Heat shock protein synthesis and thermotolerance in Salmonella typhimurium

Abstract

The resistance of stationary phase Salmonella typhimurium to heating at 55 degrees C was greater in cells grown in nutritionally rich than in minimal media, but in all media tested resistance was enhanced by exposing cells to a primary heat shock at 48 degrees C. Chloramphenicol reduced the acquisition of thermotolerance in all media but did not completely prevent it in any. The onset of thermotolerance was accompanied by increased synthesis of major heat shock proteins of molecular weight about 83, 72, 64 and 25 kDa. When cells were shifted from 48 degrees C to 37 degrees C, however, thermotolerance was rapidly lost with no corresponding decrease in the levels of these proteins. There is thus no direct relationship between thermotolerance and the cellular content of the major heat shock proteins. One minor protein of molecular weight about 34 kDa disappeared rapidly following a temperature down-shift. Its presence in the cell was thus correlated with the thermotolerant state.

Association of DnaK and GroEL with Antimicrobial Resistance in Salmonella Abortusovis

“…Almost 90% of cells pretreated at 39°C survived to antibiotic exposure comparative with cells incubated at 37°C (55% relative survival) (Figure 4). The good survival of bacterial cells to high temperature and antibiotic exposure and the drastic increase of the molecular chaperones expression after pretreatment at the moderate temperature were mentioned previously for Salmonella Typhimurium (Mackey and Derreck, 1990) and Acinetobacter baumannii (Cardoso et al, 2010), but never described in S. The mechanisms of antibiotic-resistance are different depending on the type of antimicrobial, and they can be represented by the drug inactivation or modification, target alteration or reduced accumulation associated with increased efflux or decreased permeability (Poole, 2002). The components of the antibiotic resistance mechanism are generally proteins that will be rapidly overexpressed when bacterial cells are damaged by antibiotics (Peleg et al, 2008;Cardoso et al, 2010).…”

Proteasome Inhibitors Cause Induction of Heat Shock Proteins and Trehalose, Which Together Confer Thermotolerance in Saccharomyces cerevisiae

“…6). Thus, after proteolysis was reinitiated, thermotolerance fell rapidly, while the content of hsps remained high and continued to increase for at least 2 h. Interestingly, a similar rapid loss of thermotolerance without a loss of hsps has been seen when heat-shocked yeast and bacterial cells are shifted back to the normal temperature (6,33). These results indicate that blocking proteasome function leads to an increased cell resistance to high temperature not simply through the induction of hsps but also through some additional protection mechanism involving a short-lived component.…”

“…For example, an increase in thermotolerance can be induced in yeast by incubation at 37°C even when protein synthesis is blocked (20) and in a yeast mutant which lacks the heat shock-specific transcription factor (48). In addition, upon down-shift of heat-shocked yeast or bacterial cells to 23°C, thermotolerance is lost within 1 to 2 h, even though the amounts of hsps do not fall (6,33). Thus, proteasome inhibitors, like heat treatment, elicit two protective responses.…”

Induction of Fatty Acid Composition Modifications and Tolerance to Biocides in Salmonella enterica Serovar Typhimurium by Plant-Derived Terpenes

“…It has long been known that bacteria can develop tolerance when exposed to harsh environmental conditions (29,33), including sublethal concentrations of some chemicals such as quaternary ammonium compounds, phenolics, salicylanilides, or diamidines (32,40,48). Cross-adaptation to chemically related biocides often occurs and cross-adaptation to unrelated biocides has occasionally been found.…”

“…It is well established that bacterial cells grown in nonoptimal conditions can adapt and develop resistance to the bactericidal activity of disinfectants or physical treatments (17,30,33,43,49). This acquired tolerance can be due to various cellular phenomena: genetic changes occurring through plasmid acquisition or mutation (41), synthesis of stress proteins (29), and modifications of lipid membrane composition (32). Adaptability of bacterial fatty acid membrane composition, in particular, determines the survival ability of the cell by maintaining both membrane integrity and functionality, which helps to overcome nonoptimal conditions (11,44).…”