Journal of Clinical and Cellular Immunology
Open Access

How neutrophils influence severity and immune response to tuberculosis infection in mice

Conference Series LLC Joint International Event on 5^th European Immunology & Innate Immunity

July 21-23, 2016 Berlin, Germany

Alexander Apt, Tatiana Kondratieva, Irina Linge, Elena Kondratieva, Maria Korotetskaya and Vladimir Yeremeev

Central Institute for Tuberculosis, Russia

Posters & Accepted Abstracts: J Clin Cell Immunol

Abstract :

The role of neutrophils in tuberculosis (TB) resistance and pathology is not fully defined. Neutrophil reactions are meant to target the offending pathogen but may lead to destruction of the host lung tissue, making the defending cells an enemy. Mice genetically susceptible to TB demonstrate an unusually high and prolonged neutrophil accumulation in their lungs. Compared to neutrophils from resistant mice, their neutrophils display an increased mobility and tissue influx, prolonged lifespan, low expression of the CD95 (Fas) apoptotic receptor, relative resistance to apoptosis and an increased phagocytic capacity for mycobacteria. These features, along with the poor ability of neutrophils to restrict mycobacterial growth, indicate that the prevalence of neutrophils in TB inflammation contributes to the development of pathology, rather than protection of the host and neutrophils may play the role of a "Trojan horse" for mycobacteria. This conclusion received further support in the BCG vaccination system: An advanced capture of BCG by neutrophils, which occurs in the absence of B-cells, leads to a significant decrease in numbers of IFN-gamma producing T-cells and impairs BCG performance. Selective depletion of neutrophils from infected mice results in reduced lung tissue pathology, mycobacterial CFU counts and an increase of the survival time. Furthermore, in vivo neutrophil depletion at the onset of TB infection results in a significant increase in numbers of mycobacteria-specific IFN-�?�?�?³ producing T-cells. These results suggest antagonistic activity of neutrophils and immune T-cells in the course of TB infection and provide further evidence of deleterious rather than protective role of the former.