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L-selectin shedding affects bacterial clearance in the lung: a new regulatory pathway for integrin outside-in signaling.

Abstract：

:Pneumonia induced by Gram-negative bacteria is a common and serious disease associated with high morbidity and mortality. Elimination of bacterial pathogens relies on the recruitment and functions of neutrophils. The adhesion molecule L-selectin has recently been implicated in integrin activation in neutrophils (inside-out signaling). However, the molecular mechanism by which L-selectin participates in host defense against Klebsiella pneumoniae-induced pulmonary inflammation is unknown. We demonstrate that L-selectin-deficient mice are prone to pulmonary infection compared with wild-type controls. Mechanistically, L-selectin cleavage from the neutrophil surface triggered by integrin engagement is involved in neutrophil recruitment into the lung and bacterial clearance. Downstream of integrin ligation, the metalloproteinase A disintegrin and metalloproteinase 17 (ADAM17) sheds L-selectin from the neutrophil surface in an IRhom2-dependent manner. L-selectin cleavage enhances integrin-mediated outside-in signaling, resulting in increased neutrophil effector functions. Thus, we identify a novel regulatory mechanism in neutrophils required for an adequate immune response triggered by integrin engagement during K pneumoniae-induced pulmonary inflammation.

journal_name

Blood

journal_title

Blood

authors

Cappenberg A,Margraf A,Thomas K,Bardel B,McCreedy DA,Van Marck V,Mellmann A,Lowell CA,Zarbock A

doi

10.1182/blood.2019000685

subject

Has Abstract

pub_date

2019-10-24 00:00:00

pages

1445-1457

issue

17

eissn

0006-4971

issn

1528-0020

pii

blood.2019000685

journal_volume

134

pub_type

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