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Dryad

Acinetobacter lwoffii exposure promotes PD-L1+ neutrophils and dampens viral-induced type 2 immunity

Abstract

Severe, recurrent viral infections in early life, such as those caused by respiratory syncytial virus (RSV) are associated with wheezing and asthma. Exposure to farmyard microbes protects against allergen-induced asthma, but their role in viral-induced airways disease is less understood. Here neonatal murine recurrent RSV infection promoted pulmonary eosinophilia, mucus hypersecretion and IL-13+ CD4+ T cells. These pathological features were ameliorated by concomitant inhalation of inactivated cowshed-derived bacteria, Acinetobacter lwoffii F78. The protective effect was maximal with continuous A.lwoffii exposure and protection correlated with increased circulatory, airway and lung parenchymal neutrophils. However, in contrast to pro-inflammatory neutrophils induced by RSV infection, transcriptomic and phenotypic analysis revealed A.lwoffii induced a distinct neutrophil population with reduced expression of CXCR4 and CD101, but elevated PD-L1. Induction of these PD-L1+ immunoregulatory neutrophils by inhaled A.lwoffii was linked to a concomitant reduction in Th2 immunity.