Inactivation of Surface-adherent Listeria monocytogenes Hypochlorite and Heat

1991 ◽  
Vol 54 (1) ◽  
pp. 4-6 ◽  
Author(s):  
SHIN-HO LEE ◽  
JOSEPH F. FRANK
Keyword(s):  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Cell Population ◽  
Incubation Time ◽  
Cell Populations ◽  
Adherent Cell ◽  
Adherent Cells ◽  
D Cells

Inactivation by hypochlorite of Listeria monocytogenes cells adherent to stainless steel was determined. Adherent cell populations were prepared by incubating stainless steel slides with a 24 h culture of L. monocytogenes for 4 h at 21°C. Adherent microcolonies were prepared by growing L. monocytogenes on stainless steel slides submerged in a 1:15 dilution of tryptic soy broth at 21°C. The slides were then rinsed and transferred to fresh sterile broth every 2 d with a total incubation time of 8 d. Although the 4 h and 8 d adherent populations were at similar levels, 8 d adherent cells were over 100 times more resistant than the 4 h adherent cell population when exposed to 200 ppm hypochlorite for 30 s. When stainless steel slides containing adherent cells were heated at 72°C both adherent cell populations were inactivated after 1 min. Detectable numbers of L. monocytogenes remained on stainless steel slides after treatment at 65°C for 3 min when adherent 8 d cells were tested but not when adherent 4 h cells were used.

scholarly journals The requirement for adherent cells in the Fc fragment-induced proliferative response of murine spleen cells.

1979 ◽  
Vol 150 (2) ◽  
pp. 256-266 ◽  
Author(s):  
E L Morgan ◽  
W O Weigle
Keyword(s):  
Cell Proliferation ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Population ◽  
Proliferative Response ◽  
Adherent Cell ◽  
Adherent Cells ◽  
Spleen Cells ◽  
Murine Spleen

The proliferative response of mouse B lymphocytes induced by Fc fragments was found to be dependent upon an adherent cell population. The adherent cell is esterase positive, irradiation resistant, and not susceptible to lysis by anti-thymus serum and complement. The mechanism(s) by which Fc fragments induce B-cell proliferation could be the result of the interaction of Fc with both B cells and adherent cells or with adherent cells which then release factors that trigger the B cells to proliferate. Spleen cells from the C3H/HeJ mouse were shown to be unable to respond to Fc fragments. The addition of adherent cells from either C3H/St or C3H/HeN mice to adherent cell depleted C3H/HeJ cells enabled them to respond to Fc, indicating the defect was in the adherent cell population.

scholarly journals The Listeria monocytogenes Homolog of the Escherichia coli era Gene Is Involved in Adhesion to Inert Surfaces

2007 ◽  
Vol 73 (23) ◽  
pp. 7789-7792 ◽  
Author(s):  
Frédéric Auvray ◽  
Danielle Chassaing ◽  
Cécile Duprat ◽  
Brigitte Carpentier
Keyword(s):  
Escherichia Coli ◽  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Growth Defect ◽  
Cell Populations ◽  
Lower Growth ◽  
E Coli ◽  
Attached Cell ◽  
Dimethylammonium Chloride ◽  
Inert Surfaces

ABSTRACT Two transposon-insertional mutants of Listeria monocytogenes showing smaller viable surface-attached cell populations after disinfection with N,N-didecyl-N,N-dimethylammonium chloride were identified. In both mutants, transposon Tn917-lac was found to be inserted into the same gene, lmo1462, which is homologous to the essential Escherichia coli era gene. Both L. monocytogenes lmo1462-disrupted mutants displayed lower growth rates, as was also shown for several E. coli era mutants, and the lmo1462 gene was able to complement the growth defect of an E. coli era mutant. We showed that the disruption of lmo1462 decreased the ability of L. monocytogenes cells to adhere to stainless steel. Our results suggest that this era-like gene is involved in adhesion and contributes to the presence of L. monocytogenes on surfaces.

Destruction of Listeria monocytogenes Biofilms on Stainless Steel Using Monolaurin and Heat1

1995 ◽  
Vol 58 (3) ◽  
pp. 251-255 ◽  
Author(s):  
DEOG-HWAN OH ◽  
DOUGLAS L. MARSHALL
Keyword(s):  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Food Industry ◽  
Adherent Cells ◽  
Planktonic Cells ◽  
Antimicrobial Effects ◽  
Biofilm Removal ◽  
Nutrient Environment ◽  
Physical Treatments

Individual and combined antimicrobial effects of monolaurin and heat on planktonic, 1-day adherent, or 7-day adherent cells of Listeria monocytogenes were determined to evaluate biofilm removal from stainless steel. Planktonic cells were more sensitive to heat and monolaurin than were cells attached to stainless steel. Young (1-day) biofilm cells were more sensitive to each treatment than were old (7-day) biofilm cells. Adherent cells were destroyed by 50 μg/ml monolaurin combined with heating at 65°C for 5 min. Cells in a rich nutrient environment were more resistant to treatment than were cells in a depleted nutrient environment. Results demonstrate the usefulness of combining chemical and physical treatments to control L. monocytogenes biofilm problems in the food industry.

