L-Rhamnosylation of Listeria monocytogenes Wall Teichoic Acids Promotes Resistance to Antimicrobial Peptides by Delaying Interaction with the Membrane

Listeria monocytogenes is an opportunistic Gram-positive bacterial pathogen responsible for listeriosis, a human foodborne disease. Its cell wall is densely decorated with wall teichoic acids (WTAs), a class of anionic glycopolymers that play key roles in bacterial physiology, including protection against the activity of antimicrobial peptides (AMPs). In other Gram-positive pathogens, WTA modification by amine-containing groups such as D-alanine was largely correlated with resistance to AMPs. However, in L. monocytogenes, where WTA modification is achieved solely via glycosylation, WTA-associated mechanisms of AMP resistance were unknown. Here, we show that the L-rhamnosylation of L. monocytogenes WTAs relies not only on the rmlACBD locus, which encodes the biosynthetic pathway for L-rhamnose, but also on rmlT encoding a putative rhamnosyltransferase. We demonstrate that this WTA tailoring mechanism promotes resistance to AMPs, unveiling a novel link between WTA glycosylation and bacterial resistance to host defense peptides. Using in vitro binding assays, fluorescence-based techniques and electron microscopy, we show that the presence of L-rhamnosylated WTAs at the surface of L. monocytogenes delays the crossing of the cell wall by AMPs and postpones their contact with the listerial membrane. We propose that WTA L-rhamnosylation promotes L. monocytogenes survival by decreasing the cell wall permeability to AMPs, thus hindering their access and detrimental interaction with the plasma membrane. Strikingly, we reveal a key contribution of WTA L-rhamnosylation for L. monocytogenes virulence in a mouse model of infection.     

单增李斯特菌耐药外排泵研究进展

单增李斯特菌是一种重要的人兽共患食源性胞内致病菌,广泛存在于自然环境中且易污染动物性食品,人及动物感染后可引起严重的李斯特菌病,死亡率高达30%。单增李斯特菌通常对多种药物敏感,然而,因不合理使用抗菌药或消毒剂形成的选择压力导致李斯特菌多重耐药情况的报道日渐增多。外排泵蛋白是细菌中一类重要的蛋白,可参与机体多种生物学过程,包括影响细菌对抗生素敏感性、促进有毒化合物泵出、影响细菌毒力等。本文综述了近年来关于单增李斯特菌耐药外排泵的功能及调控机制的研究进展,为深入理解李斯特菌耐药等环境适应机制及有效控制该病原污染传播和筛选抗感染药物新靶点提供理论基础。     

Antibacterial Activity of Subtilosin Alone and Combined with Curcumin, Poly-Lysine and Zinc Lactate Against Listeria monocytogenes Strains

In this paper, the antibacterial effects of the Bacillus amyloliquefaciens-produced bacteriocin subtilosin, both alone and in combination with curcumin, ε-poly-l-lysine (poly-lysine), or zinc lactate, were examined against Listeria monocytogenes. Results indicated that subtilosin inhibits both of the studied bacterial strains, Scott A (wild-type, nisin sensitive) and NR30 (nisin resistant). However, L. monocytogenes Scott A was more sensitive to subtilosin and pure curcumin. In addition, subtilosin was more active at an acidic pH. Subtilosin in combination with encapsulated curcumin displayed partial synergy against L. monocytogenes ScottA. It also had synergistic activity against both L. monocytogenes Scott A and L. monocytogenes NR30 when combined with zinc lactate. Only an additive effect was observed for subtilosin when combined with non-encapsulated curcumin or poly-lysine against the mentioned strains. Thus, using the combination of subtilosin with curcumin, poly-lysine, or zinc lactate, a lower effective dose can be used to control L. monocytogenes infection. Our findings suggest that subtilosin could be used as alternative bacteriocin to nisin, providing an opportunity to use a novel natural and efficacious biopreservative against L. monocytogenes in food preservation. This is the first report on the effects of the combination of subtilosin with natural antimicrobials on L. monocytogenes.     

