title: Salmonella enterica serovar Typhimurium infection-induced CD11b+ Gr1+ cells ameliorate allergic airway inflammation.
abstract: Allergies are mainly characterized as an unrestrained Th2-biased immune response. Epidemiological data associate protection from allergic diseases with the exposure to certain infectious agents during early stages of life. Modulation of the immune response by pathogens has been considered to be a major factor influencing this protection. Recent evidence indicates that immunoregulatory mechanisms induced upon infection ameliorate allergic disorders. A longitudinal study has demonstrated reduced frequency and incidence of asthma in children who reported a prior infection with Salmonella. Experimental studies involving Salmonella enterica serovar Typhimurium-infected murine models have confirmed protection from induced allergic airway inflammation; however, the underlying cause leading to this amelioration remains incompletely defined. In this study, we aimed to delineate the regulatory function of Salmonella Typhimurium infection in the amelioration of allergic airway inflammation in mice. We observed a significant increase in CD11b+ Gr1+ myeloid cell populations in mice after infection with S. Typhimurium. Using in vitro and in vivo studies, we confirmed that these myeloid cells reduce airway inflammation by influencing Th2 cells. Further characterization showed that the CD11b+ Gr1+ myeloid cells exhibited their inhibitory effect by altering GATA-3 expression and interleukin-4 (IL-4) production by Th2 cells. These results indicate that the expansion of myeloid cells upon S. Typhimurium infection could potentially play a significant role in curtailing allergic airway inflammation. These findings signify the contribution of myeloid cells in preventing Th2-mediated diseases and suggest their possible application as therapeutics.
authors.affiliation: Institute of Infection Immunology, Twincore, Centre for Experimental and Clinical Infection Research, Hanover, Germany.
authors.forename: Venkateswaran
authors.initials: V
authors.lastname: Ganesh
authors.forename: Abdul Mannan
authors.initials: AM
authors.lastname: Baru
authors.forename: Christina
authors.initials: C
authors.lastname: Hesse
authors.forename: Christin
authors.initials: C
authors.lastname: Friedrich
authors.forename: Silke
authors.initials: S
authors.lastname: Glage
authors.forename: Melanie
authors.initials: M
authors.lastname: Gohmert
authors.forename: Christine
authors.initials: C
authors.lastname: Jänke
authors.forename: Tim
authors.initials: T
authors.lastname: Sparwasser
mesh_terms: D000818:Animals; D039481:CD11b Antigen / Q000276:immunology*; D002454:Cell Differentiation / Q000276:immunology; D051858:Forkhead Transcription Factors / Q000276:immunology; D050990:GATA3 Transcription Factor / Q000276:immunology; D006967:Hypersensitivity / Q000276:immunology* / Q000382:microbiology; D007249:Inflammation / Q000276:immunology* / Q000382:microbiology; D015847:Interleukin-4 / Q000276:immunology; D008137:Longitudinal Studies; D008168:Lung / Q000276:immunology / Q000382:microbiology; D051379:Mice; D008807:Mice, Inbred BALB C; D022423:Myeloid Cells / Q000276:immunology / Q000382:microbiology; D019707:Receptors, Chemokine / Q000276:immunology*; D012480:Salmonella Infections / Q000276:immunology* / Q000382:microbiology; D012486:Salmonella typhimurium / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000382:microbiology; D018418:Th2 Cells / Q000276:immunology / Q000382:microbiology
chemical_list: D039481:CD11b Antigen; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D050990:GATA3 Transcription Factor; C494748:Gata3 protein, mouse; C503133:Gr-1 protein, mouse; D019707:Receptors, Chemokine; D015847:Interleukin-4