O<sub>3</sub> induced significant BAL fluid neutrophilia and eosinophilia and increased AHR and expression of IL6 and IL25 mRNA in the airway epithelium together with increased BAL fluid group 2 innate lymphoid cell (ILC2s), CD1c<sup>+</sup> myeloid dendritic cell, and CD4<sup>+</sup> T-cell counts and diminished surfactant protein D expression.
IL-6 excess is central to the pathogenesis of multiple inflammatory conditions and is targeted in clinical practice by immunotherapy that blocks the IL-6 receptor encoded by <i>IL6R</i> We describe two patients with homozygous mutations in <i>IL6R</i> who presented with recurrent infections, abnormal acute-phase responses, elevated IgE, eczema, and eosinophilia.
Concomitantly, molecular phenotyping based on a transcriptomic analysis of bronchial epithelial and sputum cells has identified a Type 2 high inflammation cluster characterized by eosinophilia and recurrent exacerbations, as well as Type 2 low clusters linked with IL-6 trans-signalling, interferon pathways, inflammasome activation and mitochondrial oxidative phosphorylation pathways.
PJE treatment inhibited OVA-induced inflammatory cell infiltration, eosinophilia, Th2 activation, and GATA-3 expression in the lung, reduced the interleukin (IL)-5 and IL-13 levels in BALF, down-regulated Th2 activation in vitro, and inhibited the macrophage production of inducible nitric oxide, cyclooxygenase-2, tumor necrosis factor-α, and IL-6.
By contrast, levels of the inflammatory cytokines IL-17A and IL-6 were significantly elevated in the J(H)(-/-) animals, and there was significantly more robust airway eosinophilia and neutrophilia than in control animals.
Schistosoma mansoni induces the synthesis of IL-6 in pulmonary microvascular endothelial cells: role of IL-6 in the control of lung eosinophilia during infection.