Thomas Tschernig

Universität des Saarlandes, Saarbrücken, Saarland, Germany

Are you Thomas Tschernig?

Claim your profile

Publications (237)716.33 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Phagocytosis activity of peripheral blood leukocytes in smokers or chronic obstructive pulmonary disease patients was found to be controversial and dependent on the phagocytic stimulus. We demonstrated that long-term exposure to cigarette smoke in mice clearly suppressed the phagocytosis of granulocytes and monocytes from peripheral blood. Impaired phagocytosis activity of peripheral blood leukocytes may have a systemic effect and potentially contribute to smoking-associated diseases such as pneumonia and lung cancer.
    BMC Research Notes 12/2015; 8(1). DOI:10.1186/s13104-015-1706-7
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Bacterial colonization and recurrent infections of the respiratory tract contribute to the progression of chronic obstructive pulmonary disease (COPD). There is evidence that exacerbations of COPD are provoked by new bacterial strains acquired from the environment. Using a murine model of colonization, we examined whether chronic exposure to cigarette smoke (CS) promotes nasopharyngeal colonization with typical lung pathogens and whether colonization is linked to inflammation in the respiratory tract. C57BL/6 N mice were chronically exposed to CS. The upper airways of mice were colonized with nontypeable Haemophilus influenzae (NTHi) or Streptococcus pneumoniae. Bacterial colonization was determined in the upper respiratory tract and lung tissue. Inflammatory cells and cytokines were determined in lavage fluids. RT-PCR was performed for inflammatory mediators. Chronic CS exposure resulted in significantly increased numbers of viable NTHi in the upper airways, whereas NTHi only marginally colonized air-exposed mice. Colonization with S. pneumoniae was enhanced in the upper respiratory tract of CS-exposed mice and was accompanied by increased translocation of S. pneumoniae into the lung. Bacterial colonization levels were associated with increased concentrations of inflammatory mediators and the number of immune cells in lavage fluids of the upper respiratory tract and the lung. Phagocytosis activity was reduced in whole blood granulocytes and monocytes of CS-exposed mice. These findings demonstrate that exposure to CS impacts the ability of the host to control bacterial colonization of the upper airways, resulting in enhanced inflammation and susceptibility of the host to pathogens migrating into the lung.
    Respiratory Research 12/2015; 16(1). DOI:10.1186/s12931-015-0204-8 · 3.09 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Conclusion: Our study illuminates a novel classification of the stromal/progenitor cell compartment in the liver and pinpoints a hitherto unrecognized injury-related alteration in progenitor subset composition in chronic liver inflammation and fibrosis.
    AJP Gastrointestinal and Liver Physiology 11/2015; DOI:10.1152/ajpgi.00344.2015 · 3.80 Impact Factor
  • Detlev Comberg · Axel Gauer · Thomas Tschernig ·

