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Blockade of interleukin-2-inducible T-cell kinase signaling attenuates acute lung injury in mice through adjustment of pulmonary Th17/Treg immune responses and reduction of oxidative stress by Nadeem, Ahmed; Al-Harbi, Naif O.; Ahmad, Sheikh F.; Al-Harbi, Mohammed M.; Alhamed, Abdullah S.; Alfardan, Ali S.; Assiri, Mohammed A.; Ibrahim, Khalid E.; Albassam, Hussam is a Immunology and Microbiology article available to read on EtoBox.

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Acute lung injury (ALI) is linked with considerable morbidity and mortality. ALI can be caused by various agents, one of them being sepsis. ALI is characterized by injury to vascular endothelium and alveolar epithelium that results in edema, pulmonary immune cells infiltration and hypoxemia. Neutrophils and T cells particularly play a huge role in amplification of pulmonary inflammation through release of multiple inflammatory mediators. Recent reports suggest a strong involvement of Th17 cells and oxidative stress in initiation/amplification of pulmonary inflammation during ALI. Interleukin-2-inducible T-cell kinase (ITK) plays a key role in Th17 cell development through control of several transcription factors. Therefore, our study explored the role of ITK on airway inflammation (total/neutrophilic cell counts, myeloperoxidase activity, E-cadherin expression, histopathological analyses) and effect of its inhibition on various inflammatory/anti-inflammatory pathways during ALI [phosphorylated-ITK (p-ITK), NFATc1, IL-17A, STAT3, Foxp3, IL-10, iNOS, nitrotyrosine, lipid peroxides). ALI was associated with increased total/neutrophilic cell counts and myeloperoxidase activity, and dec

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Author

Nadeem, Ahmed; Al-Harbi, Naif O.; Ahmad, Sheikh F.; Al-Harbi, Mohammed M.; Alhamed, Abdullah S.; Alfardan, Ali S.; Assiri, Mohammed A.; Ibrahim, Khalid E.; Albassam, Hussam

Publisher

Elsevier Science; Elsevier ; Elsevier BV (ISSN 1567-5769)

Published

2020

Language

EN

Field

Immunology and Microbiology (Life Sciences)