Highly Invasive Listeria monocytogenes Strains Have Growth and Invasion Advantages in Strain Competition

Multiple Listeria monocytogenes strains can be present in the same food sample; moreover, infection with more than one L. monocytogenes strain can also occur. In this study we investigated the impact of strain competition on the growth and in vitro virulence potential of L. monocytogenes. We identified two strong competitor strains, whose growth was not (or only slightly) influenced by the presence of other strains and two weak competitor strains, which were outcompeted by other strains. Cell contact was essential for growth inhibition. In vitro virulence assays using human intestinal epithelial Caco2 cells showed a correlation between the invasion efficiency and growth inhibition: the strong growth competitor strains showed high invasiveness. Moreover, invasion efficiency of the highly invasive strain was further increased in certain combinations by the presence of a low invasive strain. In all tested combinations, the less invasive strain was outcompeted by the higher invasive strain. Studying the effect of cell contact on in vitro virulence competition revealed a complex pattern in which the observed effects depended only partially on cell-contact suggesting that competition occurs at two different levels: i) during co-cultivation prior to infection, which might influence the expression of virulence factors, and ii) during infection, when bacterial cells compete for the host cell. In conclusion, we show that growth of L. monocytogenes can be inhibited by strains of the same species leading potentially to biased recovery during enrichment procedures. Furthermore, the presence of more than one L. monocytogenes strain in food can lead to increased infection rates due to synergistic effects on the virulence potential.     

Phagocytes produce prostaglandin E2 in response to cytosolic Listeria monocytogenes

Listeria monocytogenes is an intracellular bacterium that elicits robust CD8⁺ T-cell responses. Despite the ongoing development of L. monocytogenes-based platforms as cancer vaccines, our understanding of how L. monocytogenes drives robust CD8⁺ T-cell responses remains incomplete. One overarching hypothesis is that activation of cytosolic innate pathways is critical for immunity, as strains of L. monocytogenes that are unable to access the cytosol fail to elicit robust CD8⁺ T-cell responses and in fact inhibit optimal T-cell priming. Counterintuitively, however, activation of known cytosolic pathways, such as the inflammasome and type I IFN, lead to impaired immunity. Conversely, production of prostaglandin E₂ (PGE₂) downstream of cyclooxygenase-2 (COX-2) is essential for optimal L. monocytogenes T-cell priming. Here, we demonstrate that vacuole-constrained L. monocytogenes elicit reduced PGE₂ production compared to wild-type strains in macrophages and dendritic cells ex vivo. In vivo, infection with wild-type L. monocytogenes leads to 10-fold increases in PGE₂ production early during infection whereas vacuole-constrained strains fail to induce PGE₂ over mock-immunized controls. Mice deficient in COX-2 specifically in Lyz2⁺ or CD11c⁺ cells produce less PGE₂, suggesting these cell subsets contribute to PGE₂ levels in vivo, while depletion of phagocytes with clodronate abolishes PGE₂ production completely. Taken together, this work demonstrates that optimal PGE₂ production by phagocytes depends on L. monocytogenes access to the cytosol, suggesting that one reason cytosolic access is required to prime CD8⁺ T-cell responses may be to facilitate production of PGE₂.     

Current knowledge and perspectives on biofilm formation: the case of Listeria monocytogenes

Listeriosis is a rare, serious, and mainly food-borne infection caused by the bacterium Listeria monocytogenes. This food-borne infection primarily affects pregnant women and immunologically compromised individuals. L. monocytogenes is recognized as a problem for the food industry, mainly due to its environmental persistence, attributed in part to its ability to form biofilms. Biofilms are microbial communities adhered to biotic or abiotic surfaces coated by self-produced extracellular polymers. These structures confer protection to bacterial cells and decrease the efficiency of cleaning and disinfection procedures. This article presents a brief review of current perspectives on the formation of biofilms, with emphasis on L. monocytogenes, highlighting the importance of cell-to-cell communication and structural composition of the microbial communities. The techniques currently used to study biofilms and the need to develop new strategies for the prevention and control of biofilm-forming pathogens are also discussed.     

