Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium.

Maria J Fernandez-Cabezudo; Dietrich Lorke; Sheikh Azimullah; Milena Mechkarska; Mohammed Y Hasan; Georg A Petroianu; Basel K Al-Ramadi

Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium.

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Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium. / Fernandez-Cabezudo, Maria J; Lorke, Dietrich; Azimullah, Sheikh; Mechkarska, Milena; Hasan, Mohammed Y; Petroianu, Georg A; Al-Ramadi, Basel K.

In: IMMUNOLOGY, Vol. 130, No. 3, 3, 2010, p. 388-398.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Fernandez-Cabezudo, MJ, Lorke, D, Azimullah, S, Mechkarska, M, Hasan, MY, Petroianu, GA & Al-Ramadi, BK 2010, 'Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium.', IMMUNOLOGY, vol. 130, no. 3, 3, pp. 388-398. <http://www.ncbi.nlm.nih.gov/pubmed/20408892?dopt=Citation>

APA

Fernandez-Cabezudo, M. J., Lorke, D., Azimullah, S., Mechkarska, M., Hasan, M. Y., Petroianu, G. A., & Al-Ramadi, B. K. (2010). Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium. IMMUNOLOGY, 130(3), 388-398. [3]. http://www.ncbi.nlm.nih.gov/pubmed/20408892?dopt=Citation

Vancouver

Fernandez-Cabezudo MJ, Lorke D, Azimullah S, Mechkarska M, Hasan MY, Petroianu GA et al. Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium. IMMUNOLOGY. 2010;130(3):388-398. 3.

Bibtex

@article{efc8ba7edfc74020b170176bc6dd2bb8,

title = "Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium.",

abstract = "SUMMARY: The cholinergic nervous system has been demonstrated to attenuate the inflammatory response during sepsis via the inhibitory action of acetylcholine (ACh) on macrophages. These findings were largely based on experimental sepsis models using endotoxin as the inducing agent. Herein, however, we report that the specific inhibition of acetylcholinesterase (AChE) renders animals more resistant to infection by a virulent strain of Salmonella enterica serovar Typhimurium, a Gram-negative enteric pathogen. Inhibition of AChE was induced by a subchronic exposure to paraoxon, a potent anti-cholinesterase metabolite of the organophosphorous compound parathion. Our findings indicate that inhibition of AChE enhanced survival of infected mice in a dose-dependent fashion and this correlated with efficient control of bacterial proliferation in target organs. Immunologically, inhibition of AChE enabled the animals to mount a more effective inflammatory anti-microbial response, and to secrete higher levels of interleukin-12, a key T helper type 1-promoting cytokine. The ACh-induced enhancement in resistance to infection was abrogated by co-administration of an oxime which can reactivate AChE. Hence, in a model of Gram-negative bacterial infection, cholinergic stimulation is shown to enhance the anti-microbial immune response leading to effective control of bacterial proliferation and enhanced animal survival.",

keywords = "Animals, Male, Survival Analysis, Mice, Mice, Inbred BALB C, Nitric Oxide metabolism, Cytokines blood, Cell Count, Macrophages cytology, Acetylcholinesterase metabolism, B-Lymphocytes cytology, Cholinesterase Inhibitors pharmacology, Cholinesterase Reactivators pharmacology, Concanavalin A pharmacology, Erythrocytes drug effects, GPI-Linked Proteins, Immune System drug effects, Lipopolysaccharides pharmacology, Lymph Nodes microbiology, Oximes pharmacology, Paraoxon pharmacology, Pyridinium Compounds pharmacology, Salmonella Infections blood, Salmonella typhimurium pathogenicity, Spleen cytology, T-Lymphocytes cytology, Thymus Gland drug effects, Animals, Male, Survival Analysis, Mice, Mice, Inbred BALB C, Nitric Oxide metabolism, Cytokines blood, Cell Count, Macrophages cytology, Acetylcholinesterase metabolism, B-Lymphocytes cytology, Cholinesterase Inhibitors pharmacology, Cholinesterase Reactivators pharmacology, Concanavalin A pharmacology, Erythrocytes drug effects, GPI-Linked Proteins, Immune System drug effects, Lipopolysaccharides pharmacology, Lymph Nodes microbiology, Oximes pharmacology, Paraoxon pharmacology, Pyridinium Compounds pharmacology, Salmonella Infections blood, Salmonella typhimurium pathogenicity, Spleen cytology, T-Lymphocytes cytology, Thymus Gland drug effects",

author = "Fernandez-Cabezudo, {Maria J} and Dietrich Lorke and Sheikh Azimullah and Milena Mechkarska and Hasan, {Mohammed Y} and Petroianu, {Georg A} and Al-Ramadi, {Basel K}",

year = "2010",

language = "Deutsch",

volume = "130",

pages = "388--398",

journal = "IMMUNOLOGY",

issn = "0019-2805",

publisher = "Wiley-Blackwell",

number = "3",

}

RIS

TY - JOUR

T1 - Cholinergic stimulation of the immune system protects against lethal infection by Salmonella enterica serovar Typhimurium.

