What is it about?
e While the role of CD4+ regulatory T cells in the resolution of lung inflammation is well documented, their potential contribution to the onset of the inflammatory response has been largely neglected. Herein, we assessed the impact of germline CD4 deficiency on the alveolar macrophage (AMΦ)-neutrophil (PMN) axis in initiating the LPS-induced lung inflammation.
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Why is it important?
he levels of AMΦ and PMN in bronchoalveolar lavage fluid (BALF) and tissue histopathology were compared in wild type (WT) and CD4-deficient (CD4−/−) mice at 4 hours after local LPS challenge (2–3 µg/g: intranasally). CD4 expression (flow cytometry) and representative functions of AMΦ (phagocytosis, cytokine secretion) and PMN (migration) of WT and CD4−/− mice were compared ex vivo.
Perspectives
LPS increased PMN infiltration of alveoli in WT mice; a response severely blunted in CD4−/− mice. AMΦ isolated from WT mice captured more microbeads, but secreted less tumor necrosis factor-α, than AMΦ from CD4−/− mice. Notably, as compared to PMN of WT mice, PMN of CD4−/− mice had a diminished motility response to a relevant chemotactic stimulus (cell-free BALF). PMN expressed CD4 while AMΦ did not.
Dr. Nuha Khalid Alekhmimi
Inaya Medical College
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This page is a summary of: Pulmonary Neutrophil Recruitment in Response to Inhaled LPS is Impaired in CD4 Deficient Mice, August 2022, Research Square,
DOI: 10.21203/rs.3.rs-1796185/v1.
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