Nitric oxide (NO) releasing biomaterials are a promising approach against medical 
      device associated microbial infection. In contrast to the bacteria-killing 
      effects of NO at high concentrations, NO at low concentrations serves as an 
      important signaling molecule to inhibit biofilm formation or disperse mature 
      biofilms by regulating the intracellular nucleotide second messenger signaling 
      network such as cyclic dimeric guanosine monophosphate (c-di-GMP) for many 
      Gram-negative bacterial strains. However, Gram-positive staphylococcal bacteria 
      are the most commonly diagnosed microbial infections on indwelling devices, but 
      much less is known about the nucleotide messengers and their response to NO as 
      well as the mechanism by which NO inhibits biofilm formation. This study 
      investigated the cyclic nucleotide second messengers c-di-GMP, cyclic dimeric 
      adenosine monophosphate (c-di-AMP), and cyclic adenosine monophosphate (cAMP) in 
      both Staphylococcus aureus (S. aureus) Newman D2C and Staphylococcus epidermidis 
      (S. epidermidis) RP62A after incubating with S-nitroso-N-acetylpenicillamine 
      (SNAP, NO donor) impregnated polyurethane (PU) films. Results demonstrated that 
      NO release from the polymer films significantly reduced the c-di-GMP levels in S. 
      aureus planktonic and sessile cells, and these bacteria showed inhibited biofilm 
      formation. However, the effect of NO release on c-di-GMP in S. epidermidis was 
      weak, but rather, S. epidermidis showed significant reduction in c-di-AMP levels 
      in response to NO release and also showed reduced biofilm formation. Results 
      strongly suggest that NO regulates the nucleotide second messenger signaling 
      network in different ways for these two bacteria, but for both bacteria, these 
      changes in signaling affect the formations of biofilms. These findings provide 
      cues to understand the mechanism of Staphylococcus biofilm inhibition by NO and 
      suggest novel targets for antibiofilm interventions.
FAU - Ochetto, Alyssa
AU  - Ochetto A
AD  - Department of Biological and Biomedical Sciences, Rowan University, Glassboro, 
      New Jersey 08028, United States.
FAU - Sun, Dongxiao
AU  - Sun D
FAU - Siedlecki, Christopher A
AU  - Siedlecki CA
AUID- ORCID: 0000-0003-2163-4099
FAU - Xu, Li-Chong
AU  - Xu LC
AUID- ORCID: 0000-0001-6503-0655
LA  - eng
GR  - R01 HL153231/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20230508
PL  - United States
TA  - ACS Biomater Sci Eng
JT  - ACS biomaterials science & engineering
JID - 101654670
RN  - 0 (Nucleotides)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - H2D2X058MU (Cyclic GMP)
RN  - 415SHH325A (Adenosine Monophosphate)
SB  - IM
MH  - *Nucleotides
MH  - *Nitric Oxide/pharmacology
MH  - Staphylococcus
MH  - Staphylococcus aureus
MH  - Gene Expression Regulation, Bacterial
MH  - Cyclic GMP
MH  - Adenosine Monophosphate
PMC - PMC10355158
MID - NIHMS1900640
OTO - NOTNLM
OT  - c-di-AMP
OT  - c-di-GMP
OT  - nitric oxide
OT  - nucleotide signaling
OT  - staphylococci
COIS- The authors declare no competing financial interest.
EDAT- 2023/05/08 18:42
MHDA- 2023/06/13 06:42
PMCR- 2023/07/19
CRDT- 2023/05/08 14:44
PHST- 2023/06/13 06:42 [medline]
PHST- 2023/05/08 18:42 [pubmed]
PHST- 2023/05/08 14:44 [entrez]
PHST- 2023/07/19 00:00 [pmc-release]
AID - 10.1021/acsbiomaterials.2c01536 [doi]
PST - ppublish
SO  - ACS Biomater Sci Eng. 2023 Jun 12;9(6):3285-3296. doi: 
      10.1021/acsbiomaterials.2c01536. Epub 2023 May 8.