Seasonal Influenza A virus (IAV) epidemics cause significant morbidity and mortality each year. Severe disease during IAV infection is often associated with excessive inflammation, though the mechanisms driving this remain elusive, precluding effective treatment. To date, mechanisms of IAV-driven inflammation have been characterised in naïve cells and animals, despite most of the population having pre-existing immunity in the form of antibodies. However, IAV’s rapid evolution means many of these antibodies may still bind to the virus but no longer provide protection, necessitating seasonal vaccine reformulations. Here, we utilised both monoclonal antibodies and polyclonal serum from healthy donors to investigate whether pre-existing antibodies could contribute to pathological inflammation during IAV infection. We used recombinant haemagglutinin (HA) from two different IAV strains (pandemic H1N1, H3N2) to characterise whether these monoclonal and polyclonal anti-IAV antibodies were cross-reactive and whether they could neutralise different IAV strains. We identified a novel phenotype whereby immobilised immune complexes of antibodies and HA stimulate selective proinflammatory responses from primary human macrophages. This occurs regardless of whether antibodies are neutralising or non-neutralising against the cognate strain. We speculate that these antibodies may bind to HA present on the surface of infected cells and stimulate macrophages, initiating a predominantly proinflammatory, not antiviral, response. Fully characterising this underappreciated antibody effector function and elucidating these molecular pathways may help inform future vaccine design against common human pathogens such as IAV, to preferentially induce protective antibodies through vaccination while avoiding those that may drive aberrant inflammation. Additionally, by uncovering the responsible signalling pathways for antibody-dependent inflammation, we could identify new therapeutic targets to treat IAV-driven inflammation without compromising host defence.