    World Journal of Urology 10/2015; DOI:10.1007/s00345-015-1717-y · 2.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Phagocytosis of bacteria is an important process during early host defence. It has been directly observed only ex vivo or in vitro. Here, we report on the observation of phagocytosis under in vivo conditions by using intravital microscopy in the murine lung. Suspensions of fluorescently labelled Streptococcus pneumoniae, Staphylococcus aureus and Pseudomonas aeruginosa cells were each instilled intratracheally to anaesthetized mice. After thoracotomy, the alveolar surface was observed for 30 min. Alveolar phagocytes exhibiting ingested bacteria could be detected and counted. The highest numbers were found after the infection with P. aeruginosa. By using intravital microscopy, cellular host defence could be observed in living mice lungs. The initial phagocytic reaction crucially depends on the species of applied bacteria invading the lung.
    Inflammation 10/2015; DOI:10.1007/s10753-015-0274-2 · 2.21 Impact Factor
  • Abdulrahman Raslan · Nadine Hainz · Anja Beckmann · Thomas Tschernig · Carola Meier ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Pannexin1 (Panx1) is one of three members of the pannexin protein family. The expression of Panx1 mRNA has been extensively investigated from late embryonic to adult stages. In contrast, expression during early embryonic development is largely unknown. Our aim is to examine the temporal and spatial expression of Panx1 in mouse embryonic development by focusing on embryonic days (E) 9.5 to 12.5. Whole embryos are investigated in order to provide a comprehensive survey. Analyses were performed at the mRNA level by using reverse transcription plus the polymerase chain reaction and whole-mount in situ hybridization. Panx1 mRNA was detected in the heads and bodies of embryos at all developmental stages investigated (E9.5, E10.5, E11.5, E12.5). In particular, the nervous system expressed Panx1 at an early time point. Interestingly, Panx1 expression was found in afferent ganglia of the cranial nerves and spinal cord. This finding is of particular interest in the context of neuropathic pain and other Panx1-related neurological disorders. Our study shows, for the first time, that Panx1 is expressed in the central and peripheral nervous system during early developmental stages. The consequences of Panx1 deficiency or inhibition in a number of experimental paradigms might therefore be predicated on changes during early development.
    Cell and Tissue Research 10/2015; DOI:10.1007/s00441-015-2294-5 · 3.57 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives: Our previous data demonstrated that allergic airway inflammation induces migration of dendritic cells (DC) into airway sensory jugular and nodose ganglia (jugular-nodose ganglion complex; JNC). Here we investigated the effects of steroid treatment regarding the expression and migration of DC and calcitonin gene-related peptide (CGRP)-immunoreactive neurons of vagal sensory ganglia during allergic airway inflammation. Methods: A house dust mite (HDM) model for allergic airway inflammation was used. The mice received 0.3 mg fluticasone propionate per kilogram of body weight in the last 9 days. JNC slices were analyzed on MHC II, the neuronal marker PGP9.5, and the neuropeptide CGRP. Results: Allergic airway inflammation increased the numbers of DC and CGRP-expressing neurons in the JNC significantly in comparison to the controls (DC/neurons: HDM 44.58 ± 1.6% vs. saline 33.29 ± 1.6%, p < 0.05; CGRP-positive neurons/total neurons: HDM 30.65 ± 1.9% vs. saline 19.49 ± 2.3%, p < 0.05). Steroid treatment did not have any effect on the numbers of DC and CGRP-expressing neurons in the JNC compared to HDM-treated mice. Conclusions: The present findings indicate an important role of DC and CGRP-containing neurons in the pathogenesis of allergic airway inflammation. However, steroid treatment did not have an effect on the population of DC and neurons displaying CGRP in the JNC, whereas steroid treatment was found to suppress allergic airway inflammation.
    NeuroImmunoModulation 10/2015; DOI:10.1159/000440622 · 1.88 Impact Factor
  • Anja Beckmann · Alexander Grissmer · Elmar Krause · Thomas Tschernig · Carola Meier ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Pannexins (Panx) are proteins with a similar membrane topology to connexins, the integral membrane protein of gap junctions. Panx1 channels are generally of major importance in a large number of system and cellular processes and their function has been thoroughly characterized. In contrast, little is known about channel structure and subcellular distribution. We therefore determine the subcellular localization of Panx1 channels in cultured cells and aim at the identification of channel morphology in vitro. Using freeze-fracture replica immunolabeling on EYFP-Panx1-overexpressing HEK 293 cells, large particles were identified in plasma membranes, which were immunogold-labeled using either GFP or Panx1 antibodies. There was no labeling or particles in the nuclear membranes of these cells, pointing to plasma membrane localization of Panx1-EYFP channels. The assembly of particles was irregular, this being in contrast to the regular pattern of gap junctions. The fact that no counterparts were identified on apposing cells, which would have been indicative of intercellular signaling, supported the idea of Panx1 channels within one membrane. Control cells (transfected with EYFP only, non-transfected) were devoid of both particles and immunogold labeling. Altogether, this study provides the first demonstration of Panx1 channel morphology and assembly in intact cells. The identification of Panx1 channels as large particles within the plasma membrane provides the knowledge required to enable recognition of Panx1 channels in tissues in future studies. Thus, these results open up new avenues for the detailed analysis of the subcellular localization of Panx1 and of its nearest neighbors such as purinergic receptors in vivo.
