Lu Huang

Assistant Professor of Virology, Immunology & Microbiology

See BU Profile for additional information and publications

Research Interest

Tuberculosis (TB), a disease caused by Mycobacterium tuberculosis (Mtb) infection, remains one of the biggest infectious disease threats and a leading cause of death worldwide. Progress toward an effective vaccine has been limited by a fundamental gap in our understanding of protective immunity against TB. The overall goal of my laboratory is to define the mechanisms of protective immunity to Mtb using a combination of genetics, immunology, metabolism, genomics and animal models of disease. Our research focuses on innate immune responses in the lung, with particular emphasis on how cell-intrinsic mechanisms shape the function of lung macrophages and neutrophils during Mtb infection. Both macrophages and neutrophils are the predominant host cells at site of Mtb infection and have been implicated in both disease control and progression. The complexity of macrophages and neutrophils is reflected by their origins, heterogeneity and metabolism, all of which govern the functions of these cells in various tissues under homeostatic and inflammatory conditions. We have previously demonstrated that lung macrophages with distinct developmental lineages acquire unique metabolic states and exhibit differential levels of permissiveness to Mtb survival and growth at early stages of infection. In parallel, we uncovered that lipid metabolism in neutrophils functions as a key pathway to promote Mtb pathogenesis. These studies implicate that cell-intrinsic features of myeloid cells dominate the host response to Mtb infection. We are particularly interested in unveiling the ontogeny and immunometabolism of lung myeloid cells during Mtb infection. Ultimately, the knowledge from our studies will inform the development of vaccines and novel therapeutic interventions against this pathogen. Moreover, these studies may also have a broad impact on other pulmonary diseases.