MurA escape mutations uncouple peptidoglycan biosynthesis from PrkA signaling

Gram-positive bacteria are protected by a thick mesh of peptidoglycan (PG) completely engulfing their cells. This PG network is the main component of the bacterial cell wall, it provides rigidity and acts as foundation for the attachment of other surface molecules. Biosynthesis of PG consumes a high amount of cellular resources and therefore requires careful adjustments to environmental conditions. An important switch in the control of PG biosynthesis of Listeria monocytogenes, a Gram-positive pathogen with a high infection fatality rate, is the serine/threonine protein kinase PrkA. A key substrate of this kinase is the small cytosolic protein ReoM. We have shown previously that ReoM phosphorylation regulates PG formation through control of MurA stability. MurA catalyzes the first step in PG biosynthesis and the current model suggests that phosphorylated ReoM prevents MurA degradation by the ClpCP protease. In contrast, conditions leading to ReoM dephosphorylation stimulate MurA degradation. How ReoM controls degradation of MurA and potential other substrates is not understood. Also, the individual contribution of the ~20 other known PrkA targets to PG biosynthesis regulation is unknown. We here present murA mutants which escape proteolytic degradation. The release of MurA from ClpCP-dependent proteolysis was able to activate PG biosynthesis and further enhanced the intrinsic cephalosporin resistance of L. monocytogenes. This latter effect required the RodA3/PBP B3 transglycosylase/transpeptidase pair. One murA escape mutation not only fully rescued an otherwise non-viable prkA mutant during growth in batch culture and inside macrophages but also overcompensated cephalosporin hypersensitivity. Our data collectively indicate that the main purpose of PrkA-mediated signaling in L. monocytogenes is control of MurA stability during standard laboratory growth conditions and intracellular growth in macrophages. These findings have important implications for the understanding of PG biosynthesis regulation and β-lactam resistance of L. monocytogenes and related Gram-positive bacteria.     

Listeria monocytogenes Internalin and E-cadherin: From Bench to Bedside

Listeria monocytogenes is a Gram-positive bacterium responsible for a severe infection associated with different clinical features (gastroenteritis, meningoencephalitis, and abortion in pregnant women). These pathologies are caused by the unusual capacity of the bacterium to cross three host barriers during infection and to invade nonphagocytic cells. To invade host cells, Listeria uses two proteins, InlA and InlB, which have specific receptors on the host-cell surface, E-cadherin and Met, respectively. Here, we discuss the specificity of the InlA–E-cadherin interaction, the signaling cascade activated on E-cadherin engagement by InlA, and the role of InlA and E-cadherin in the breaching of host barriers and the dissemination of the infection.Listeriosis is a potentially lethal food-borne infection with a mortality rate up to 30%. It has emerged as a significant human infection in industrialized countries along with the development of large-scale agro-industrial plants and refrigerated food. Opposite to most food-borne infections, listeriosis is rare but potentially very severe, because it remains often under-diagnosed at its early stages (Lecuit 2007). The etiological agent of listeriosis is Listeria monocytogenes, a Gram-positive bacterium that contaminates meat, dairy products, and ready to eat food. Upon ingestion of contaminated food, L. monocytogenes can colonize the intestine and gives rise to gastroenteritis in case of the absorption of a high inoculum. Strikingly, L. monocytogenes has the capacity to cross the intestinal barrier and disseminate to the mesenteric lymph nodes, spleen, and liver. In immunocompromised individuals, L. monocytogenes may replicate in the spleen and liver, cause prolonged and sustained bacteremia, cross the blood–brain barrier and the placental barrier, and disseminate to the brain and placenta, causing meningitis, encephalitis, abortion in pregnant women, and neonatal infections (Hamon et al. 2006; Bonazzi et al. 2009).The capacity of L. monocytogenes to cross multiple host barriers relies on the ability of the bacterium to invade nonphagocytic cells, such as epithelial cells, by interacting with host cell-surface receptors. Adhesion to host cells is a key step underlying bacterial pathogenicity and it is required to counteract the mechanical clearance at tissue surfaces provided by intestinal peristaltism and blood flow. Internalization allows persistence in a shielded niche, away from the soluble effectors of the host immune system (Cossart and Sansonetti 2004; Pizarro-Cerda and Cossart 2006), and access to target organs, as illustrated by L. monocytogenes (Bonazzi et al. 2009).Bacterial surface proteins that engage host receptors are generally called adhesins, although it is now clear that many of them not only mediate adhesion, but also bacterial internalization (Boyle and Finlay 2003; Hauck et al. 2006; Pizarro-Cerda and Cossart 2006). Adhesion to and internalization of L. monocytogenes within epithelial cells is mainly mediated by two bacterial surface protein members of the internalin family, namely internalin (InlA) and InlB, that use E-cadherin and Met as receptors, respectively, on the surface of host cells (Hamon et al. 2006; Pizarro-Cerda and Cossart 2006; Bonazzi et al. 2009). Upon receptor-mediated internalization, L. monocytogenes is engulfed into the cell and becomes surrounded by a tight phagocytic vacuole that the bacterium can lyse by means of the pore-forming toxin listeriolysin O (LLO). Once free in the cytoplasm of the host cell, L. monocytogenes uses the protein ActA to harness the actin polymerization machinery and facilitate its intracellular movement via the formation of so-called actin “comet tails.” Actin-based motility is fundamental for L. monocytogenes direct cell-to-cell spread, a typical feature that allows the dissemination of the infection to neighboring cells via the formation of plasma membrane protrusions. Once internalized by neighboring cells, L. monocytogenes is confined in a double-membrane vacuole from which it escapes to restart its life cycle (Fig. 1) (Hamon et al. 2006).Open in a separate windowFigure 1.The cell cycle of L. monocytogenes. (1) L. monocytogenes adheres to the surface of epithelial cells via the interactions of the surface proteins InlA and InlB with E-cadherin and the Met receptor, respectively. (2) On internalization, L. monocytogenes is engulfed in a phagocytic vacuole. (3) L. monocytogenes lyses vacuolar membranes by means of the toxin LLO. (4) L. monocytogenes uses the protein ActA to harness the actin polymerization machinery and facilitate its intracellular movement via the formation of so-called actin “comet tails.” (5) L. monocytogenes exploits actin-based motility for direct cell-to-cell spread to allow the dissemination of the infection to neighboring cells via the formation of plasma membrane protrusions. (6) Once internalized by neighboring cells, L. monocytogenes is confined in a double-membrane vacuole from which it escapes to restart its life cycle.Its remarkable adaptation to the cellular environment and its capacity to exploit cellular receptor-mediated signaling pathways and the actin polymerization machinery have made L. monocytogenes an exceptional tool for the study of a wide array of cellular functions (Cossart and Sansonetti 2004; Bonazzi and Cossart 2006; Hamon et al. 2006; Pizarro-Cerda and Cossart 2006; Veiga and Cossart 2005a; Bonazzi et al. 2009). Here, we review the interaction of InlA with E-cadherin, the signaling pathway initiated by this interaction that results in the internalization of L. monocytogenes, and the role of InlA-E-cadherin interaction during listeriosis.     

