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John Johnson
Education
- Postdoctoral Fellowship - Integrative Physiology Department and the Center for Neurosciences, University of Colorado at Boulder, 2002-05
- PhD, Neuroscience, University of Colorado at Boulder, 2002
- MA, Psychology, University of Colorado at Boulder, 1999
- BS, Zoology, Michigan State University, 1995
Courses Taught
- Advanced Human Physiology
- Introduction to Neuroscience
Research Interests
I have broad interests in understanding the interactions between the nervous and immune systems, particularly with respect to alterations in behavior. It has only recently been appreciated that the nervous system and immune system communicate and influence one another. It is now recognized that products (e.g. cytokines) released by immune cells alter brain-mediated responses (e.g. behavioral, hormonal, and cognitive processes). For example, in response to foreign microorganisms cytokines are released by immune cells and stimulate brain-mediated physiological and behavioral responses, which are commonly referred to as sickness responses (e.g. fever, decreasing appetite, increasing sleep, amplifying pain, altering hormone levels, and impairing cognitive processes).
Brain cytokine levels also increase when an organism is exposed to stressful events, during normal aging and during neurodegenerative diseases. It has been proposed that elevated brain cytokines may mediate some of the behavioral, cognitive, and emotional changes that are associated with these times. My laboratory is interested in understanding the regulation of brain cytokines, what role brain cytokines play in mediated various physiological/behavioral responses, and how the regulations/production of brain cytokines change with repeated stressor exposure.
Recent Abstracts
An Animal Model of Recurrent Depression: Sensitized Depression-like Behavior When Rats Re-exposed to Chronic Mild Stress
Jennifer Remus, Destiny Jamison, and John Johnson; Biological Sciences, Kent State University Kent, OH 44242
Major depression is a debilitating disorder, characterized by feelings of worthlessness, persistent sadness and lack of motivation. Depression is also recognized to be a chronic, recurrent disorder with each episode of depression increasing the likelihood of another occurrence. The current study aimed to develop an animal model of recurrent depression in order to examine possible biological mechanisms responsible for this increased susceptibility. We hypothesized that animals with a prior depressive episode would be sensitized to future stressors, causing the animals to display depressive-like behaviors more rapidly or to a greater extent. Fisher rats (n=15) were exposed to chronic mild stress for 35 days or remained in their home cage as control animals during which animals showed a slow decrease in sucrose consumption. Following the 35 days, animals went through a 20 day recovery phase where no stressors were present and animal showed a steady increase in sucrose consumption back to baseline levels. At this time animals were re-exposed to chronic mild stress for 15 days. A rapid decline in sucrose consumption was observed. Linear regression lines were calculated for each animal’s sucrose consumption during the first and second stressor exposure and a paired t-test of the slope of each line revealed re-exposure to stress resulted in a significantly more rapid decline in sucrose consumption compared to that observed during the initial stressor exposure.
Repeated Stressor Exposure Regionally Sensitizes b-Adrenoceptor-Mediated Induction of Brain IL-1
Kristin Gabella, Veronica M. Porterfield, John D. Johnson
Chronic or repeated stressor exposure is associated with elevated brain cytokines, which are linked to poor health consequences including metabolic syndrome, heart disease, neurodegenerative conditions, cognitive decline, and depression. During non-pathogenic times the production of brain cytokines, particularly IL-1, is largely mediated by beta-adrenergic receptors (b-ADRs). Here, we tested the hypothesis that changes in b-ADR signaling following repeated stressor exposure favors increased brain cytokine production. Fischer rats were exposed to repeated mild stressors or remained in their home cage. Twenty-four hours after the last stressor animals were injected centrally with either saline or 10ug (1ug/ml) isoproterenol, a b-ADR agonist, via intra-cistera magna injections. As previously demonstrated, isoproterenol stimulated widespread IL-1 protein production 2h later in control animals. Interestingly, animals repeatedly exposed to stressors had similar basal cytokine levels but significantly greater IL-1 production in the hypothalamus and amygdala compared to controls, while levels were equal to controls in the hippocampus, prefrontal cortex, and brainstem. These data demonstrate repeated stressor exposure cause regional changes in b-ADR signaling that favors greater brain cytokine production. This is particularly interesting because to date only widespread priming of cytokine production to immunological stimuli has been reported following stressor exposure. These data indicate stressor exposure also primes cytokine production to stimuli that are not immunogens and this likely involves a different underlying mechanism to result in regional brain changes.
Recent Publications
Johnson, J.D., Zimomra, Z.R., Stewart, L.T. Beta-Adrenergic Receptor Activation Primes Microglia Cytokine Production. Journal of Neuroimmunology (2013) 254:161-164.
Porterfield, V.M., Gabella, K.M., Simmons, M.A., Johnson, J.D. Repeated Stressor Exposure Regionally Enhances Beta-Adrenergic Receptor Mediated Brain IL-1b Production.
Brain, Behavior, and Immunity (2012) 26:1249-1255.