    Cell and Tissue Research 09/2015; DOI:10.1007/s00441-015-2281-x · 3.57 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pulmonary infection with influenza virus is frequently complicated by bacterial superinfection with Streptococcus pneumoniae being the most prevalent causal pathogen and hence, often associated with high morbidity and mortality rates. Local immunosuppression due to pulmonary influenza virus infection has been identified as a major cause in the pathogenesis of secondary bacterial lung infection. Thus, specific local stimulation of the pulmonary innate immune system in subjects with influenza infection might improve host defense against secondary bacterial pathogens. Here, we examined the effect of pulmonary immunostimulation with TLR-2 stimulating macrophage-activating lipopeptide-2 (MALP-2) in influenza A virus (IAV)-infected mice on the course of subsequent pneumococcal superinfection. Female C57BL/6N mice infected with IAV were treated with MALP-2 on day 5 and challenged with S. pneumoniae on day 6. Intratracheal MALP-2 application increased proinflammatory cytokine and chemokine release and enhanced recruitment of leukocytes, mainly neutrophils into the alveolar space of IAV-infected mice without detectable systemic side effects. Local pulmonary instillation of MALP-2 in IAV-infected mice 24 h before transnasal pneumococcal infection considerably reduced bacterial numbers in the lung tissue without inducing exaggerated inflammation. Pulmonary viral load was not altered by MALP-2. Clinically, MALP-2 treatment in IAV-infected mice increased survival rates and reduced hypothermia and body weight loss after pneumococcal superinfection compared with untreated co-infected mice. In conclusion, local immunostimulation with MALP-2 in influenza virus-infected mice improved pulmonary bacterial elimination and increased survival after subsequent pneumococcal superinfection.
    Infection and Immunity 09/2015; DOI:10.1128/IAI.00948-15 · 3.73 Impact Factor
  • Nadine Hainz · Sandra Wolf · Thomas Tschernig · Carola Meier ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. Neurological impairments are caused by axonal damage due to demyelination and neuroinflammation within the central nervous system. T cells mediate the neuroinflammation. The activation of T cells is induced by the release of adenosine triphosphate and involves purinergic receptors as well as pannexin (Panx) proteins. As Panx1 is expressed on T cells, we here propose that application of probenecid, a known Panx inhibitor, will prevent the onset of clinical symptoms in a mouse model of MS, the experimental autoimmune encephalomyelitis (EAE) model. EAE-induced mice received daily injections of probenecid. Disease scores, T cell numbers, and microglia activation were compared between experimental groups. Probenecid treatment resulted in lower disease scores as compared to EAE animals. Probenecid-treated animals also displayed fewer inflammatory lesions. Microglia activation was not altered by treatment. In conclusion, probenecid prevented the onset of EAE.
    Inflammation 08/2015; DOI:10.1007/s10753-015-0230-1 · 2.21 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Janus kinase (JAK) inhibitors have recently been developed for allergic diseases. We focused on the 2 different JAK inhibitors, tofacitinib (selective for JAK3) and oclacitinib (selective for JAK1 and 2), to clarify the mechanism of anti-inflammatory and anti-itching potency of these drugs. In the process of detecting anti-itching potency, we observed that tofacitinib treated mice showed aggression behaviour. The objective of the study reported here was to investigate the aggressive behaviour induced by tofacitinib by using a mouse model of allergic dermatitis and the resident-intruder test. For the allergic dermatitis model, female BALB/c mice were sensitized and challenged topically with toluene-2,4-diisocyanate (TDI). Vehicle, tofacitinib or oclacitinib, was administered orally 30min before TDI challenge. Scratching, aggression and standing behaviours were monitored in the 60min period immediately following challenge of TDI. Another group of male BALB/c mice treated with vehicle, tofacitinib or oclacitinib was evaluated in the resident-intruder test and brains were obtained to determine blood brain barrier penetration. In the allergic dermatitis model, a significant increase in aggression and standing behaviour was only obvious in the tofacitinib treatment group. There was no effect in non-sensitized mice, but similar aggression was also induced by tofacitinib in male resident-intruder test. Penetration of blood-brain barrier was observed both in tofacitinib and oclacitinib treated mice. These results suggest that aggression was induced by tofacitinib under some kind of stressful environment. This study indicates a possible role of the JAK-STAT pathway in modulation of aggression behaviour. Copyright © 2015. Published by Elsevier B.V.
    European journal of pharmacology 07/2015; 764. DOI:10.1016/j.ejphar.2015.06.060 · 2.53 Impact Factor
  • N.T. Veith · W. Knopp · A. Pizanis · T. Tschernig · T. Pohlemann · P. Mörsdorf ·

