Abstract

Coxiella burnetii is a Gram-negative, obligate intracellular bacterium and the causative agent of Q fever. Infections are usually acquired after inhalation of contaminated particles, where C. burnetii infects its cellular target cells, alveolar macrophages. Respiratory pathogens encounter the C-type lectin surfactant protein D (SP-D) during the course of natural infection. SP-D is a component of the innate immune response in the lungs and other mucosal surfaces. Many Gram-negative pulmonary pathogens interact with SP-D, which can cause aggregation, bactericidal effects and aid in bacterial clearance. Here we show that SP-D binds to C. burnetii in a calcium-dependent manner with no detectable bacterial aggregation or bactericidal effects. Since SP-D interactions with bacteria often alter macrophage interactions, it was determined that SP-D treatment resulted in a significant decrease in C. burnetii interactions to a mouse alveolar macrophage model cell line MH-S indicating SP-D causes a significant decrease in phagocytosis. The ability of SP-D to modulate macrophage activation by C. burnetii was tested and it was determined that SP-D does not alter the correlates measured for macrophage activation. Taken together these studies support those demonstrating limited activation of alveolar macrophages with C. burnetii and demonstrate interactions with SP-D participate in reduction of phagocyte attachment and phagocytosis.

Highlights

  • Coxiella burnetii is a Gram-negative zoonotic bacterial pathogen that is the etiologic agent of Q Fever in humans and coxiellosis in animals [1]

  • To determine if surfactant protein D (SP-D) was bactericidal towards C. burnetii we incubated the bacteria with SP-D and the ability to replicate was monitored in ACCM-2

  • Our data demonstrate that C. burnetii interacts with SP-D in a calcium-dependent manner that can be inhibited by carbohydrate

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Summary

Introduction

Coxiella burnetii is a Gram-negative zoonotic bacterial pathogen that is the etiologic agent of Q Fever in humans and coxiellosis in animals [1]. SP-D Binds C. burnetii and Decreases Host Cell Interactions “rough” LPS, which occurs after serial passage in a non-immunocompetent host [3]. This transition can occur via the deletion of O-antigen or core carbohydrate biosynthesis genes. Smooth variants, designated phase I are virulent during animal infection, whereas, rough variants designated phase II are attenuated in immunocompetent animal infection. Both phase I and phase II infect and multiply in a variety of cell types [5]

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