Advances in Microbial Physiology (eBook)

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2009 | 1. Auflage
202 Seiten
Elsevier Science (Verlag)
978-0-08-088831-6 (ISBN)

Advances in Microbial Physiology is one of the most successful and prestigious series from Academic Press, an imprint of Elsevier. It publishes topical and important reviews, interpreting physiology to include all material that contributes to our understanding of how microorganisms and their component parts work. First published in 1967, it is now in its 56th volume. The Editors have always striven to interpret microbial physiology in the broadest context and have never restricted the contents to traditional views of whole cell physiology. Now edited by Professor Robert Poole, University of Sheffield, Advances in Microbial Physiology continues to be an influential and very well reviewed series. - 2007 impact factor of 4.9, placing it 13th in the highly competitive category of microbiology - Contributions by leading international scientists - The latest research in microbial physiology

Advances in Microbial Physiology is one of the most successful and prestigious series from Academic Press, an imprint of Elsevier. It publishes topical and important reviews, interpreting physiology to include all material that contributes to our understanding of how microorganisms and their component parts work. First published in 1967, it is now in its 56th volume. The Editors have always striven to interpret microbial physiology in the broadest context and have never restricted the contents to traditional views of whole cell physiology. Now edited by Professor Robert Poole, University of Sheffield, Advances in Microbial Physiology continues to be an influential and very well reviewed series. - 2007 impact factor of 4.9, placing it 13th in the highly competitive category of microbiology- Contributions by leading international scientists- The latest research in microbial physiology

Front Cover 1
Advances in Microbial Physiology 2
Copyright Page 5
Contents 6
Contributors to Volume 56 8
All Stressed Out. Salmonella Pathogenesis and Reactive Nitrogen Species 10
Abbreviations 11
1. Overview 12
2. Reactive Nitrogen Species (RNS): An Important Component of the Innate Immune System 12
3. Salmonella: Epidemiology 17
4. Salmonella and RNS 21
5. Nitrate Reductase Systems 27
6. Conclusion 29
References 29
Microbial Metropolis 38
Abbreviations 39
1. Introduction 40
2. A Multiplicity of Manifestations 45
3. Sticking to Things 49
4. The Matrix 54
5. On Communicating: Quorum Sensing (QS) 57
6. Biofilm Formation 62
7. Evolution and Social Microbiology 64
8. Model Building: The Glass Bead Game? 72
9. Multicellular Development – Getting it all Together 77
Postscript 85
References 85
Carbon Monoxide in Biology and Microbiology: Surprising Roles for the "Detroit Perfume" 94
Abbreviations 96
1. Introduction 97
2. The Chemistry of CO and Other Heme Ligands and Implications for Biological Interactions 100
3. CO in the Biosphere and the Origin of Life 106
4. CO as a Heme Ligand 107
5. CO as an Inhibitor of Respiration 108
6. Bacterial Metabolism of CO 109
7. Microbial HO 115
8. Experimental Administration of CO and the Development of CO-RMs 121
9. New Applications of CO in Physiology and Medicine 129
10. Consequences of Microbial Exposure to CO and CO-RMs 145
11. Future Prospects and Unanswered Questions 156
Acknowledgments 156
References 157
Author Index 178
A 178
B 178
C 180
D 181
E 182
F 182
G 183
H 184
I 185
J 185
K 185
L 186
M 187
N 189
O 189
P 190
Q 191
R 191
S 192
T 193
U/ 194
V 194
W 195
X 196
Y 196
Z 196
Subject Index 198
A 198
B 198
C 198
D 199
E 199
F 199
G 199
H 199
I 200
K 200
L 200
M 200
N 200
O 200
P 200
Q 201
R 201
S 201
T 202
V 202
W 202
Z 202

All Stressed Out. Salmonella Pathogenesis and Reactive Nitrogen Species

K. Prior1, I. Hautefort2, J.C.D. Hinton3, D.J. Richardson1 and G. Rowley1

1School of Biological Sciences, University of East Anglia, Norwich, UK

2Molecular Microbiology Group, Institute of Food Research, Norwich Research Park, Norwich, UK

3School of Genetics and Microbiology, Trinity College, Dublin, Ireland

Abstract

Bacterial pathogens must overcome a range of challenges during the process of infecting their host. The ability of a pathogen to sense and respond appropriately to changes in host environment is vital if the pathogen is to succeed. Mammalian defense strategies include the use of barriers like skin and epithelial surfaces, the production of a chemical arsenal, such as stomach acid and reactive oxygen and nitrogen species, and a highly coordinated cellular and humoral immune response.