    Der Chirurg 05/2015; DOI:10.1007/s00104-015-0025-9 · 0.57 Impact Factor
  • B Wonnenberg · M Voss · A Honecker · M Bischoff · C Meier · T Tschernig · R Bals · C Beisswenger ·

    Pneumologie 04/2015; 69(04). DOI:10.1055/s-0035-1548642
  • Yulin Qi · Nadine Hainz · Thomas Tschernig · Carola Meier · Dietrich A Volmer ·
    [Show abstract] [Hide abstract]
    ABSTRACT: We demonstrate, by means of on-tissue mass spectrometry of tissue sections, that the drug probenecid can penetrate the blood-brain barrier. This method holds general promise for the detection and distribution of small molecule drugs within organ and tissue compartments.
    Cell and Tissue Research 03/2015; 360(2). DOI:10.1007/s00441-015-2153-4 · 3.57 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Asthma is the consequence of allergic inflammation in the lung compartments and lung-draining lymph nodes. Dendritic cells initiate and promote T cell response and drive it to immunity or allergy. However, their modes of action during asthma are poorly understood. In this study, an allergic inflammation with ovalbumin was induced in 38 mice versus 42 control animals. After ovalbumin aerosol challenge, conventional dendritic cells (CD11c/MHCII/CD8) were isolated from the lungs and the draining lymph nodes by means of magnetic cell sorting followed by fluorescence-activated cell sorting. A comparative transcriptional analysis was performed using gene arrays. In general, many transcripts are up- and downregulated in the CD8(-) dendritic cells of the allergic inflamed lung tissue, whereas few genes are regulated in CD8(+) dendritic cells. The dendritic cells of the lymph nodes also showed minor transcriptional changes. The data support the relevance of the CD8(-) conventional dendritic cells but do not exclude distinct functions of the small population of CD8(+) dendritic cells, such as cross presentation of external antigen. So far, this is the first approach performing gene arrays in dendritic cells obtained from lung tissue and lung-draining lymph nodes of asthmatic-like mice.
    International Journal of Genomics 02/2015; 2015:638032. DOI:10.1155/2015/638032 · 0.95 Impact Factor
  • Ebru Diler · Stephanie Saul · Ivan Bogeski · Carola Meier · Thomas Tschernig ·
    [Show abstract] [Hide abstract]
    ABSTRACT: The influence of extracellular calcium on phagocytosis is limited, and the involvement of extracellular magnesium is unclear. The role of extracellular calcium and magnesium on phagocytosis efficiency was investigated. Extracellular calcium had no influence on the internalization of 1 μm polystyrene particles by primary monocytes as has been shown before for the human lymphoma-derived, differentiated cell line U937 and murine alveolar macrophage-derived MH-S cells. In contrast, the phagocytosis by differentiated U937 cells was positively affected by the presence of extracellular magnesium whereas that of MH-S cells was not. An extracellular increase in the magnesium level did not cause an increase in the free cytosolic magnesium concentration in either cell line. In contrast to magnesium, extracellular calcium caused an increase in intracellular divalent cation levels in differentiated U937 cells. A phagocytosis-enhancing effect in the extracellular space was observed in relation to extracellular magnesium rather than with an intracellular increase in magnesium levels, indicating that murine and human immune cells might be regulated differently.
    Magnesium research: official organ of the International Society for the Development of Research on Magnesium 02/2015; 28(1):23-31. DOI:10.1684/mrh.2015.0378 · 0.77 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abundant microbial colonization is a hallmark of COPD and smoke exposure likely increases the susceptibility to colonization and infection. The aim of the present study was to characterize the pulmonary changes of a combined exposure to cigarette smoke (CS) and microbial challenge in a preclinical murine COPD model. Animals were exposed to CS for 2 weeks, 3, and 6 months. Low and high doses of heat inactivated nontypeable Haemophilus influenzae (NTHi) were administered by inhalation during the whole exposure time. Pulmonary changes were analyzed by stereology, pulmonary function tests, measurements of inflammatory cells and mediators, and histopathology.
    Experimental and Toxicologic Pathology 01/2015; 67(3). DOI:10.1016/j.etp.2015.01.002 · 1.86 Impact Factor
  • N T Veith · T Tschernig · B J Braun · T Pohlemann · G Aßmann ·
    [Show abstract] [Hide abstract]
