Inflammatory Cells Involved in Asthma

Rayees, Sheikh; Din, Inshah

doi:10.1007/978-3-030-70270-0_5

Cited by 1 publication

(2 citation statements)

References 29 publications

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“…The primary inflammatory cells implicated in allergy disorders are eosinophils. Eosinophils are not often found in healthy lungs, but their buildup in the lungs indicates an airway inflammation present in mild to severe forms of asthma (Rayees & Din, 2021). Reactive oxygen species such as hypobromite, superoxide, and peroxide are released by eosinophils, along with other cationic proteins such as eosinophil peroxidase.…”

Section: Discussionmentioning

confidence: 99%

“…Eosinophil builds up in the lungs results in inflammation of the upper and lower airways. They are known to emit strong pro-inflammatory substances, particularly eosinophil peroxidase and leukotrienes, which are known to remodel the epithelial membrane in asthmatic airways (Rayees & Din, 2021). Neutrophils are one of the first innate immune cells to be recruited into the lungs after specific asthma-related events such allergenic challenges, virus-induced asthma exacerbations, or nocturnal crises, even though they are not always present in the airways of allergic asthmatic patients (Ramirez-Velazquez et al, 2013;Ilmarinen et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

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Ellagic acid alleviates pulmonary inflammation and oxidative stress in mouse model of diisononyl phthalate-induced asthma

Olajide

Olayinka

Ore

et al. 2023

LSMB

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Polyvinyl chloride is plasticized using diisononyl phthalate (DiNP), and exposure to phthalates has been linked to the emergence of asthma and allergies. The adjuvant impact of DiNP exposure results in allergic airway inflammation. In the current study, we looked into how ellagic acid (ELA) impacted asthma brought on by DiNP. Male BALB/c mice (n=40, 20-30 g) were divided into 4 groups of 10 mice each, and the following treatments were given to each group: group 1 (control) received saline orally for 30 days; group 2 (ELA) received 10 mg/kg of ELA (oral) for 30 days; group 3 (DiNP & ELA) received 10 mg/kg of ELA (oral) for 7 days prior to DiNP (50mg/kg) exposure (intraperitoneal and intranasal); group 4 (DiNP) received 50 mg/kg DiNP. After the last administration, mice were sacrificed, lungs were removed and their bronchoalveolar lavage fluid was collected which was used for biochemical and histopathological analysis. The mice given DiNP had changes in their histoarchitecture, inflammatory cells, antioxidant status, and inflammation markers. Malondialdehyde (MDA) and inflammatory biomarkers (NO, MPO) were considerably higher (p< 0.05) in the lungs of DiNP-treated mice than in the control group. In the lungs, DiNP reduced the concentration of non-enzymatic antioxidants (GSH and AA), and the activity of enzymatic antioxidants (SOD, CAT, and GST). DiNP also altered inflammatory cells (eosinophils, neutrophils, lymphocytes, monocytes, leucocytes) in the BALF. ELA administration ameliorated these changes. Histopathological analysis revealed airway inflammation characterized by inflammatory cell infiltration, oedema, hemorrhage, and constricted alveoli space. Additionally, the mice co-treated with ELA and DiNP experienced mild inflammation of the alveoli and interstitial spaces as well as mild thickening of the alveolar septae. ELA offered a protective effect against DiNP-induced allergic asthma in mice.

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Section: Discussionmentioning

confidence: 99%