Effect of Cleaners and Sanitizers on Listeria monocytogenes Attached to Product Contact Surfaces

1992 ◽  
Vol 55 (4) ◽  
pp. 246-251 ◽  
Author(s):  
E. P. KRYSINSKI ◽  
L. J. BROWN ◽  
T. J. MARCHISELLO
Keyword(s):  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Hazard Analysis ◽  
Control Point ◽  
Adherent Cells ◽  
Chemical Cleaning ◽  
Critical Control Point ◽  
Biofilm Removal ◽  
Good Manufacturing Practices ◽  
Conveyor Belts

A variety of chemical cleaning and sanitizing compounds were evaluated for their ability to remove and/or inactivate surface adherent Listeria monocytogenes. Adherent cells were obtained by incubating 1-cm2 chips of stainless steel or plastic conveyor belts with a multistrain cocktail of L. monocytogenes for 24 h at 25°C. Resistance of adherent cells to sanitizers was dependent upon the surface studied, being greatest on polyester/polyurethane followed by polyester and stainless steel. Biofilm removal with cleaners followed the same pattern as sanitizers with the polyester/polyurethane surface being most difficult to clean. Complete biofilm removal and/or inactivation was obtained in many cases where the surface was first cleaned prior to exposure to sanitizer. The data support conventional wisdom in that cleaning must precede sanitizing in order to remove and inactivate microorganisms. Listeria biofilms should be controllable by combining Good Manufacturing Practices with the discipline of a Hazard Analysis Critical Control Point Program.

Survival of Listeria monocytogenes Attached to Stainless Steel Surfaces in the Presence or Absence of Flavobacterium spp.

2001 ◽  
Vol 64 (9) ◽  
pp. 1369-1376 ◽  
Author(s):  
PHILIP J. BREMER ◽  
IAN MONK ◽  
CAROLYN M. OSBORNE
Keyword(s):  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Mixed Culture ◽  
Cell Population ◽  
Exposure Time ◽  
Food Processing ◽  
Pure Culture ◽  
Bacterial Biofilm ◽  
Selective Agar ◽  
Steel Surfaces

Contaminated surfaces of food processing equipment are believed to be a significant source of Listeria monocytogenes to foods. However, very little is known about the survival of Listeria in processing environments. In a mixed bacterial biofilm of L. monocytogenes and Flavobacterium spp., the number of L. monocytogenes cells attaching to stainless steel increased significantly compared to when L. monocytogenes was in a pure culture. The L. monocytogenes cells in the mixed biofilms were also recoverable for significantly longer exposure periods. On colonized coupons held at 15°C and 75% humidity, decimal reduction times were 1.2 and 18.7 days for L. monocytogenes in pure and mixed biofilms, respectively. With increasing exposure time, the proportion of cells that were sublethally injured (defined as an inability to grow on selective agar) increased from 8.1% of the recoverable cell population at day 0 to 91.4% after 40 days' exposure. At 4 and −20°C, decimal reduction times for L. monocytogenes in pure culture were 2.8 and 1.4 days, respectively, and in mixed culture, 10.5 and 14.4 days, respectively. The enhanced colonization and survival of L. monocytogenes on “unclean” surfaces increase the persistence of this pathogen in food processing environments, while the increase in the percentage of sublethally injured cells in the population with time may decrease the ability of enrichment regimes to detect it.

Novel Microtechnology System for Cytometric Analysis of Adherent Cell Populations

2010 ◽  
Author(s):  
Nicholas M. Gunn ◽  
Mark Bachman ◽  
Lifeng Zheng ◽  
G.-P. Li ◽  
Edward L. Nelson
Keyword(s):  
Single Cells ◽  
Pulsed Laser ◽  
Cellular Heterogeneity ◽  
Cell Populations ◽  
Adherent Cell ◽  
Adherent Cells ◽  
Microscope Slide ◽  
Glass Microscope Slide ◽  
Glass Microscope

The increasing appreciation of tissue cellular heterogeneity and recent identification of rare cell populations within tissues that are associated with specific biological behaviors, e.g., progenitor cells, has illuminated a limitation of current technologies to study such adherent cells directly from primary tissues. The micropallet array is a recently-developed technology designed to address this limitation by virtue of its capacity to isolate and recover single adherent cells on individual micropallets [1]. Micropallet arrays consist of hundreds of thousands of microscale polymer pedestals (“micropallets”) uniformly arrayed on a glass microscope slide. The micropallets are made from a high aspect photopolymerizable polymer using photolithographic methods. Cells are applied to the arrays and fall stochastically upon its surface, with single cells adhering to individual micropallets. Cells are then analyzed in situ and single, unperturbed cells can be selected and collected from the array by releasing the underlying micropallets using a focused pulsed laser.

