CCR7 modulates pulmonary and lymph node inflammatory responses in cigarette smoke-exposed mice

The Journal of Immunology : Official Journal of the American Association of Immunologists
Tine DemoorGuy G Brusselle

Abstract

Peribronchial lymphoid follicles have recently been identified as one of the hallmark features of (severe) chronic obstructive pulmonary disease (COPD). However, little is known about the relative contribution of peribronchial lymphoid follicles vs mediastinal lymph nodes in inflammatory responses in COPD patients and animal models. In a murine model of COPD, we studied inflammatory responses in airways, lungs, and mediastinal lymph nodes of wild-type (WT) vs CCR7 knockout (CCR7(-/-)) mice upon subacute or chronic exposure to cigarette smoke (CS). Although crucial for the organization of the secondary lymphoid organs, CCR7 was not required for the development of chronic CS-induced pulmonary lymphoid follicles. Moreover, T cell numbers were significantly increased in airways and lungs of air-exposed CCR7(-/-) mice, and they continued to increase upon chronic CS exposure. Unexpectedly, subacute CS-induced inflammation in airways and lungs, including airway neutrophilia and the recruitment of inflammatory-type CD11b(+) dendritic cells, depended greatly on CCR7. In the draining lymph nodes, chronic CS exposure induced CCR7-dependent recruitment of airway-derived dendritic cells, accompanied by increases in CD4(+) and CD8(+) T cells...Continue Reading

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Sep 21, 2012·Respiratory Research·Angela Haczku
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Mar 19, 2021·Respiratory Research·Jef SerréGhislaine Gayan-Ramirez
Apr 17, 2021·The European Respiratory Journal·Jeffrey L Curtis

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