    ABSTRACT: A 51-year-old female patient with history of longterm drug abusus, was admitted to our hospital with large, stocking-shaped areas of painful, non-displaceable confluent bruising reaching up to the groin. The emergency laboratory tests showed leucopenia, thrombocytopenia and anemia as well as a distinct protein C deficiency. Purpura fulminans was diagnosed and treated with an initial dose of protein C. The patient survived and the skin necrosis can be treated. Purpura fulminans is an internistic and dermatological emergency situation which can lead to shock through consumptive coagulopathy. The serious course of disease can be prevented by rapid treatment with protein C. © Georg Thieme Verlag KG Stuttgart · New York.
    DMW - Deutsche Medizinische Wochenschrift 12/2014; 139(50):2597-601. DOI:10.1055/s-0034-1387428 · 0.54 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Surfactant proteins (SP) secreted by alveolar type 2 cells, play an essential role in maintaining the air-liquid barrier of the lung and are also involved in the opsonisation and clearance of bacteria by phagocytes. We have recently described a novel surfactant protein, SP-H (SFTA3). Expression of SP-H was earlier demonstrated to be upregulated by LPS and negatively regulated by IL-1beta and IL-23 in vitro. The influence of SP-H on phagocytosis was measured using a murine and a human phagocytic cell line and fluorescent latex beads. SP-H markedly increases phagocytosis in vitro in the murine-derived alveolar macrophage cell lines MH-S and in human-derived differentiated U937 cells. It can be assumed that SP-H is involved in regulating phagocytic activity of macrophages. SP-H is a new player in pulmonary host defence.
    BMC Research Notes 11/2014; 7(1):851. DOI:10.1186/1756-0500-7-851
  • M.W. Laschke · V. Augustin · S. Kleer · T. Tschernig · M.D. Menger ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Porous polyethylene (Medpor(®)) is frequently used in craniofacial reconstructive surgery. Rapid vascularization of the biomaterial crucially contributes to its adequate incorporation without complications. Macrophage-activating lipopeptide-2 (MALP-2) is a toll-like receptor (TLR)-2/6 agonist with pro-angiogenic properties. Herein we analyzed, whether local single-shot application of MALP-2 improves the angiogenic host tissue response to Medpor(®). Medpor(®) (3 x 3 x 0.25mm) was implanted into dorsal skinfold chambers of BALB/c mice topically exposed to different MALP-2 doses (0.1μg and 0.5μg) or vehicle (control). The vascularization of the implants and the inflammatory foreign body reaction was analyzed using intravital fluorescence microscopy, histology and immunohistochemistry over 14 days. MALP-2 treatment dose-dependently improved the vascularization of Medpor(®), as indicated by a significantly higher functional microvessel density at the border and center of the implants when compared to controls. This was associated with a temporary increase of adherent leukocytes in host tissue venules during the first 3 days after implantation. At day 14, implants in MALP-2-treated chambers were surrounded by a granulation tissue, which exhibited a significantly higher density of CD31-positive microvessels and number of F4/80-positive macrophages when compared to controls. Additional biomaterial-free chambers did not show any signs of angiogenesis when treated with MALP-2. This indicates that locally applied MALP-2 effectively stimulates the early vascularization of Medpor(®) without inducing any local or systemic side effects. Accordingly, this easy approach may further improve the rapid incorporation of this biomaterial at the implantation site.
    Acta Biomaterialia 11/2014; 10(11). DOI:10.1016/j.actbio.2014.07.004 · 6.03 Impact Factor

Publication Stats

4k Citations
716.33 Total Impact Points


  • 2010-2015
    • Universität des Saarlandes
      • Institut für Medizinische Mikrobiologie und Hygiene
      Saarbrücken, Saarland, Germany
  • 1995-2011
    • Hannover Medical School
      • • Institute for Functional and Applied Anatomy
      • • Centre for Anatomy
      Hanover, Lower Saxony, Germany
  • 2006
    • VU University Amsterdam
      • Department of Molecular Cell Biology and Immunology
      Amsterdamo, North Holland, Netherlands
  • 2005-2006
    • Fraunhofer Institute for Toxicology and Experimental Medicine ITEM
      Hanover, Lower Saxony, Germany
  • 2002
    • University of Pittsburgh
      • Department of Environmental and Occupational Health
      Pittsburgh, Pennsylvania, United States
    • University Hospital Essen
      Essen, North Rhine-Westphalia, Germany
  • 1998
    • Technische Universität Dresden
      • Institut für Pathologie
      Dresden, Saxony, Germany