Strain-Specific Interactions of Listeria monocytogenes with the Autophagy System in Host Cells

Listeria monocytogenes is an intracellular bacterial pathogen that can replicate in the cytosol of host cells. These bacteria undergo actin-based motility in the cytosol via expression of ActA, which recruits host actin-regulatory proteins to the bacterial surface. L. monocytogenes is thought to evade killing by autophagy using ActA-dependent mechanisms. ActA-independent mechanisms of autophagy evasion have also been proposed, but remain poorly understood. Here we examined autophagy of non-motile (ΔactA) mutants of L. monocytogenes strains 10403S and EGD-e, two commonly studied strains of this pathogen. The ΔactA mutants displayed accumulation of ubiquitinated proteins and p62/SQSTM1 on their surface. However, only strain EGD-e ΔactA displayed colocalization with the autophagy marker LC3 at 8 hours post infection. A bacteriostatic agent (chloramphenicol) was required for LC3 recruitment to 10403S ΔactA, suggesting that these bacteria produce a factor for autophagy evasion. Internalin K was proposed to block autophagy of L. monocytogenes in the cytosol of host cells. However, deletion of inlK in either the wild-type or ΔactA background of strain 10403S had no impact on autophagy evasion by bacteria, indicating it does not play an essential role in evading autophagy. Replication of ΔactA mutants of strain EGD-e and 10403S was comparable to their parent wild-type strain in macrophages. Thus, ΔactA mutants of L. monocytogenes can block killing by autophagy at a step downstream of protein ubiquitination and, in the case of strain EGD-e, downstream of LC3 recruitment to bacteria. Our findings highlight the strain-specific differences in the mechanisms that L. monocytogenes uses to evade killing by autophagy in host cells.     

