Heike L. Rittner

ORCID: 0000-0003-4867-0188
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About
Contact & Profiles
Research Areas
  • Pain Mechanisms and Treatments
  • Neuropeptides and Animal Physiology
  • Pain Management and Treatment
  • Cancer, Stress, Anesthesia, and Immune Response
  • Musculoskeletal pain and rehabilitation
  • Anesthesia and Pain Management
  • Barrier Structure and Function Studies
  • Pain Management and Opioid Use
  • Pain Management and Placebo Effect
  • Myofascial pain diagnosis and treatment
  • Pediatric Pain Management Techniques
  • Ion Channels and Receptors
  • Fibromyalgia and Chronic Fatigue Syndrome Research
  • Hereditary Neurological Disorders
  • Pharmacological Effects of Natural Compounds
  • Nerve injury and regeneration
  • Nerve Injury and Rehabilitation
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Hernia repair and management
  • Inflammatory mediators and NSAID effects
  • Spine and Intervertebral Disc Pathology
  • Receptor Mechanisms and Signaling
  • Autoimmune Bullous Skin Diseases
  • Drug-Induced Adverse Reactions
  • Peripheral Nerve Disorders

Universitätsklinikum Würzburg
2016-2025

University of Würzburg
2009-2024

Klinikum Würzburg Mitte
2014-2020

Masaryk University
2019

University Medical Center of the Johannes Gutenberg University Mainz
2019

Johannes Gutenberg University Mainz
2019

Central European Institute of Technology
2019

University Hospital Brno
2019

Klinik und Poliklinik für Urologie
2009-2018

Charité - Universitätsmedizin Berlin
2003-2017

Background Inflammatory pain can be effectively controlled by an interaction of opioid receptors on peripheral sensory nerve terminals with peptides released from immune cells upon stressful stimulation. To define the source peptide production, we sought to identify and quantify populations opioid-containing during course Freund's complete adjuvant-induced hind paw inflammation in rat. In parallel, examined development stress-induced local analgesia paw. Methods At 2, 6, 96 h after adjuvant...

10.1097/00000542-200108000-00036 article EN Anesthesiology 2001-08-01

Giant cell arteritis (GCA) is a systemic vasculitis preferentially affecting large and medium-sized arteries. Inflammatory infiltrates in the arterial wall induce luminal occlusion with subsequent ischemia degradation of elastic membranes, allowing aneurysm formation. To identify pathways relevant to disease process, differential display–PCR was used. The enzyme aldose reductase (AR), which implicated regulation tissue osmolarity, found be upregulated arteritic lesions. Upregulated AR...

10.1172/jci4711 article EN Journal of Clinical Investigation 1999-04-01

Different sensory profiles in diabetic distal symmetrical sensory-motor polyneuropathy (DSPN) may be associated with pain and the responsiveness to analgesia. We aimed characterize phenotypes of patients painful painless neuropathy assess demographic, clinical, metabolic, electrophysiological parameters related presence neuropathic a large cohort well-defined DSPN subjects. This observational cross-sectional multi-center study (performed as part ncRNAPain EU consortium) 232 subjects...

10.1097/j.pain.0000000000001034 article EN Pain 2017-08-03

Recent studies have provided evidence of pathology and functional abnormalities small nerve fibers as a potential correlate pain in the fibromyalgia syndrome. Here, we aimed to quantify dermal unmyelinated fiber diameter at electron microscopic level find morphological disturbance. Thirty-two patients with syndrome, 12 neuropathy, 24 healthy controls were prospectively recruited. Skin biopsies distal proximal legs index finger taken processed for immunofluorescence microscopy. We determined...

10.1097/j.pain.0000000000000285 article EN Pain 2015-07-08

Cancer-induced bone pain (CIBP) is a frequent complication in patients suffering from metastases. Previous studies have demonstrated pivotal role of reactive oxygen species (ROS) inflammatory and neuropathic pain, ROS scavengers exhibited potent antinociceptive effect. However, the spinal remains unclear. In this study, we investigated analgesic effect two well-established CIBP model. Our results found that intraperitoneal injection N-tert-Butyl-α-phenylnitrone (PBN, 50 100mg/kg)...

10.1016/j.redox.2017.10.011 article EN cc-by Redox Biology 2017-10-16

Abstract —Giant cell arteritis (GCA) is an inflammatory vasculopathy in which T cells and macrophages infiltrate the wall of medium large arteries. Clinical consequences such as blindness stroke are related to arterial occlusion. Formation aortic aneurysms may result from necrosis smooth muscle fragmentation elastic membranes. The molecular mechanisms injury GCA not understood. To identify damage, gene expression inflamed unaffected temporal artery specimens was compared by differential...

10.1161/01.res.84.9.1050 article EN Circulation Research 1999-05-14

Giant cell arteritis (GCA) is a vasculitic syndrome that preferentially affects medium and large-sized arteries. Glucocorticoid therapy resolves clinical symptoms within hours to days, but has be continued over several years prevent disease relapses. It not known whether how glucocorticoids affect the function of inflammatory infiltrate or why persists subclinically despite chronic treatment. GCA self-sustained in temporal arteries engrafted into SCID mice, providing model which mechanisms...

10.1172/jci119477 article EN Journal of Clinical Investigation 1997-06-15

Although opioids are highly effective analgesics, they also known to induce cellular adaptations resulting in tolerance. Experimental studies often performed the absence of painful tissue injury, which precludes extrapolation clinical situation. Here we show that rats with chronic morphine treatment do not develop signs tolerance at peripheral mu-opioid receptors (micro-receptors) presence CFA-induced paw inflammation. In sensory neurons these animals, internalization mu-receptors was...

