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Updated: Jan 26, 2026

Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
Published on: January 17, 2025
Effect of Sodium Chloride on Uptake of Substrate by Staphylococcus aureus 196E
J L Smith1, M J Maurer1, M M Bencivengo1
1Eastern Regional Research Center, U.S. Department of Agriculture, 600 East Mermaid Lane, Philadelphia, Pennsylvania 19118.
Abstract:
Sodium chloride inhibited a number of biochemical parameters in Staphylococcus aureus 196E. Induction of phospho-β-galactosidase, synthesis of staphylococcal enterotoxin A, enzyme activity (phospho-β-galactosidase) and glucose utilization were approximately four times more sensitive to the inhibitory effects of salt than was growth. Uptake of 14C-2-deoxyglucose and respiratory activity with a number of substrates were inhibited also. The breakdown of o-nitrophenyl-β-galactoside (ONPG) by lactose-grown S. aureus 196E was inhibited by NaCl as well as by other solutes (salts, carbohydrates, amino acids) which suggested that the inhibitory effect is a general one of solutes and not restricted to NaCl. Various ionophores (gramicidin, valinomycin, monensin, lasalocid, m-chlorophenylhydrazone), the H+-ATPase inhibitor (N,N',-dicyclohexylcarbodiimide), and ion channel blockers (quinine, quinidine, chlorpromazinc, tetracaine, verapamil) reversed the inhibitory action of salt on ONPG breakdown by lactose-grown cells; however, these compounds did not reverse NaCl inhibition of glucose utilization. The effects observed here suggest that NaCl (and probably other solutes) exerts an inhibitory effect on transport of substrates into the cells of S. aureus 196E.
Insights
Sodium chloride inhibits Staphylococcus aureus growth and biochemical processes. This salt impacts substrate transport into cells, affecting key functions like enzyme activity and glucose utilization.
Area of Science:
- Microbiology
- Biochemistry
- Cell Biology
Background:
- Staphylococcus aureus is a common pathogen.
- Understanding how external factors like sodium chloride affect bacterial physiology is crucial for developing control strategies.
Purpose of the Study:
- To investigate the inhibitory effects of sodium chloride (NaCl) on various biochemical parameters in Staphylococcus aureus 196E.
- To determine the specificity of NaCl's inhibitory action and explore potential mechanisms.
Main Methods:
- Assessing the impact of NaCl on bacterial growth, enzyme induction (phospho-β-galactosidase), enterotoxin A synthesis, glucose utilization, substrate uptake (¹⁴C-2-deoxyglucose), and respiratory activity.
- Evaluating the effect of various solutes and ion modulators (ionophores, ATPase inhibitors, ion channel blockers) on NaCl-induced inhibition.
Main Results:
- NaCl significantly inhibited multiple biochemical parameters, including enzyme activity and glucose utilization, more than growth.
- The inhibitory effect of NaCl on o-nitrophenyl-β-galactoside (ONPG) breakdown was reversed by ion modulators, suggesting a role for ion transport.
- However, these modulators did not reverse NaCl's inhibition of glucose utilization, indicating a complex mechanism.
Conclusions:
- Sodium chloride, and likely other solutes, exerts a general inhibitory effect on substrate transport into Staphylococcus aureus cells.
- The findings suggest that NaCl interferes with the transport mechanisms essential for bacterial metabolism and function.
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