Nuclear factor-kappa B and its role in inflammatory lung disease

Alharbi, Khalid Saad; Fuloria, Neeraj Kumar; Fuloria, Shivkanya; Rahman, Sk Batin; Almalki, Waleed Hassan; Shaikh, Mohammad Arshad Javed; Thangavelu, Lakshmi; Singh, Sachin Kumar; Allam, Venkata Sita Rama Raju; Jha, Niraj Kumar; Chellappan, Dinesh Kumar; Dua, Kamal; Gupta, Gaurav

doi:10.1016/j.cbi.2021.109568

Cited by 160 publications

(71 citation statements)

References 66 publications

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“…The decreased GSH and increased MDA levels are responsible for airway inflammation [33], and may contribute to the pathogenesis of the atopic march. It is well known that nuclear factor kappa-B (NF-κB) pathways are activated by oxidative stress, which can then participate in inflammation regulation [34]. Consistent with oxidative stress detection, the level of NF-κB in the lung was exacerbated in the atopic march group compared to the OVA group (Fig 7C and D).…”

Section: Discussionsupporting

confidence: 72%

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Li¹,

Zhang²,

Ren

et al. 2021

Bioscience Reports

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Purpose: The pathological process of atopic dermatitis (AD) progressing into other types of allergic diseases such as asthma and allergic rhinitis during the first several years of life is often referred to as the atopic march. Although the phenomenon of atopic march has been recognized for decades, how asthma stems from AD is still not fully understood, confounding a universal strategy to effectively protect people from the atopic march. Methods: We established experimental atopic march mice by first inducing allergic dermatitis with 0.5% fluorescein isothiocyante applied to the skin, followed by an OVA airway challenge. In addition, by examining serum immunoglobulin concentrations, airway cytokines, the levels of oxidative stress markers, histopathological changes in lung tissue and airway hyperresponsiveness, we were able to validate the successful establishment of the model. Furthermore, by detecting the attenuating effects of melatonin (MT) and the levels of oxidative stress in the atopic march mice, we explored the potential molecular mechanisms involved in the development of atopic march. Results: By successfully establishing an experimental atopic march mouse model, we were able to demonstrate that overproduction of oxidative stress in the lung significantly upregulated the activation of NF-κB signaling pathways causing TSLP release, which further promotes the development of atopic march. Conclusions: To mitigate the development of the atopic march, antioxidants such as MT may be imperative to inhibit NF-κB activation in the lung, especially after the onset of AD.

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Section: Discussionsupporting

confidence: 72%

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Li¹,

Zhang²,

Ren

et al. 2021

Bioscience Reports

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“…It is noted that Nlrp3, NF-κB, p38, and ERK signal pathways participated in modulating the production of inflammatory cytokines ( 4 , 31 – 33 ). Therefore, we examined whether Nlrp3 inflammasome, NF-κB, p38, and ERK signal pathways in N. caninum- infected PMs were modulated by the mitophagy-ROS axis.…”

Section: Resultsmentioning

confidence: 99%

Neospora caninum Evades Immunity via Inducing Host Cell Mitophagy to Inhibit Production of Proinflammatory Cytokines in a ROS-Dependent Manner

et al. 2022

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Neospora caninum is an intracellular protozoan that mainly infects cattle to cause abortion and significant economic losses worldwide. A better understanding of the immune evasion mechanisms of N. caninum could help to search for an effective approach to prevent and treat neosporosis. Mitophagy is used by some viruses to evade host immune surveillance. However, host cell mitophagy and its effect on N. caninum infection is unclear. In the present study, N. caninum-induced host cell mitophagy and its role in parasite infection were investigated in vitro and in vivo. Furthermore, the regulation of N. caninum-induced host cell mitophagy on the production of Reactive Oxygen Species (ROS), the secretions of proinflammatory cytokines, and the signals of p38, ERK, and Nlrp3 inflammasome were explored. Our results showed that autophagosomes and co-localization of LC3 with mitochondria were observed in N. caninum-infected macrophages. The mtDNA/nDNA ratio and the levels of mitochondrial marker proteins (Hsp60 and Tim23) were decreased with the increase of N. caninum numbers or infection time. N. caninum could induce mitophagy in brain and peritoneal lavage fluid cells of mice. Promoting mitophagy via mitophagy inducers (CCCP) could shorten survival time, decrease body weight, increase parasite load, and attenuate secretion of cytokines in N. caninum infected mice. CCCP treatment decreased the production of cytokines and Reactive Oxygen Species (ROS), and increased parasite burden in N. caninum-infected macrophages. Furthermore, CCCP or NAC (ROS inhibitor) treatment could inhibit ERK signal, Nlrp3 inflammasome, and cytokine production, while promote p38 signal in N. caninum-infected macrophages. The opposite results were obtained when using a mitophagy inhibitor (Mdivi1). Taken together, N. caninum-induced mitophagy could regulate the activations of p38, ERK, Nlrp3 inflammasome to inhibit the production of inflammatory cytokines in a ROS-dependent manner to escape host immune surveillance.

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“…However, the capacity of these naturally occurring antioxidants is limited [ 140 ]. This explains why excessive ROS formation cannot be adequately compensated, consequently leading to cell and organ damage [ 141 , 142 , 143 ]. In ARDS, the breakdown of the endothelial/epithelial barrier is an important hallmark of disease progression [ 144 , 145 ].…”

Section: Methodsmentioning

confidence: 99%

Antioxidants as Therapeutic Agents in Acute Respiratory Distress Syndrome (ARDS) Treatment—From Mice to Men

et al. 2022

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Acute respiratory distress syndrome (ARDS) is a major cause of patient mortality in intensive care units (ICUs) worldwide. Considering that no causative treatment but only symptomatic care is available, it is obvious that there is a high unmet medical need for a new therapeutic concept. One reason for a missing etiologic therapy strategy is the multifactorial origin of ARDS, which leads to a large heterogeneity of patients. This review summarizes the various kinds of ARDS onset with a special focus on the role of reactive oxygen species (ROS), which are generally linked to ARDS development and progression. Taking a closer look at the data which already have been established in mouse models, this review finally proposes the translation of these results on successful antioxidant use in a personalized approach to the ICU patient as a potential adjuvant to standard ARDS treatment.

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Nuclear factor-kappa B and its role in inflammatory lung disease

Cited by 160 publications

References 66 publications

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Melatonin prevents allergic airway inflammation in epicutaneously sensitized mice

Neospora caninum Evades Immunity via Inducing Host Cell Mitophagy to Inhibit Production of Proinflammatory Cytokines in a ROS-Dependent Manner

Antioxidants as Therapeutic Agents in Acute Respiratory Distress Syndrome (ARDS) Treatment—From Mice to Men

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