Campisi, J., Sharkey, C., Johnson, J.D., Asea, A.A., Maslanik, T., Bernstein-Hanley, I., Fleshner, M. Stress-induced facilitation of host response to bacterial challenge is dependent on extracellular Hsp72 and independent of alpha beta T cells. Stress (2012) 15(6):637-646
Camp, R.M., Remus, J.L., Kalburgi, S.N.,Porterfield, V.M.,Johnson, J.D. Fear Conditioning Can Contribute to Behavioral Changes Observed in a Repeated Stress Model Behavioural Brain Research (2012) 233(2):536-544.
Zimomra, Z.R., Porterfield, V.M., Camp, R., Johnson, J.D. Time-Dependent Mediators of HPA Activation Following Peripheral E.coli Am.J.Physiol Regul Integr Comp Physiol (2011) Dec;301(6):R1648-57.
Hains, L.E., Loram, L.C., Taylor, F., Strand, K., Weiseler, J.L., Barrientos, R., Young, J.J., Frank, M.G., Sobesky, J., Martin, T.J., Eisenach, J.C., Maier, S.F., Johnson, J.D., Fleshner, M., Watkins, L.R. Immune Priming with prior Laparotomy or Corticosterone Potentiates Lipopolysaccharide-induced Fever and Sickness Behaviors. Journal of Neuroimmunology (2011) Oct 28;239(1-2):53:60.
Porterfield, V.M., Zimomra, Z.R., Caldwell, E., Camp, R.M., Johnson, J.D. Strain Differences in Restraint Stress Induced Brain Cytokines. Neuroscience (2011) 188:48-54.
Fleshner, M., Kennedy, S.L., Johnson, J.D., Day, H.E.W., Greenwood, B.N. Exercise and Stress Resistance: Neural-Immune Mechanisms. The Neuroimmunological Basis of Behavior and Mental Disorders, (2009) Editors: Allan Siegel and Steven S. Zalcman
Johnson, J.D., Cortez, V., Kennedy, S.L., Foley, T.E., Hanson, H, Fleshner, M. Role of Central b-Adrenergic Receptors in Regulating Proinflammatory Cytokine Responses to a Peripheral Bacterial Challenge. Brain, Behavior, and Immunity (2008) 22:1078-1086.
Recent Grants
National Institute of Mental Health
“Regulation of Brain IL-1 & Sickness Responses Following E.coli Challenge”
1/1/07 - 5/31/10
Ohio Board of Regents Research Incentive Program
“Development of an Interdisciplinary Translational Research Model to Study Depression in Laboratory Animals and Human Subjects”
6/15/09 – 6/14/11
Defense Advanced Research Projects Agency (DARPA)
“Targeting Stress Resilience Without Detriment to Adaptive Stress Response”
5/28/10-5/27/13Scholarly, Creative & Professional Activities
Fleshner, M., Johnson, J.D., Friedman, J. Extracellular Hsp72: A double-edged sword for host defense. In: Heat Shock Proteins: Potent Mediators of Inflammation & Immunity, Springer Publishing New York, NY (2007) Vol. 1: 235-264.
Fleshner, M., Sharkey, C.M., Nickerson, M., Johnson, J.D. Endogenous extracellular Hsp72 release is an adaptive feature of the acute stress response. Psychoneuroimmunology 4th Ed, Elsevier/Academic Press, San Diego, CA. (2006). Vol. 2: 1013-1034
Johnson, J.D. and Fleshner, M. Releasing signals, secretory pathways, and immune function of endogenous extracellular heat shock protein 72. (2006). J. Leukoc Biol. Mar, 79(3):425-434.
Nickerson, M., Kennedy, S.L., Johnson, J.D., Fleshner, M. Sexual dimorphism of the intracellular heat shock protein 72 response. (2006). J. Appl Physiol., 101:566-575.
Johnson, J.D., Campisi, J., Sharkey, C.M., Kennedy, S.S., Nickerson, M., & Fleshner, M. (2005). Adrenergic Receptors Mediate Stress-Induced Elevations in Extracellular Hsp72. J. Applied Physiol., 99:1789-1795.
Johnson, J.D., Campisi, J., Sharkey, C.M., Kennedy, S.L., Nickerson, M., Greenwood, B.N., & Fleshner, M. (2005). Catecholamines Mediate Stress-Induced Release of Peripheral and Central Inflammatory Cytokines. Neuroscience, 135:1295-1307.
Fleshner, M. & Johnson, J.D. (2005). Endogenous extracellular Heat Shock Protein 72: Releasing signal(s) and function. Int. J. Hyperthermia, 21(5):457-471.
Kennedy, S.L., Nickerson, M., Campisi, J., Johnson, J.D., Smith, T.P., & Fleshner, M., (2005). Splenic norepinephrine depletion and suppression of in vivo antibody. Journal of Neuroimmunology, 165:150-160.
O'Connor, K.A., Ginsberg, A.B., Maksimova, E., Wieseler-Frank, J.L., Johnson, J.D., Spencer, R.L., Campeau, S., Watkins, L.R., & Maier, S.F., (2004). Stress-induced sensitization of the hypothalamic-pituitary adrenal axis is associated with alterations of hypothalamic and pituitary gene expression. Neuroendocrinology. 80:252-263.