A Listeria monocytogenes clone in human breast milk associated with severe acute malnutrition in West Africa: A multicentric case-controlled study

BackgroundSevere acute malnutrition (SAM) is a major public health problem affecting children under the age of five in many low- and middle-income countries, and its resolution would contribute towards achieving the several sustainable development goals. The etiology of SAM is pluri-factorial, including delayed maturation of the gut microbiota, suboptimal feeding practices and dysfunctional breastfeeding. The recent serendipitous detection of Listeria monocytogenes in the breast milk of Malian women, in contrast to French women, suggests a possible association with SAM.Methodology/ Principal findingsTo investigate the possible association of L. monocytogenes carriage in breast milk and SAM, a case-control study was performed in Senegal, with subjects recruited from two areas. Using 16S amplicon sequencing, a culture independent method, 100% (152/152) of the mothers were positive for L. monocytogenes in their breast milk while qPCR analysis gave lower recovery rates. Interestingly, after enrichment in Fraser broth and seeding on PALCALM agar, all 10 isolated strains were isolated from the milk of 10 mothers who had SAM children which also had a significantly increased relative abundance of L. monocytogenes (0.34 (SD 0.35) vs 0.05 (SD 0.07) in controls, p<0.0001). The high genomic similarity between these strains and Malian breast milk strains from a previous study supports the hypothesis of endemic clone carriage in West Africa. Moreover, the in vitro growth inhibition of L. monocytogenes using breast milk samples was obtained from only 50% of the milk of mothers who had SAM children, in contrast to control samples which systematically inhibited the growth of L. monocytogenes with a higher inhibition diameter (15.7 mm (SD 2.3) in controls versus 3.5 mm (SD 4.6) in SAM, p = 0.0001). Lactobacillus and Streptococcus isolated from the breast milk of controls inhibit L. monocytogenes in a species-dependent manner.Conclusions/SignificanceOur study reveals a previously unsuspected carriage of L. monocytogenes in the breast milk of West African women, which is associated with SAM. The inhibitory effect of human selected lactic acid bacterial species against L. monocytogenes might provide new therapeutic and inexpensive options to prevent and treat this neglected public health issue.     

Inflammasome-Mediated Inhibition of Listeria monocytogenes-Stimulated Immunity Is Independent of Myelomonocytic Function

Activation of the Nlrc4 inflammasome results in the secretion of IL-1β and IL-18 through caspase-1 and induction of pyroptosis. L. monocytogenes engineered to activate Nlrc4 by expression of Legionella pneumophilia flagellin (L. monocytogenes L.p.FlaA) are less immunogenic for CD8⁺ T cell responses than wt L. monocytogenes. It is also known that IL-1β orchestrates recruitment of myelomonocytic cells (MMC), which have been shown to interfere with T cell-dendritic cells (DC) interactions in splenic white pulp (WP), limiting T cell priming and protective immunity. We have further analyzed the role of MMCs in the immunogenicity of L. monocytogenes L.p.FlaA. We confirmed that MMCs infiltrate the WP between 24–48 hours in response to wt L. monocytogenes infection and that depletion of MMCs enhances CD8⁺ T cell priming and protective memory. L. monocytogenes L.p.FlaA elicited accelerated recruitment of MMCs into the WP. While MMCs contribute to control of L. monocytogenes L.p.FlaA, MMC depletion did not increase immunogenicity of L.p.FlaA expressing strains. There was a significant decrease in L. monocytogenes L.p.FlaA in CD8α⁺ DCs independent of MMCs. These findings suggest that limiting inflammasome activation is important for bacterial accumulation in CD8α⁺ DCs, which are known to be critical for T cell response to L. monocytogenes.     

Anthropogenic impact on the presence of L. monocytogenes in soil, fruits, and vegetables

The aim of this study was to determine the prevalence of Listeria sp. and Listeria monocytogenes in soil samples with reference to type of fertilizers (natural and artificial) and distance from places intensively exploited by men, as well as to determine the relationship between the presence of L. monocytogenes in the soil and in fruits and vegetables. The examined 1,000 soil samples originated from 15 different areas, whilst 140 samples of fruits and 210 samples of vegetables were collected from those areas. L. monocytogenes was isolated only from 5.5 % of all soil samples coming exclusively from meadows intensively grazed by cattle (27.8 %) and areas near food processing plants (25 %) and wild animal forests (24 %). Listeria sp. and L. monocytogenes were not present on artificially fertilized areas and wastelands. L. monocytogenes was detected in 10 % of samples of strawberry, 15 % of potato samples, and 5 % of parsley samples. Our data indicate that Listeria spp. and particularly L. monocytogenes were found in the soil from (1) arable lands fertilized with manure, (2) pasture (the land fertilized with feces of domestic animals), and (3) forests (again, the land fertilized with feces of animals, not domestic but wild). The bacteria were not detected in the soil samples collected at (1) artificially fertilized arable lands and (2) wastelands (the lands that were not fertilized with manure or animal feces). Moreover, a correlation was determined in the presence of L. monocytogenes between soil samples and samples of the examined fruits and vegetables.     

