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S16 Acquired immune responses to the seasonal trivalent influenza vaccination in COPD
  1. KJ Staples1,
  2. NP Williams1,
  3. O Bonduelle2,
  4. AJ Hutton2,
  5. D Cellura1,
  6. B Combadiere2,
  7. TMA Wilkinson1
  1. 1University of Southampton Faculty of Medicine, Southampton, UK
  2. 2INSERM, Centre d’Immunologie et des Maladies Infectieuses, Paris, France

Abstract

Background Influenza A virus (IAV) is a major global public health burden, particularly in the elderly and those with underlying respiratory conditions such as COPD. Epidemiological data suggests that influenza vaccination protects against all-cause mortality in COPD patients. However recent work has called the efficacy of the vaccine in COPD into question, suggesting there is a defect in the ability of COPD patients to mount an adequate humoral response to influenza vaccination.

Objectives The aim of our study was to investigate mechanisms driving the acquired immune responses to the seasonal trivalent influenza vaccination (TIV), in COPD subjects and healthy controls

Methods 47 subjects were enrolled into the study; 23 COPD patients, 13 age-matched healthy control (HC –≥50) and 11 young healthy control subjects (YC –≤40). Serum and PBMC were isolated pre-TIV vaccination and at 7d, 28d and 6 months post vaccine for antibody titre, T cell and ELISpot analysis.

Results The antibody titre to each of the three strains of virus was significantly increased 7 d post-vaccine (p<0.001), peaking at 28 d post whilst beginning to wane 6 months post-vaccine. The kinetics of the vaccine response were similar between YH, HC and COPD patients and there was no significant difference in antibody titres between the groups 28 d post-vaccine. This increase in antibody titre was reflected by a significant increase in H1N1-specific CD4 +T helper cells in the cohort 28 d post-vaccine (p<0.01) but there was no significant difference in the fold-induction of specific CD4 +T cells at any time point between groups. As there were no disease-dependent differences we investigated if there was any association of these measures with age. H1N1 (r=−0.4253, p=0.0036) and Flu B (r=−0.344, p=0.0192) antibody titre at 28 d negatively correlated with age as did H1N1-specific CD4 +T helper cells (r=−0.4276, p=0.0034).

Conclusions These results suggest that age is the primary determinant of response to trivalent vaccine and that there is no defect in COPD per se. The yearly trivalent vaccine should therefore be continued as an adjunct to COPD disease management.

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