Gary B. Huffnagle, Ph.D.

Nina and Jerry D Luptak Professor of Food Allergy
Professor, Molecular, Cellular & Developmental Biology (MCDB)
Associate Chair for Undergraduate Studies, MCDB
Professor, Pulmonary & Critical Care Medicine
Research Professor, Mary H Weiser Food Allergy Center
Professor, Microbiology & Immunology
734-936-9369

Biography

Gary B. Huffnagle, PhD holds faculty appointments (Professor) in Internal Medicine, Microbiology & Immunology, and Molecular Cellular & Developmental Biology, as well as the Mary H. Weiser Food Allergy Center at the University of Michigan. He also holds the Nina and Jerry D Luptak Professorship in Food Allergy at the University of Michigan.  He received his PhD in immunology from the University of Texas Southwestern Medical School and was elected to the American Academy of Microbiology of the American Society for Microbiology in 2013. 

Areas of Interest

Dr. Huffnagle's research interests fall into three areas: (1) the microbiome & respiratory diseases, (2) the mucosal immunobiology and microbiology of food allergies, and (3) the microbiology, immunology and microbial ecology of the yeast Candida albicans. 

(1) With over 200 species, Pseudomonas is one of the largest, most genetically diverse and ecologically adaptable of all Gram-negative genera. Despite this diversity, the only Pseudomonas species recognized as a common colonizer of humans is the opportunistic pathogen Pseudomonas aeruginosa. However, non-aeruginosa Pseudomonas species (NAPS) can often be detected in clinical specimens, but they have been assumed to be clinically insignificant. We have ongoing studies in humans and mice that pulmonary inflammation results in a bloom of two NAPS in the lungs that have the potential to act as co-factors in chronic inflammation and disease, as demonstrated by in vitro, in vivo and in silico analyses.

(2) Our laboratory is interested in the role of the microbiota in shaping mucosal immunity and protection from food allergies. Epidemiologic and clinical data support the hypothesis that perturbations in the microbiota due to differences in "westernized" countries have disrupted the normal microbiota-mediated mechanisms of immunological tolerance in the mucosa, leading to an increase in the incidence of allergic diseases and other inflammatory conditions. Our laboratory demonstrated that mice can develop allergic responses to allergens if their endogenous microbiota is altered at the time of first allergen exposure. These experimental and clinical observations are consistent with other studies demonstrating that the endogenous microbiota plays a significant role in shaping the development of the immune system.

(3) In conjunction with our mucosal immunity interest, our laboratory also studies the microbial ecology of mucosal surfaces and how colonization by Candida albicans and other yeast can modify the resistance and resilience of the bacterial community structure in the gastrointestinal tract in response to ecologic stress or perturbation, as well as downstream effects on immune system regulation.

Published Articles or Reviews

Huffnagle GB, McNeil LK, McDonald RA, Murphy JW, Toews GB, Maeda N, Kuziel WA. Cutting Edge: Role of CCR5 in organ-specific and innate immunity to Cryptococcus neoformans. J Immunol1999, 163: 4642-4646.

Traynor TR, Kuziel WA, Toews GB, Huffnagle GB. CCR2 expression determines T1 vs. T2 polarization during pulmonary Cryptococcus neoformans infection. J Immunol 2000, 164(4):2021-2027.

Aliberti J, Reis e Sousa C, Schito M, Hieny S, Wells T, Huffnagle GB, Sher A. CCR5 provides a signal for microbial induced production of IL-12 by CD8a+ dendritic cells. Nature Immunol 2000, 1:83-87.

Olszewski MA, Huffnagle GB, McDonald RA, Lindell DM, Cook DN, Toews GB. The role of MIP-1a/CCL3 in regulation of T cell-mediated immunity to Cryptococcus neoformans infection. J Immunol 2000, 165(11):6429-36.

Noverr MC, Phare SM, Toews GB, Coffey MJ, Huffnagle GB. Pathogenic yeasts of Cryptococcus neoformans and Candida albicans produce immunomodulatory prostaglandins. Infect Immun 2001, May;69(5):2957-63.