title: Immortalized MH-S cells lack defining features of primary alveolar macrophages and do not support mouse pneumovirus replication.
abstract: The SV-40-transformed MH-S cell line maintains some, but not all, features of primary alveolar macrophages (AMs) from BALB/c mice. We show here that MH-S cells produce inflammatory cytokines IL-6 and CXCL10 in response to challenge with Gram-positive Lactobacillus reuteri, and to TLR2 and NOD2 ligands Pam3CSK4 and MDP, respectively. In contrast, although wild-type AMs are infected in vivo by pneumonia virus of mice (PVM), no virus replication was detected in MH-S cells. Interestingly, the surface immunophenotype of MH-S cells (CD11c(+)Siglec F(-)) differs from that of wild-type AMs (CD11c(+) Siglec F(+)) and is similar to that of immature AMs isolated from granulocyte macrophage-colony stimulating factor (GM-CSF) gene-deleted mice; AMs from GM-CSF(-/-) mice also support PVM replication. However, MH-S cells do not express the GM-CSF receptor alpha chain (CD116) and do not respond to GM-CSF. Due to these unusual features, MH-S cells should be used with caution as experimental models of AMs.
authors.affiliation: Inflammation Immunobiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States.
authors.forename: Todd A
authors.initials: TA
authors.lastname: Brenner
authors.affiliation: Inflammation Immunobiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States.
authors.forename: Tyler A
authors.initials: TA
authors.lastname: Rice
authors.affiliation: Inflammation Immunobiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States.
authors.forename: Erik D
authors.initials: ED
authors.lastname: Anderson
authors.affiliation: Inflammation Immunobiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States.
authors.forename: Caroline M
authors.initials: CM
authors.lastname: Percopo
authors.affiliation: Inflammation Immunobiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: hrosenberg@niaid.nih.gov.
authors.forename: Helene F
authors.initials: HF
authors.lastname: Rosenberg
mesh_terms: D000818:Animals; D002461:Cell Line, Transformed; D054357:Chemokine CXCL10 / Q000378:metabolism; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000235:genetics; D015850:Interleukin-6 / Q000378:metabolism; D052200:Limosilactobacillus reuteri / Q000276:immunology*; D055666:Lipopeptides / Q000276:immunology; D016676:Macrophages, Alveolar / Q000473:pathology / Q000821:virology*; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D018111:Pneumovirus / Q000502:physiology*; D018186:Pneumovirus Infections / Q000276:immunology*; D051195:Toll-Like Receptor 2 / Q000378:metabolism; D014779:Virus Replication
chemical_list: D054357:Chemokine CXCL10; D015850:Interleukin-6; D055666:Lipopeptides; C508075:Pam(3)CSK(4) peptide; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2; D016178:Granulocyte-Macrophage Colony-Stimulating Factor
keywords: Granulocyte-macrophage colony stimulating factor; Inflammation; Macrophage; Pattern recognition receptor; Pneumovirus; Siglec F