AU - Fernandez-Cabezudo, Maria J

AU - Lorke, Dietrich

AU - Azimullah, Sheikh

AU - Mechkarska, Milena

AU - Hasan, Mohammed Y

AU - Petroianu, Georg A

AU - Al-Ramadi, Basel K

PY - 2010

Y1 - 2010

N2 - SUMMARY: The cholinergic nervous system has been demonstrated to attenuate the inflammatory response during sepsis via the inhibitory action of acetylcholine (ACh) on macrophages. These findings were largely based on experimental sepsis models using endotoxin as the inducing agent. Herein, however, we report that the specific inhibition of acetylcholinesterase (AChE) renders animals more resistant to infection by a virulent strain of Salmonella enterica serovar Typhimurium, a Gram-negative enteric pathogen. Inhibition of AChE was induced by a subchronic exposure to paraoxon, a potent anti-cholinesterase metabolite of the organophosphorous compound parathion. Our findings indicate that inhibition of AChE enhanced survival of infected mice in a dose-dependent fashion and this correlated with efficient control of bacterial proliferation in target organs. Immunologically, inhibition of AChE enabled the animals to mount a more effective inflammatory anti-microbial response, and to secrete higher levels of interleukin-12, a key T helper type 1-promoting cytokine. The ACh-induced enhancement in resistance to infection was abrogated by co-administration of an oxime which can reactivate AChE. Hence, in a model of Gram-negative bacterial infection, cholinergic stimulation is shown to enhance the anti-microbial immune response leading to effective control of bacterial proliferation and enhanced animal survival.

AB - SUMMARY: The cholinergic nervous system has been demonstrated to attenuate the inflammatory response during sepsis via the inhibitory action of acetylcholine (ACh) on macrophages. These findings were largely based on experimental sepsis models using endotoxin as the inducing agent. Herein, however, we report that the specific inhibition of acetylcholinesterase (AChE) renders animals more resistant to infection by a virulent strain of Salmonella enterica serovar Typhimurium, a Gram-negative enteric pathogen. Inhibition of AChE was induced by a subchronic exposure to paraoxon, a potent anti-cholinesterase metabolite of the organophosphorous compound parathion. Our findings indicate that inhibition of AChE enhanced survival of infected mice in a dose-dependent fashion and this correlated with efficient control of bacterial proliferation in target organs. Immunologically, inhibition of AChE enabled the animals to mount a more effective inflammatory anti-microbial response, and to secrete higher levels of interleukin-12, a key T helper type 1-promoting cytokine. The ACh-induced enhancement in resistance to infection was abrogated by co-administration of an oxime which can reactivate AChE. Hence, in a model of Gram-negative bacterial infection, cholinergic stimulation is shown to enhance the anti-microbial immune response leading to effective control of bacterial proliferation and enhanced animal survival.

KW - Animals

KW - Male

KW - Survival Analysis

KW - Mice

KW - Mice, Inbred BALB C

KW - Nitric Oxide metabolism

KW - Cytokines blood

KW - Cell Count

KW - Macrophages cytology

KW - Acetylcholinesterase metabolism

KW - B-Lymphocytes cytology

KW - Cholinesterase Inhibitors pharmacology

KW - Cholinesterase Reactivators pharmacology

KW - Concanavalin A pharmacology

KW - Erythrocytes drug effects

KW - GPI-Linked Proteins

KW - Immune System drug effects

KW - Lipopolysaccharides pharmacology

KW - Lymph Nodes microbiology

KW - Oximes pharmacology

KW - Paraoxon pharmacology

KW - Pyridinium Compounds pharmacology

KW - Salmonella Infections blood

KW - Salmonella typhimurium pathogenicity

KW - Spleen cytology

KW - T-Lymphocytes cytology

KW - Thymus Gland drug effects