Luo Laboratory Research

Ongoing Projects

  1. How maternal immune factors regulate neonatal microbiota. Gut colonization of commensal bacteria decreases the risk of neonatal sepsis. This suggests that dysbiosis of the neonatal gut microbiota may represent a risk factor and contribute to increased incidence of infection in infants. Our ongoing experiments show that host adaptive immune status plays a key role in shaping the gut microbiota. They beg the question, however, of the relative contributions of maternal and de novo immunity sources to the observed microbiota changes. In an NIH-funded project, we propose to focus on the effects of maternal factors, in particular those transferred through the milk and placenta, on the development of neonatal microbiota.
  2. Role of gut microbiota in systemic lupus erythematosus (SLE). SLE is a very complex autoimmune disorder with no known cure. It is characterized by severe and persistent inflammation that damages multiple organs, including skin, kidney, lung, joint, heart, and brain. More than half of patients suffer from lupus nephritis, a leading cause of death in patients with SLE. Current treatments for lupus nephritis are primarily nonselective immunosuppressants. They can effectively reduce the risk for renal failure, but the side effects are a major cause of concern. There is an imperative need for new treatment strategies against lupus nephritis, for which a better understanding of disease pathogenesis is required. Perturbation of gut microbiota has been shown to be associated with many autoimmune diseases, but little is known about the role of gut microbiota in SLE. We study both protective and pathogenic roles of gut microbiota in mouse models of SLE as well as in human patients.
  3. Complex roles of vitamin A in autoimmunity. Vitamin A and its active metabolite, retinoic acid (RA), are known to exert both pro-inflammatory and anti-inflammatory functions depending on different contexts. RA can suppress inflammation and induce tolerance under steady state. Paradoxically, it can also act as an adjuvant to promote ongoing inflammation against infections. This conundrum on the functions of RA is much less understood for autoimmunity. Evidence is lacking on whether and how RA affects the initiation and progression of autoimmune disorders, which as a whole are a leading cause of death and disability in the United States. In an NIH-funded project, we aim to define the complex roles of RA in autoimmunity.
  4. Generation of humanized lupus mouse model. Numerous mouse models have been employed to understand the pathogenesis of lupus and to test potential therapies. Although each model has unique advantages, effective treatments in mouse models often do not translate to human disease. We therefore aim to generate human-mouse chimeras for lupus research.

Collaborators

Virginia Tech

Other Institutions