Mitochondrial Function in Allergic Disease

Iyer, Divyaanka; Mishra, Navya; Agrawal, Anurag

doi:10.1007/s11882-017-0695-0

Cited by 47 publications

(39 citation statements)

References 86 publications

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“…The alveolar macrophage functions of patients with COPD were shown to be impaired due to mitochondrial dysfunction [97]. Other chronic pulmonary diseases, such as pulmonary fibrosis, asthma, cystic fibrosis, and pulmonary hypertension were also shown to be associated with mitochondrial dysfunction [98,99].…”

Section: Mitochondrial Dysfunction and Mtdna Mutations In Chronic Patmentioning

confidence: 99%

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Orekhov

Nikiforov

Ivanova

et al. 2020

JCM

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Chronification of inflammation is the process that lies at the basis of several human diseases that make up to 80% of morbidity and mortality worldwide. It can also explain a great deal of processes related to aging. Atherosclerosis is an example of the most important chronic inflammatory pathology in terms of public health impact. Atherogenesis is based on the inflammatory response of the innate immunity arising locally or focally. The main trigger for this response appears to be modified low-density lipoprotein (LDL), although other factors may also play a role. With the quick resolution of inflammation, atherosclerotic changes in the arterial wall do not occur. However, a violation of the innate immunity response can lead to chronification of local inflammation and, as a result, to atherosclerotic lesion formation. In this review, we discuss possible mechanisms of the impaired immune response with a special focus on mitochondrial dysfunction. Some mitochondrial dysfunctions may be due to mutations in mitochondrial DNA. Several mitochondrial DNA mutations leading to defective mitophagy have been identified. The regulatory role of mitophagy in the immune response has been shown in recent studies. We suggest that defective mitophagy promoted by mutations in mitochondrial DNA can cause innate immunity disorders leading to chronification of inflammation.

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Section: Mitochondrial Dysfunction and Mtdna Mutations In Chronic Patmentioning

confidence: 99%

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Orekhov

Nikiforov

Ivanova

et al. 2020

JCM

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“…On the other hand, there are also many exogenous sources of ROS, such as cigarette smoke, ultraviolet light, ionizing radiation, pollutants, ozone, organic solvents, metals, and some medicaments (e.g., chemotherapeutic agents). Both endogenous and exogenous sources of ROS can play an important role in the pathogenesis and worsening of various inflammatory conditions, especially through continual accumulation of the oxidative changes in biomolecules (8, 10–13). …”

Section: Oxidative Stress and Ba Developmentmentioning

confidence: 99%

“…Based on the development and persistence of oxidative stress, several crucial aspects and mechanisms can be identified (11): Overproduction of ROS and RNS in chronic inflammation (13, 14). …”

Section: Oxidative Stress and Ba Developmentmentioning

confidence: 99%

Oxidative Stress and Bronchial Asthma in Children—Causes or Consequences?

2017

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Bronchial asthma is one of the most common chronic inflammatory diseases of the airways. In the pathogenesis of this disease, the interplay among the genes, intrinsic, and extrinsic factors are crucial. Various combinations of the involved factors determine and modify the final clinical phenotype/endotype of asthma. Oxidative stress results from an imbalance between the production of reactive oxygen species and reactive nitrogen species and the capacity of antioxidant defense mechanisms. It was shown that oxidative damage of biomolecules is strongly involved in the asthmatic inflammation. It is evident that asthma is accompanied by oxidative stress in the airways and in the systemic circulation. The oxidative stress is more pronounced during the acute exacerbation or allergen challenge. On the other hand, the genetic variations in the genes for anti-oxidative and pro-oxidative enzymes are variably associated with various asthmatic subtypes. Whether oxidative stress is the consequence of, or the cause for, chronic changes in asthmatic airways is still being discussed. Contribution of oxidative stress to asthma pathology remains at least partially controversial, since antioxidant interventions have proven rather unsuccessful. According to current knowledge, the relationship between oxidative stress and asthmatic inflammation is bidirectional, and genetic predisposition could modify the balance between these two positions—oxidative stress as a cause for or consequence of asthmatic inflammation.

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“…As for the role of mitochondria in inflammation, oxidative stress may cause release to the cytosol of compounds such as damage-associated molecular pattern molecules, adenosine triphosphate, cardiolipins, and mitochondrial DNA, subsequently activating immune signalling cascades via intracellular activation of TLR agonists [85]. Mitochondrial dynamics are directly altered by the presence of airborne particles and protease allergens, leading to changes in membrane potential and proteosomal activity that ultimately leads to proapoptotic events [86,87].…”

Section: Lung and Redox Biology: Role In Respiratory Allergic Inflammmentioning

confidence: 99%

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

López-Rodríguez

Benedé

Barderas

et al. 2017

J Investig Allergol Clin Immunol

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Airway epithelium is the cellular structure with the greatest surface exposed to a plethora of environmental airborne substances, including microorganisms, respiratory viruses, air pollutants, and allergens. In addition to being a protective physical barrier at the air-liquid interface, the airway epithelium acts as an effective chemical and immunological barrier that plays a crucial role in orchestrating the immune response in the lungs, by supporting the activation, recruitment, and mobilization of immune cells. Airway epithelium dysfunction has been clearly associated with various airway inflammatory diseases, such as allergic asthma. Although it is not fully understood why a person develops respiratory allergy, a growing body of evidence shows that the nature of the host's immune response is strongly determined by the state of the airway epithelium at the time of contact with the inhaled allergen. Our review highlights the physiological state of airway epithelium as a key element in the development of allergy and, particularly, in exacerbation of asthma. We review the role of physiological oxidants as signaling molecules in lung biology and allergic diseases and examine how high exposure to air pollutants (eg, cigarette smoke and diesel particles) can contribute to the increased incidence of respiratory allergy and exacerbation of the disease. Key words: Airway epithelium. Barrier dysfunction. Respiratory allergy. Redox biology. Air pollutants. ResumenEl epitelio pulmonar constituye la barrera celular más susceptible a la acción deletérea de la multitud de agentes que se encuentran en el ambiente, incluidos los alérgenos. Además de prevenir su acceso al organismo, la barrera epitelial de las vías respiratorias juega un papel inmunomodulador crucial, regulando de forma local la acción de las células del sistema inmune subyacentes. Una disfunción epitelial, provocada tanto directa como indirectamente por la acción de los aeroalérgenos, parece ser una de las causas principales de desregulación de la homeostasis pulmonar, causando una respuesta proinflamatoria descontrolada que cada vez más autores atribuyen al origen de las reacciones alérgicas. En esta revisión se quiere destacar el papel de la barrera epitelial pulmonar como regulador de la respuesta inmune en el contexto de la alergia. Las enfermedades crónicas que afectan a las vías respiratorias, tales como el asma alérgica, muestran frecuentemente una función epitelial defectuosa, apoyando así la hipótesis antes mencionada que subyace al origen de la alergia. El impacto de otros contaminantes ambientales -como virus respiratorios, bacterias, humo del tabaco y partículas diésel-sobre la integridad epitelial, así como su influencia en la biología redox pulmonar relacionada con el desarrollo de la respuesta alérgica, también se abordarán en la presente revisión.

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Mitochondrial Function in Allergic Disease

Cited by 47 publications

References 86 publications

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Possible Role of Mitochondrial DNA Mutations in Chronification of Inflammation: Focus on Atherosclerosis

Oxidative Stress and Bronchial Asthma in Children—Causes or Consequences?

Airway Epithelium Plays a Leading Role in the Complex Framework Underlying Respiratory Allergy

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