Norbert Kaminski

Professor of Toxicology, Director of the Institute for Integrative Toxicology | Michigan State University

East Lansing, MI, UNITED STATES

Expert on cannabinoid research and toxicology.

Biography

Norbert Kaminski is the director of the MSU Institute for Integrative Toxicology and a professor in the Department of Pharmacology and Toxicology.

Kaminski has studied the effects of marijuana on the immune system since 1990. His lab was the first to identify the proteins that can bind marijuana compounds on the surface of immune cells. Up until then, it was unclear how these compounds, also known as cannabinoids, affected the immune system. His latest research looked at the effects THC, or tetrahydrocannabinol, a chemical found in marijuana, had on mental decline in HIV patients.

Kaminski is a member of the Society of Toxicology and Immunotoxicology Specialty Section, the American Association of Immunologists and the International Cannabinoid Research Society.

Industry Expertise (4)

Research

Education/Learning

Health and Wellness

Health Care - Services

Areas of Expertise (4)

Experimental therapeutics

Cannabinoids

Toxicology

Immunotoxicology

Accomplishments (1)

President, Society of Toxicology (professional)

2014 The Society of Toxicology (SOT) is a learned society (professional association) based in the United States that supports scientific inquiry in the field of toxicology.

Education (3)

North Carolina State University: PhD, Toxicology & Physiology 1985

North Carolina State University: MS, Toxicology 1981

Loyola University of Chicago: BA, Chemistry 1978

Affiliations (2)

Journal of Pharmacology and Experimental Therapeutics
Insititute for Integrative Toxicology

Links (1)

MSU Profile

News (3)

Norbert Kaminski named CRIS interim director

MSU Today online

2017-12-01

"Norbert Kaminski was named interim director of the Center for Research on Ingredient Safety (CRIS) at Michigan State University (MSU). He replaces Michael Holsapple, who resigned in November..."

Marijuana may help HIV patients keep mental stamina longer

MSUToday online

2017-12-11

A chemical found in marijuana, known as tetrahydrocannabinol, or THC, has been found to potentially slow the process in which mental decline can occur in up to 50 percent of HIV patients, says a new Michigan State University study.

New study shows marijuana might help HIV patients

Yahoo

2017-12-14

The stereotypical pot user isn’t exactly known to be mentally sharp, but new research has found that the drug might do just that — for HIV patients, at least.

Journal Articles (3)

CLARITY-BPA: Effects of Chronic Bisphenol A Exposure on the Immune System: Part 1 – Quantification of the relative number and proportion of leukocyte populations in the spleen and thymus

Toxicology

Li J, Bach A, Crawford RB, Phadnis-Moghe AS, Chen W, D'Ingillo S, Kovalova N, Suarez-Martinez JE, Zhou J, Kaplan BLF, Kaminski NE3

2018 Bisphenol A (BPA) is extensively used in manufacturing of a broad range of consumer products worldwide. Due to its widespread use, human exposure to BPA is virtually ubiquitous. Broad human exposure coupled with a large scientific literature describing estrogenic activity of BPA in animals has raised public health concerns. To comprehensively evaluate the health effects of BPA exposure, a chronic toxicity study using a wide-range of BPA doses (2.5-25000 μg/kg bw/day) was conducted jointly by the NTP, thirteen NIEHS-supported grantees, and the FDA, which is called the Consortium Linking Academic and Regulatory Insights on Toxicity of BPA (CLARITY-BPA). As a participant in the CLARITY-BPA project, the objective of the current study was to evaluate the effects of chronic BPA exposure in Sprague-Dawley rats on the relative number and proportion of defined leukocyte populations in the spleen and the thymus. Toward this end, lymphoid tissues from a total of 641 rats were assayed after being continuously dosed with BPA or controls for up to one year. To comprehensively evaluate the effects of BPA on leukocyte compositions, extensive endpoints that cover major populations of leukocytes were assessed, including B cells, T cells, NK cells, granulocytes, monocytes, macrophages and dendritic cells. In total, of the 530 measurements in BPA-treated rats, 10 measurements were statistically different from vehicle controls and were mainly associated with either the macrophage or dendritic cell populations. Most, if not all, of these alterations were found to be transient with no persistent trend over the one-year time period. In addition, the observed BPA-associated alterations were mostly moderate in magnitude and not dose-dependent. Due to the aforementioned, it is unlikely that the observed BPA-mediated changes alone would adversely affect immune competence.

