Abstract
Abstract Mechanisms responsible for pulmonary tissue homeostasis and regeneration are incompletely understood. This study investigated whether Trefoil factor family (TFF) proteins, regulators of gastrointestinal restitution, served any role in the pulmonary tract under steady state conditions or pathogen infection. At baseline, TFF2 lung mRNA transcript levels were highest compared to TFF1 and TFF3. Strikingly, TFF2 deficient mice (TFF2-/-) were hypoxic by 6-8 weeks of age, with abnormal alveoli, reduced blood oxygen levels, and defective integrin expression on alveolar type 1 cells. TFF2 was essential for mucosal barrier function in tracheal epithelia and TFF2 deficiency caused multiple transcriptional defects in adhesion, motility, and wound repair. Unexpectedly, TFF2 expression in hematopoietic cells was necessary for Type 2 immunity and recovery of pulmonary function after inoculation with the hookworm Nippostrongylus brasiliensis. TFF2 served a cell-intrinsic role in promoting macrophage polarization towards the M2 subset. Thus, in addition to epithelial restitution, TFF2 derived from hematopoietic cells instructs macrophage subset differentiation, promotes host immunity, and stimulates tissue repair within the pulmonary tract.
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