Science: revealing the mechanism of neutrophils inhibiting allergic airway inflammation

November 16, 2019 / bioun / - -- allergic airway inflammation, including asthma, is a complex disease A variety of immune and non immune factors promote the occurrence and progress of this disease Mobilization, recruitment and clearance of neutrophils must be strictly controlled because of the involvement of hyperactive neutrophil inflammation in chronic diseases, including asthma Efforts to target neutrophils in therapy do not take into account their pleiotropic function and the effects of disrupting the basic regulatory pathways that control their turnover in homeostasis and inflammation In a new study, researchers from the Imperial College of technology, the bison Cancer Institute, the University of Glasgow in Scotland and the University of Valencia in Spain confirmed that neutrophil depletion caused, in addition to the exacerbation of T helper type 2 (Th2) inflammation, epithelial remodeling and airway resistance by using the allergic airway disease model induced by house dust mite (HDM) In mechanism, this is due to a significant increase in the concentration of systemic granulocyte colony-stimulating factor (G-CSF), which is usually negatively regulated by migrating neutrophils around the lung The relevant research results were recently published in the Journal of science immunology, and the title of the paper is "neutrophils train effective airway information by limiting ilc2 function and monocyte – dental cell antigen presentation" Picture from science immunology, 2019, DOI: 10.1126/sciimmunologol.aax7006 Interestingly, these researchers found that the increased G-CSF directly affects the type 2 innate lymphoid cell (ilc2) in human and mouse airway, causing the production of Th2 cytokines IL-5 and IL-13, thus increasing the allergic sensitization in animals exposed to house dust mites In addition, the increased systemic G-CSF promoted the proliferation of bone marrow mononuclear progenitor cells, which enhanced antigen presentation by increasing the dendritic cell pool derived from peripheral monocytes By modeling the effects of neutrophil depletion, this study found that G-CSF had previously unrecognized roles in regulating ilc2 function and antigen presentation More broadly, this highlights the unexpected regulatory role of neutrophils in limiting Th2 allergic airway inflammation (BIOON Com) reference: Dhiren F Patel et al Neutrophils training allergic airway information by limiting ilc2 function and monocyte – dendritic cell antigen presentation Science immunology, 2019, DOI: 10.1126/scientific.aax7006