Toxoplasma gondii Profilin Promotes Recruitment of Ly6Chi CCR2+ Inflammatory Monocytes That Can Confer Resistance to Bacterial Infection

Ly6C⁺ inflammatory monocytes are essential to host defense against Toxoplasma gondii, Listeria monocytogenes and other infections. During T. gondii infection impaired inflammatory monocyte emigration results in severe inflammation and failure to control parasite replication. However, the T. gondii factors that elicit these monocytes are unknown. Early studies from the Remington laboratory showed that mice with a chronic T. gondii infection survive lethal co-infections with unrelated pathogens, including L. monocytogenes, but a mechanistic analysis was not performed. Here we report that this enhanced survival against L. monocytogenes is due to early reduction of bacterial burdens and elicitation of Ly6C⁺ inflammatory monocytes. We demonstrate that a single TLR11/TLR12 ligand profilin (TgPRF) was sufficient to reduce bacterial burdens similar to T. gondii chronic infection. Stimulation with TgPRF was also sufficient to enhance animal survival when administered either pre- or post-Listeria infection. The ability of TgPRF to reduce L. monocytogenes burdens was dependent on TLR11 and required IFN-γ but was not dependent on IL-12 signaling. TgPRF induced rapid production of MCP-1 and resulted in trafficking of Ly6C^hi CCR2⁺ inflammatory monocytes and Ly6G⁺ neutrophils into the blood and spleen. Stimulation with TgPRF reduced L. monocytogenes burdens in mice depleted with the Ly6G specific MAb 1A8, but not in Ly6C/Ly6G specific RB6-8C5 depleted or CCR2^−/− mice, indicating that only inflammatory monocytes are required for TgPRF-induced reduction in bacterial burdens. These results demonstrate that stimulation of TLR11 by TgPRF is a mechanism to promote the emigration of Ly6C^hi CCR2⁺ monocytes, and that TgPRF recruited inflammatory monocytes can provide an immunological benefit against an unrelated pathogen.     

Acquired cellular resistance following transfer of lymphocytes from mice infected repeatedly with Staphylococcus aureus

Cell-mediated immunity following multiple staphylococcal infections of mice was found to differ from other established experimental models of infection with facultative intracellular microorganisms in that acquired cellular resistance was of extremely short duration. This is perhaps a reflection of the fact that Staphylococcus aureus does not multiply or survive within mononuclear phagocytes and are eliminated from the tissues within a few days. Thus, a sustained antigenic stimulus required for maintenance of cellular immunity does not occur. Spleen cells from immunized mice transferred simultaneously with staphylococcal antigen conferred resistance against Listeria monocytogenes on unimmunized syngeneic mice. Treatment of immune splenic lymphocytes with antilymphocyte serum and complement markedly inhibited or abolished capacity of the lymphocytes to transfer resistance to Listeria. These results support and extend our previous data which suggest that mice infected repeatedly with staphylococci are able to suppress the growth of L. monocytogenes via cellular rather than humoral mechanisms.     

Control of Relative Air Humidity as a Potential Means to Improve Hygiene on Surfaces: A Preliminary Approach with Listeria monocytogenes

Relative air humidity fluctuations could potentially affect the development and persistence of pathogenic microorganisms in their environments. This study aimed to characterize the impact of relative air humidity (RH) variations on the survival of Listeria monocytogenes, a bacterium persisting on food processing plant surfaces. To assess conditions leading to the lowest survival rate, four strains of L. monocytogenes (EGDe, CCL500, CCL128, and LO28) were exposed to different RH conditions (75%, 68%, 43% and 11%) with different drying kinetics and then rehydrated either progressively or instantaneously. The main factors that affected the survival of L. monocytogenes were RH level and rehydration kinetics. Lowest survival rates between 1% and 0.001% were obtained after 3 hours of treatment under optimal conditions (68% RH and instantaneous rehydration). The survival rate was decreased under 0.001% after prolonged exposure (16h) of cells under optimal conditions. Application of two successive dehydration and rehydration cycles led to an additional decrease in survival rate. This preliminary study, performed in model conditions with L. monocytogenes, showed that controlled ambient RH fluctuations could offer new possibilities to control foodborne pathogens in food processing environments and improve food safety.