Time-Dependent Airway Epithelial and Inflammatory Cell Responses Induced by Influenza Virus A/PR/8/34 in C57BL/6 Mice

Toxicologic Pathology

John P. Buchweitz, Jack R. Harkema, Norbert E. Kaminski

2007 The present study examines the kinetics of airway epithelial remodeling and inflammation in the airways of C57BL/6J mice infected with influenza virus A/PR/8/34 (PR8). Mice were intranasally instilled with 50 plaque forming units (pfu) of virus or its respective vehicle, saline, and then were sacrificed at 3, 7, 10, 15, or 21 days postinfection (dpi). PR8 treatment resulted in airway epithelial cell regeneration as suggested by proliferating cell nuclear antigen (PCNA) positive staining at 7 and 10 dpi and mucous cell metaplasia (MCM) evident at 10, 15, and 21 dpi. PR8 treatment resulted in a classic pattern of inflammation observed in bronchoalveolar lavage fluid (BALF), in which neutrophils peaked at 3 and 7 dpi and monocytes, lymphocytes, and eosinophils peaked at 10 dpi before returning to background levels of detection. Chemokine (MCP-1) and cytokine (IL-6, TNF-α, IFN-γ, IL-5, IL-4, and IL-9) levels peaked at 7 dpi in BALF. IL-13 levels were unaffected by PR8 treatment. Concurrent with inflammation, MUC5AC gene expression was markedly increased by PR8 treatment at 7 dpi. Collectively, the results of this study indicate that the onset of MCM in airway epithelium occurs during the remodeling process and persists after the inflammatory response has diminished.

Interactions at a dioxin responsive element (DRE) and an overlapping κB site within the hs4 domain of the 3′α immunoglobulin heavy chain enhancer

Toxicology

Courtney E.W Sulentic, Jong Soon Kang, Yong Joo Nab, Norbert E. Kaminski

2004 Our previous results describing the CH12.LX (AhR-expressing) and BCL-1 (AhR-deficient) B cell lines have supported an AhR/dioxin-responsive element (DRE)-mediated mechanism for TCDD-induced inhibition of μ heavy chain expression and thus of IgM secretion. Transcriptional regulation of the Ig heavy chain genes involves several regulatory elements including the 3′α Ig heavy chain enhancer, which is composed of four regulatory domains that span approximately 40 kb. One of these domains, hs4, contains a DRE-like site that overlaps a κB motif. We have previously demonstrated TCDD-inducible binding of both the AhR nuclear complex and NF-κB/Rel proteins to the DRE and κB motifs, respectively, as well as TCDD and LPS-induced transcriptional activity through the hs4 domain. The objective of the present study was to determine if the AhR nuclear complex and NF-κB/Rel proteins converge at these two overlapping cis-elements and act cooperatively to influence enhancer activity. To eliminate the potential influence of other transcription factors which bind to the hs4 domain, the approach was to construct a series of luciferase reporters containing a variable heavy chain (VH) promoter and a 42 bp fragment of the 1.4 kb hs4 regulatory domain, that included only the overlapping DRE and κB motif or mutations of these motifs for transient transfection experiments in CH12.LX and BCL-1 cells. In the CH12.LX cells, TCDD activated the hs4 fragment; however, co-treatment with LPS led to a marked and synergistic activation as previously observed with the wild type 1.4 kb hs4 domain. Mutation of either or both of the DRE and κB motifs diminished the effect of TCDD and LPS on the luciferase reporters possessing the 42 bp portion of hs4, and resembled the effect of these treatments on the promoter alone. In the BCL-1 cells, activity of the hs4 fragment was not induced by TCDD and/or LPS treatment. These results suggest that the AhR nuclear complex and NF-κB/Rel proteins converge at the DRE and κB motif to influence transcriptional activity of the hs4 enhancer fragment.