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Nutrition in Inflammatory Lung Diseases

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Oxidative Stress in Lung Diseases

Abstract

The lung is a specialized organ that facilitates the gas exchange between an organism and the environment. Its function is to supply the blood with oxygen that the body uses and eliminate the carbon dioxide produced by metabolism. Chronic inhalation of environmental contaminants can result in the overwhelming production of reactive oxygen species (ROS). Oxidative stress in tissues is a process of cellular deterioration dependent on the production of free radicals by an imbalance between ROS and antioxidant agents of endogenous. In the pathogenesis and evolution of numerous pulmonary diseases of high prevalence, inflammation and oxidative stress seem to coexist with an important degree of interaction between both. During the inflammatory process, increased production of ROS may induce damage to lipid structures, proteins, and DNA, the inhibition of apoptosis, and activation of proto-oncogenes when initiating signal transduction pathways. Diet and nutrition are becoming recognized as modifiable contributors to the development and progression of pulmonary diseases. Polyphenols are secondary metabolites of plants and are commonly present in the human diet. Because of their antioxidant and anti-inflammatory properties, polyphenols represent a potential to improve the treatments of pulmonary diseases. Several studies have shown the Mediterranean diet appears to benefit patients with airways disease, such as asthma and chronic obstructive pulmonary disease. However, more studies are needed to elucidate the molecular role of nutrition as well as more clinical trial interventions to assess the nutritional management of respiratory diseases and the prevention of these disorders.

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Abbreviations

OH:

Hydroxyl radical

AG:

Gallic acid

AGEs:

Advanced glycation end products

APCs:

Antigen-presenting cells

COPD:

Chronic obstructive pulmonary disease

COX:

Cyclooxygenase

DCs:

Dendritic cells

DHA:

Docosahexaenoic acid

EPA:

Eicosapentaenoic acid

FEV1:

Forced expiratory volume in 1 s

GSH:

Reduced glutathione

GST:

Glutathione S-transferase

H2O2:

Hydrogen peroxide

HOCl:

Hypochlorous acid

ICAM-1:

Intracellular adhesion molecule

IgE:

Immunoglobulin E

IL:

Interleukin

iNOS:

Nitric oxide synthase

IκK:

Iκ kinase

LOX:

Lipoxygenase

LPS:

Lipopolysaccharides

LTB4:

Leukotriene B4

MAPK:

Mitogen-activated protein kinase

MCP-1:

Monocyte chemotactic protein-1

MMPs:

Metalloproteinases

MOD:

Monoamine oxidase

MUFAs :

Monounsaturated fatty acids

NF-κB:

Nuclear factor κB

NK:

Natural killer

NKT:

Natural killer T cells

NLRP3:

NOD-like receptor pyrin domain containing

NO:

Nitric oxide

O2:

Molecular oxygen

O2•-:

Superoxide anion

PGE2:

Prostaglandin E2

PPAR :

Proliferator-activated receptor

PUFAs:

Polyunsaturated fatty acids

RAGE:

Receptor for advanced glycation end products

RNS:

Reactive nitrogen species

ROS:

Reactive oxygen species

SOD:

Superoxide dismutase

SP:

Surfactant proteins

TNFα:

Tumor necrosis factor α

TREG:

Regulatory T cells

VCAM-1:

Vascular cell adhesion protein

WHO:

World Health Organization

XO:

Xanthine oxidase

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Aguilar-López, D.K., Olvera-Sandoval, C., Estrada-Luna, D., Izquierdo-Vega, J.A., Sharma, A., Betanzos-Cabrera, G. (2019). Nutrition in Inflammatory Lung Diseases. In: Chakraborti, S., Chakraborti, T., Das, S., Chattopadhyay, D. (eds) Oxidative Stress in Lung Diseases. Springer, Singapore. https://doi.org/10.1007/978-981-13-8413-4_1

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