• Florry E van den Boogaard, Xanthe Brands, Joris J T H Roelofs, Regina de Beer, Onno J de Boer, Cornelis van 't Veer, and Tom van der Poll.
• Center for Experimental and Molecular Medicine Center for Infection and Immunity Amsterdam.
• J. Infect. Dis. 2014 Nov 1;210(9):1376-84.

BackgroundStreptococcus pneumoniae is the most common causative pathogen in community-acquired pneumonia. Mast cells (MCs) are located mainly at the host-environment interface where they function as sentinels.ObjectiveOur goal was to study the role of MCs during pneumonia caused by S. pneumoniae.MethodsLung tissue of patients who had died from pneumococcal pneumonia or a nonpulmonary cause was stained for MCs and tryptase. Wild-type (WT) and MC-deficient (Kit(W-sh/W-sh)) mice were observed or sacrificed after induction of pneumonia by intranasal inoculation of S. pneumoniae. In separate experiments, WT mice were treated with doxantrazole or cromoglycate, which are MC stabilizing agents.ResultsThe constitutive presence of tryptase-positive MCs was reduced in affected lungs from pneumonia patients. Kit(W-sh/W-sh) mice showed a prolonged survival during the first few days after median lethal dose (LD)100 and LD50 infection, while overall mortality did not differ from that in WT mice. Relative to WT mice, Kit(W-sh/W-sh) mice showed reduced bacterial counts with less bacterial dissemination to distant organs and less inflammation. Neither doxantrazole nor cromoglycate influenced antibacterial defense or inflammatory responses after airway infection with S. pneumoniae.ConclusionsMCs exhibit an unfavorable role in host defense during pneumococcal pneumonia by a mechanism independent of degranulation.© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

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