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            <funder>The Laboratory of Cellular and Molecular Immunology is supported by the F.R.S.-FNRS for the FRFS-WELBIO under grant CR-2012S-01R, by the Belgian Program on Interuniversity Attraction Poles (IUAP; T-TIME; P7/39), and by an “Action de Recherche Concertée de la Fédération Wallonie-Bruxelles de Belgique” (12/07-03-ITPKC). C.S. and C.R. are research fellows of the F.R.S.-FNRS, L.F. is supported by the FRFS-WELBIO (CR-2012S-01R), T.M. is supported by the Acteria Foundation, and C.D. and T.M. are research associates of the F.R.S.-FNRS.</funder>
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                <title xml:lang="en">Exposure to Bacterial CpG DNA Protects from Airway Allergic Inflammation by Expanding Regulatory Lung Interstitial Macrophages.</title>
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                    <forename type="first">Fabrice</forename>
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                <title level="j">Immunity</title>
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                  <publisher>Elsevier</publisher>
                  <biblScope unit="volume">46</biblScope>
                  <biblScope unit="issue">3</biblScope>
                  <biblScope unit="pp">457-473</biblScope>
                  <date type="datePub">2017-03-21</date>
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              <idno type="doi">10.1016/j.immuni.2017.02.016</idno>
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              <keywords scheme="author">
                <term xml:lang="en">asthma</term>
                <term xml:lang="en">spleen</term>
                <term xml:lang="en">regulatory macrophages</term>
                <term xml:lang="en">CpG</term>
                <term xml:lang="en">CCR2</term>
                <term xml:lang="en">monocytes</term>
                <term xml:lang="en">lung</term>
                <term xml:lang="en">hygiene hypothesis</term>
                <term xml:lang="en">IL-10</term>
                <term xml:lang="en">TLR9</term>
              </keywords>
              <classCode scheme="mesh">Animals</classCode>
              <classCode scheme="mesh">Chemotaxis, Leukocyte/immunology*</classCode>
              <classCode scheme="mesh">Hypersensitivity/immunology*</classCode>
              <classCode scheme="mesh">Macrophage Activation/immunology</classCode>
              <classCode scheme="mesh">Macrophages/immunology</classCode>
              <classCode scheme="mesh">Macrophages, Alveolar/immunology*</classCode>
              <classCode scheme="mesh">Mice</classCode>
              <classCode scheme="mesh">Mice, Inbred C57BL</classCode>
              <classCode scheme="mesh">Mice, Knockout</classCode>
              <classCode scheme="mesh">Oligodeoxyribonucleotides/immunology</classCode>
              <classCode scheme="mesh">Respiratory Hypersensitivity/immunology*</classCode>
              <classCode scheme="mesh">Spleen/immunology</classCode>
              <classCode scheme="mesh">DNA, Bacterial/immunology*</classCode>
              <classCode scheme="mesh">Disease Models, Animal</classCode>
              <classCode scheme="mesh">Flow Cytometry</classCode>
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              <p>Living in a microbe-rich environment reduces the risk of developing asthma. Exposure of humans or mice to unmethylated CpG DNA (CpG) from bacteria reproduces these protective effects, suggesting a major contribution of CpG to microbe-induced asthma resistance. However, how CpG confers protection remains elusive. We found that exposure to CpG expanded regulatory lung interstitial macrophages (IMs) from monocytes infiltrating the lung or mobilized from the spleen. Trafficking of IM precursors to the lung was independent of CCR2, a chemokine receptor required for monocyte mobilization from the bone marrow. Using a mouse model of allergic airway inflammation, we found that adoptive transfer of IMs isolated from CpG-treated mice recapitulated the protective effects of CpG when administered before allergen sensitization or challenge. IM-mediated protection was dependent on IL-10, given that Il10(-/-) CpG-induced IMs lacked regulatory effects. Thus, the expansion of regulatory lung IMs upon exposure to CpG might underlie the reduced risk of asthma development associated with a microbe-rich environment.</p>
            </abstract>
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              <org type="consortium">We thank Dr. François Trottein (Institut Pasteur de Lille) for providing Influenza A virus; Prof. Hans Nauwynck (Ghent University) for advice; Dr. Natalia Kosovilka from the Stanford PAN facility; Dr. Sandra Ormenese and Raafat Stephan from the Cell Imaging and Flow Cytometry GIGA Platform; Dr. Pierre Drion and other staff members from the Mouse Facility and Transgenics GIGA Platform; Dr. Chantal Humblet from the GIGA Immunohistology Platform; and Raja Fares, Cédric François, and Ilham Sbai for excellent technical and secretarial assistance.</org>
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