Literature DB >> 20646008

Indication for a role of regulatory T cells for the advent of influenza A (H1N1)-related pneumonia.

M Raftogiannis1, A Antonopoulou, F Baziaka, A Spyridaki, P Koutoukas, T Tsaganos, A Savva, A Pistiki, M Georgitsi, E J Giamarellos-Bourboulis.   

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.
© 2010 British Society for Immunology.

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Year:  2010        PMID: 20646008      PMCID: PMC2962977          DOI: 10.1111/j.1365-2249.2010.04208.x

Source DB:  PubMed          Journal:  Clin Exp Immunol        ISSN: 0009-9104            Impact factor:   4.330


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