scholarly journals Effect of Environmental Stress on the Ability of Listeria monocytogenes Scott A To Attach to Food Contact Surfaces

1998 ◽  
Vol 61 (10) ◽  
pp. 1293-1298 ◽  
Author(s):  
L. MICHELE SMOOT ◽  
MERLE D. PIERSON
Keyword(s):  
Stainless Steel ◽  
Listeria Monocytogenes ◽  
Cell Growth ◽  
Cell Populations ◽  
Sterile Phosphate Buffer ◽  
Food Contact Surfaces ◽  
Alkaline Conditions ◽  
Ph Conditions ◽  
Growth Ph ◽  
Holding Temperature

Attachment of Listeria monocytogenes Scott A to Buna-N rubber and stainless Steel under different temperature and pH conditions at the time of cell growth or at the time of attachment was investigated. AU experiments were conducted using sterile phosphate buffer to avoid cell growth during exposure to the test surfaces. Numbers of attached cells increased with increasing attachment temperature (10 to 45°C) and exposure time for both test surfaces. Maximum levels of attached cells were obtained when cell growth occurred at 30°C. Downward, but not upward, shifts in the cell suspension holding temperature prior to attachment to Buna-N rubber resulted in reduced adhered cell populations. Maximum levels of adhered cells to Buna-N rubber were not affected by adjustments of the attachment medium pH between 4 and 9. However, after short contact times (i.e., less than 30 min), levels of attached cells were lower when attachment occurred under alkaline conditions. Growth pH was also found to affect the levels of adhered cell populations to Buna-N rubber. L. monocytogenes Scott A attached to stainless Steel at higher levels for all temperature and pH parameters evaluated in this study.

scholarly journals Prostaglandin E inhibits the production of human interleukin 2.

1982 ◽  
Vol 155 (3) ◽  
pp. 943-948 ◽  
Author(s):  
R S Rappaport ◽  
G R Dodge
Keyword(s):  
Mononuclear Cell ◽  
Human Lymphocytes ◽  
Interleukin 2 ◽  
Cell Populations ◽  
Adherent Cell ◽  
Prostaglandin E ◽  
Enhancement Effect ◽  
Adherent Cells ◽  
Normal Human ◽  
Nonadherent Cell

Prostaglandins of the E type specifically inhibited the production of interleukin 2 (IL-2) by normal human lymphocytes, whereas PG synthetase inhibitors such as indomethacin and fentiazac raised IL-2 production above normal levels. Removal of adherent cells from mononuclear cell populations also resulted in enhanced IL-2 production. The resultant nonadherent cell population lost sensitivity to the enhancement effect of PG synthetase inhibitors, suggesting that a PGE-producing adherent cell plays a major role in the regulation of IL-2.

scholarly journals Discrete and continuum phenotype-structured models for the evolution of cancer cell populations under chemotherapy

2020 ◽  
Vol 15 ◽  
pp. 14 ◽  
Author(s):  
Rebecca E.A. Stace ◽  
Thomas Stiehl ◽  
Mark A.J. Chaplain ◽  
Anna Marciniak-Czochra ◽  
Tommaso Lorenzi
Keyword(s):  
Cancer Cell ◽  
Cell Population ◽  
Evolutionary Dynamics ◽  
Analytical Description ◽  
Chemotherapeutic Agents ◽  
Cell Populations ◽  
Theoretical Ground ◽  
Individual Based Model ◽  
Nonlocal Parabolic Equation ◽  
Epigenetic Drug

We present a stochastic individual-based model for the phenotypic evolution of cancer cell populations under chemotherapy. In particular, we consider the case of combination cancer therapy whereby a chemotherapeutic agent is administered as the primary treatment and an epigenetic drug is used as an adjuvant treatment. The cell population is structured by the expression level of a gene that controls cell proliferation and chemoresistance. In order to obtain an analytical description of evolutionary dynamics, we formally derive a deterministic continuum counterpart of this discrete model, which is given by a nonlocal parabolic equation for the cell population density function. Integrating computational simulations of the individual-based model with analysis of the corresponding continuum model, we perform a complete exploration of the model parameter space. We show that harsher environmental conditions and higher probabilities of spontaneous epimutation can lead to more effective chemotherapy, and we demonstrate the existence of an inverse relationship between the efficacy of the epigenetic drug and the probability of spontaneous epimutation. Taken together, the outcomes of the model provide theoretical ground for the development of anticancer protocols that use lower concentrations of chemotherapeutic agents in combination with epigenetic drugs capable of promoting the re-expression of epigenetically regulated genes.

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