Salmonella serovars are significant human and animal pathogens which have evolved several mechanisms to overcome mammalian host defense. Here we focus on the interplay which occurs between Salmonella and the host during the infection process, with particular emphasis on the complex bacterial response to reactive nitrogen species produced by the host. We discuss recent advances in our understanding of the key mechanisms which confer bacterial resistance to nitrogen species, which in response to nitric oxide include the flavohemoglobin, HmpA, the flavorubredoxin, NorV, and the cytochrome c nitrite reductase, NrfA, whilst in response to nitrate include a repertoire of nitrate reductases. Elucidating the precise role of different aspects of microbial physiology, nitrogen metabolism, and detoxification during infection will provide valuable insight into novel opportunities and potential targets for the development of therapeutic approaches.

Abbreviations

ATR: acid tolerance response
eNOS: endothelial NOS
Hb(Fe ii): oxy-ferrous hemoglobin
IFN-?: gamma-interferon
IFN-?R: gamma-interferon receptor
IL-1: interleukin-1
iNOS: inducible NOS
IRF-1: interferon regulatory factor 1
JAK: Janus kinase
LPS: lipopolysaccharide
MDR: multi-drug resistant
NF-?B: a transcription factor (nuclear factor kappa-light-chain-enhancer of activated B cells)
nNOS: neuronal NOS
NOS: nitric oxide synthase
NR-A: nitrate reductase system comprising NarGHJI operon
NR-Z: nitrate reductase system comprising NarZYWV operon
PAMP: pathogen-associated molecular pattern
PMN: polymorphonuclear leukocytes
RNI: reactive nitrogen intermediate
RNS: reactive nitrogen species
ROI: reactive oxygen intermediate
ROS: reactive oxygen species
SCV: Salmonella-containing vacuole
SPI-1, SPI-2: Salmonella Pathogenicity Island 1, 2
STAT: signal transducers and activators of transcription
TGF-?: transforming growth factor beta
TLR: Toll-like receptor
TNF-?: tumor necrosis factor alpha
TTSS: type-III secretion system

1. Overview

The ability of a pathogen to sense and respond to its ever changing environment is critical to its success. Using Salmonella enterica serovar Typhimurium ( S. Typhimurium) as a model intracellular organism, this review explores the interplay between the host and pathogen during the infection process. We discuss the strategies that Salmonella, and other pathogens, employ to respond to reactive nitrogen species (RNS) produced by the host to resist bacterial infection.

2. Reactive Nitrogen Species (RNS): An important component of the innate immune system

2.1. Innate Mammalian Defense

Innate host defense systems respond non-specifically to the presence of pathogens. The responses do not confer long-lasting or protective immunity or the establishment of immunological memory, such as occurs in the adaptive immune response (Levy et al., 2005). However, activity of the innate defenses may later result in activation of the adaptive immune system, through presentation of antigens (Kindt et al., 2007).

Innate immunity includes barrier defenses, such as the integrity of the skin, which prevents entry of pathogens. The skin surface is also maintained at a slightly acidic pH by secretions, produced by hair follicles which contain lactic acid and fatty acids (Maggini et al., 2007). Ciliary activity in the lungs expels foreign particles, including pathogenic microbes, by beating of the hair-like cilia in an upward direction (Levy et al., 2005). Coughing and sneezing responses also expel irritants. Mucus is produced in both the respiratory and gastrointestinal tracts, and this can trap microbes, preventing their further activity (Levy et al., 2005). The normal flushing by tears, saliva, and urine also removes pathogens. Indeed, tears and saliva contain lysozyme which can destroy the cell membrane of gram-positive bacteria, leading to bacterial lysis (Abergel et al., 2007). The immune processes function together to help mammals to prevent infection by bacterial pathogens.