Johnson, J.D., O'Connor, K.A., Watkins, L.R., Maier, S.F., (2004). The role of IL-1b in stress-induced sensitization of proinflammatory cytokine and corticosterone responses. Neuroscience, 127:569-577.
Fleshner, M., Campisi, J., Johnson, J.D., (2003). Can exercise stress facilitate innate immunity? A functional role for stress-induced extracellular Hsp72. Exercise Immunology Review. 9:6-24.
Johnson, J.D., (2003). Cycles of sex and disease. Trends in Endocrinol. Metab. 14(3):105-106.
O'Connor, K.A., Johnson, J.D., Hansen, M.K., Wieseler-Frank, J.L., Maksimova, E., Watkins, L.R., Maier, S.F., (2003). Peripheral and central proinflammatory cytokine response to a severe acute stressor. Brain Res. 991(1-2):123-32.
O'Connor, K.A., Johnson, J.D., Hammack, S.E., Brooks, L.M., Spencer, R.L., Watkins, L.R., Maier, S.F., (2003). Inescapable shock induces resistance to the effects of dexamethasone. Psychoneuroendocrinology, 28:481-500.
Johnson, J.D., O'Connor K.A., Hansen, M.K., Biedenkapp, J.C., Watkins, L.R., Maier, S.F., (2003). Effects of prior stress on LPS-induced cytokine and sickness responses. Am. J. Physiol.284: R422-R432.
O'Connor, K.A., Hansen, M.K., Pugh, C.R., Deak, M.M., Biedenkapp, J.C., Milligan, E.D., Johnson, J.D., Wang, H., Maier, S.F., Tracey, K.J., Watkins, L.R., (2003). Further characterization of high mobility group box 1 (HMGB1) as a proinflammatory cytokine: central nervous system effects. Cytokine, 24:254-265.
Johnson, J.D., O'Connor, K.A., Deak, T., Stark, M., Watkins, L.R., Maier, S.F., (2002). Prior stressor exposure sensitizes LPS-induced cytokine production. Brain, Behavior, and Immunity, 16, 461-476.
Johnson, J.D., O'Connor, K.A., Deak, T., Spencer, R.L., Watkins, L.R., Maier, S.F., (2002). Prior stressor exposure primes the HPA axis. Psychoneuroendocrinology, 27:353-365.
Pugh, C.R., Johnson, J.D., Martin, D., Rudy, J.W., Maier, S.F., Watkins, L.R., (2000). Human innumodeficiency virus-1 coat protein gp120 impairs contextual fear conditioning: a potential role in AIDS related learning and memory impairments. Brain Res. 861(1): 8-15.
Durham, R.A., Johnson, J.D., Eaton, M.J., Moore, K.E., Lookingland, K.J., (1998). Opposing roles for dopamine D1 and D2 receptors in the regulation of hypothalamic tuberinfundibular dopamine neurons. Eur J Pharmacol, 355 (2-3): 141-7.
Cheung, S., Johnson, J.D., Moore K.E., Lookingland, K.J., (1997). Dopamine receptor-mediated regulation of expression of Fos and its releated antigens (FRA) in somatostatin neurons in the hypothalamic periventricular nucleus. Brain Res. 770(1-2):176-83.
Durham, R.A., Johnson, J.D., Moore, K.E., and Lookingland, K.J., (1996). Evidence that D2 receptor-mediated activation of hypothalamic tuberoinfundibular dopaminergic neurons in the male rat occurs via inhibition of tonically active afferent dynorphinergic neurons. Brain Res, 732(1-2):113-20.
Research Areas
- Neuroimmune Interactions
- Regulation of Brain Cytokines
- Physiological & Pathological Consequences of Elevated Brain Cytokines
- Stress, Immune, and Behavior
OFFICE
Department of Biological SciencesCONTACT INFO
Phone: 330-672-3849jjohns72@kent.edu
COURSES TEACHING
Spring 2013- BSCI 40099 - 003 Senior Honors Thesis
- BSCI 40196 - 019 Individual Investigation
- BSCI 40434 - 001 Mammalian Physiology Ii
- BSCI 40600 - 016 Writing In Biological Sciences
- BSCI 50196 - 001 Individual Investigation
- BSCI 50434 - 001 Mammalian Physiology Ii
- BMS 60198 - 028 Research
- BSCI 70434 - 001 Mammalian Physiology Ii
- BSCI 80299 - 006 Dissertation Ii
- BMS 60198 - 031 Research
- BSCI 80199 - 007 Dissertation I
- BSCI 80299 - 006 Dissertation Ii
- BSCI 30520 - 001 Introduction To Neuroscience
- BSCI 40600 - 004 Writing In Biological Sciences
- BSCI 80198 - 010 Research
- BSCI 80199 - 004 Dissertation I
- BSCI 80299 - 010 Dissertation Ii
EXPERTISE
- Faculty Advisor
- stress
- cytokines
- depression
- neuroscience
