title: Indication for a role of regulatory T cells for the advent of influenza A (H1N1)-related pneumonia.
abstract: Regulatory T cells (T(regs) ) have an anti-inflammatory role. A former study in a limited number of patients found that absolute counts of T(regs) increase when infection by the new influenza H1N1 virus is complicated with pneumonia. These results generate the question if H1N1-related pneumonia is associated with a state of hypo-inflammation. A total of 135 patients were enrolled with blood sampling within less than 24 h from diagnosis; 23 with flu-like syndrome; 69 with uncomplicated H1N1-infection; seven with bacterial pneumonia; and 36 with H1N1-related pneumonia. T(regs) and CD14/HLA-DR co-expression were estimated by flow cytometry; concentrations of tumour necrosis factor-alpha (TNF-α), of interleukin (IL)-6 and of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) by an enzyme immunoassay; those of procalcitonin (PCT) by immuno-time-resolved amplified cryptate technology assay. Expression of human leucocyte antigen D-related (HLA-DR) on monocytes was similar between groups; absolute T(reg) counts were greater among patients with H1N1-related pneumonia than flu-like syndrome or H1N1-uncomplicated infection. Serum TNF-α of patients with bacterial pneumonia was greater than those of other groups, but IL-10 was similar between groups. Serum PCT was greater among patients with H1N1-related pneumonia and sTREM-1 among those with H1N1-related pneumonia. Regression analysis revealed that the most important factors related with the advent of pneumonia were the existence of underlying illnesses (P = 0·006) and of T(regs) equal to or above 16 mm(3) (P = 0·013). It is concluded that the advent of H1N1-related pneumonia is related to an early increase of the absolute T(reg) counts. This increase is probably not part of a hypo-inflammatory state of the host.
authors.affiliation: 4th Department of Internal Medicine, University of Athens, Medical School, Athens, Greece. mraftogiann@med.uoa.gr
authors.forename: M
authors.initials: M
authors.lastname: Raftogiannis
authors.forename: A
authors.initials: A
authors.lastname: Antonopoulou
authors.forename: F
authors.initials: F
authors.lastname: Baziaka
authors.forename: A
authors.initials: A
authors.lastname: Spyridaki
authors.forename: P
authors.initials: P
authors.lastname: Koutoukas
authors.forename: T
authors.initials: T
authors.lastname: Tsaganos
authors.forename: A
authors.initials: A
authors.lastname: Savva
authors.forename: A
authors.initials: A
authors.lastname: Pistiki
authors.forename: M
authors.initials: M
authors.lastname: Georgitsi
authors.forename: E J
authors.initials: EJ
authors.lastname: Giamarellos-Bourboulis
mesh_terms: D000328:Adult; D000368:Aged; D005260:Female; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D016130:Immunophenotyping; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology*; D007251:Influenza, Human / Q000097:blood / Q000150:complications / Q000276:immunology*; D015850:Interleukin-6 / Q000097:blood; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood; D008875:Middle Aged; D018410:Pneumonia, Bacterial / Q000097:blood / Q000150:complications / Q000276:immunology*; D011971:Receptors, Immunologic / Q000097:blood; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055815:Young Adult
chemical_list: D006684:HLA-DR Antigens; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1; D014409:Tumor Necrosis Factor-alpha