2.1.1. Stomach Acidity and RNS

One of the first innate mammalian defenses to be encountered by ingested enteric pathogens is the acidic environment of the stomach. Here, acidity may dip as low as pH 1 in the immediate post-prandial period (Levy et al., 2005; Rychlik and Barrow, 2005). Bacterial survival of the transit through the stomach is achieved through activation of the acid tolerance response (ATR), the mechanisms of which will be discussed in more detail later.

As well as directly stressing the bacteria, the acidity of the stomach converts dietary and salivary nitrite to nitric oxide (NO), to generate nitrosative stress which the bacteria must also survive. Nitrosative stress can cause changes to bacterial proteins which inhibit their normal functions, or inhibit DNA replication (Fang, 2004), rendering the bacteria non-viable. Exogenous nitrogen species are introduced to the gut in the diet. Most dietary nitrate present in the gastrointestinal tract is produced from vegetables (Lundberg et al., 2004); beets, celery, and leafy vegetables are especially rich in nitrates (Bryan, 2006). In the oral cavity, salivary nitrate is reduced to nitrite by commensal bacteria on the tongue. In the stomach, the nitrite is acidified in a reaction with stomach acid, to nitrous acid (HNO 2) (Equation 1(a)). Nitrous acid comprises dinitrogen trioxide (N 2O 3) as an intermediary compound (Equation 1(b)) with water, which subsequently disproportionates to other nitrogen species, including NO (Equation 1(c)) (Benjamin et al., 1994; van Wonderen et al., 2008). Nitrite is also ingested in the diet, most often with cured and processed meats, to which nitrite is added as a preservative (Bryan, 2006). Residual nitrate and nitrite are ultimately excreted in the urine, at levels similar to those ingested in the diet (Lundberg et al., 2004), ensuring that in the normal, uninfected system, a steady state of nitrate and nitrite levels is maintained. Feces and sweat have been shown to constitute only minor routes for excretion of nitrate and nitrite ions (Weller et al., 1996; Ten Bruggencate et al., 2004). Nitrogen species are consequently found distributed throughout the length of the gastrointestinal tract, representing a serious problem for enteric pathogens.

Equation (1a), (1b) and (1c)– The disproportionation of nitrite to NO

(1a)

(1b)

(1c)

2.1.2. Macrophages and RNS

NO is produced by the normal constitutive activity of the l-arginine–NO pathway, which maintains various physiological functions like vascular tone, neurotransmission, and platelet function (Levy et al., 2005). Endogenous NO is vital as a signaling molecule for many processes in the mammalian system, and is produced from the amino acid l-arginine and molecular oxygen by NO synthases (NOS) (Nelson and Cox, 2004). There are three NOS isoforms; endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). (Moncada et al., 1997). Basal plasma NO levels are generated by the endogenous l-arginine–NO pathway. The NO can be detoxified by reacting with oxy-ferrous hemoglobin (Hb(FeII)) (Gow and Stamler, 1998), to produce nitrate (Lundberg et al., 2004).

Macrophages use iNOS to produce NO, without the need for elevated intracellular calcium (Ca 2+) which is required by eNOS and nNOS (Marletta, 1994; Nathan and Xie, 1994; Griffith and Stuehr, 1995; Michel...

Erscheint lt. Verlag	10.11.2009
Mitarbeit	Herausgeber (Serie): Robert K. Poole
Sprache	englisch
Themenwelt	Studium ► 1. Studienabschnitt (Vorklinik) ► Physiologie
	Naturwissenschaften ► Biologie ► Mikrobiologie / Immunologie
	Naturwissenschaften ► Biologie ► Zoologie
	Technik
ISBN-10	0-08-088831-3 / 0080888313
ISBN-13	978-0-08-088831-6 / 9780080888316

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