10.1172/jci25911 article EN Journal of Clinical Investigation 2008-01-27

Opioid-containing leukocytes can counteract inflammatory hyperalgesia. Under stress or after local injection of corticotropin releasing factor (CRF), opioid peptides are released from leukocytes, bind to receptors on peripheral sensory neurons and mediate antinociception. Since polymorphonuclear cells (PMN) the predominant opioid-containing leukocyte subpopulation in early inflammation, we hypothesized that PMN their recruitment by chemokines important for opioid-mediated antinociception at...

10.1016/j.pain.2004.08.029 article EN Pain 2004-10-13

Leukocytes counteract inflammatory pain by releasing opioid peptides, which bind to receptors on peripheral sensory neurons. In the early phase of inflammation, polymorphonuclear cells (PMN) are major source opioids. Their recruitment is governed ligands at chemokine receptor CXCR2. Here, we examined whether chemokines can also induce peptide secretion from PMN and thus inhibit pain. rats with hindpaw intraplantar injection CXCL2/3, but not CXCR4 ligand CXCL12, elicited naloxone-reversible...

10.1096/fj.06-6077fje article EN The FASEB Journal 2006-10-23

The analgesic effects of leukocyte-derived opioids have been exclusively demonstrated for somatic inflammatory pain, example, the pain associated with surgery and arthritis. Neuropathic results from injury to nerves, is often resistant current treatments, can seriously impair a patient's quality life. Although it has recognized that neuronal damage involve inflammation, generally assumed immune cells act predominately as generators neuropathic pain. However, in this study we leukocytes...

10.1172/jci36246 article EN Journal of Clinical Investigation 2009-01-12

Selective targeting of sensory or nociceptive neurons in peripheral nerves remains a clinically desirable goal. Delivery promising analgesic drugs is often impeded by the perineurium, which functions as diffusion barrier attributable to tight junctions. We used perineurial injection hypertonic saline tool open transiently rats and elucidated molecular action principle mechanistic detail: Hypertonic acts via metalloproteinase 9 (MMP9). The noncatalytic hemopexin domain MMP9 binds low-density...

10.1073/pnas.1120800109 article EN Proceedings of the National Academy of Sciences 2012-06-25

The interplay of specific leukocyte subpopulations, resident cells and proalgesic mediators results in pain inflammation. Proalgesic like reactive oxygen species (ROS) downstream products elicit by stimulation transient receptor potential (TRP) channels. contribution subpopulations however is less clear. Local injection neutrophilic chemokines elicits neutrophil recruitment but no hyperalgesia rats. In meta-analyses the monocytic chemoattractant, CCL2 (monocyte chemoattractant protein-1;...

10.1371/journal.pone.0063564 article EN cc-by PLoS ONE 2013-05-02

Fibromyalgia syndrome (FMS) is a chronic widespread pain condition probably comprising subgroups with different underlying pathomechanisms. There increasing evidence for small nerve fiber impairment in of patients FMS. MicroRNAs (miRNAs) regulate molecular factors determining de- and re-generation. We investigated whether systemic cutaneous miRNA expression FMS related to pathology. confirmed previous findings disturbed function reduced intraepidermal density found 51 aberrantly expressed...

10.1097/j.pain.0000000000000668 article EN Pain 2016-07-15

Complex regional pain syndrome (CRPS) presents postinjury with disproportionate and neuropathic, autonomic, motor symptoms, skin texture affection. However, the origin of these multiplex changes is unclear. Skin biopsies offer a window to analyze somatosensory vascular system as well trophicity their protecting barriers. In previous studies, barrier-protective exosomal microRNAs were altered in CRPS. We here postulated that tissue architecture barrier proteins are already at beginning...

10.1097/j.pain.0000000000003168 article EN cc-by-nc-nd Pain 2024-02-07

Pain can be effectively controlled by endogenous mechanisms based on neuroimmune interactions. In inflamed tissue immune cell-derived opioid peptides activate receptors peripheral sensory nerves leading to potent analgesia. This is brought about a release of opioids from inflammatory cells after stimulation stress or corticotropin-releasing hormone (CRH). Immunocytes migrate the circulation in multiple steps, including their rolling, adhesion, and transmigration through vessel wall....

10.1523/jneurosci.22-13-05588.2002 article EN Journal of Neuroscience 2002-07-01

Abstract Polymorphonuclear cells (PMN) are recruited in early inflammation and believed to contribute inflammatory pain. However, studies demonstrating a hyperalgesic role of PMN did not examine selective recruitment or document effective recruitment. We hypothesized that hyperalgesia does develop after chemokine-induced is independent infiltration complete Freund's adjuvant (CFA)-induced, local inflammation. were by intraplantar injection CXC chemokine ligand 1 (CXCL1; keratinocyte-derived...

10.1189/jlb.0805452 article EN Journal of Leukocyte Biology 2006-03-07

In inflammation, pain is regulated by a balance of pro- and analgesic mediators. Analgesic mediators include opioid peptides which are secreted neutrophils at the site leading to activation receptors on peripheral sensory neurons. humans, local opioids significantly downregulate postoperative as well arthritic pain. rats, inflammatory induced intraplantar injection heat inactivated Mycobacterium butyricum, component complete Freund's adjuvant. We hypothesized that mycobacterially derived...

10.1371/journal.ppat.1000362 article EN cc-by PLoS Pathogens 2009-04-02
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