Thomas P. Kohler

ORCID: 0000-0002-0530-6813
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About
Contact & Profiles
Research Areas
  • Pneumonia and Respiratory Infections
  • Streptococcal Infections and Treatments
  • Bacterial Infections and Vaccines
  • Antimicrobial Resistance in Staphylococcus
  • Platelet Disorders and Treatments
  • Biochemical and Structural Characterization
  • Pneumocystis jirovecii pneumonia detection and treatment
  • Respiratory viral infections research
  • Bacterial biofilms and quorum sensing
  • Antimicrobial Peptides and Activities
  • Glycosylation and Glycoproteins Research
  • Immune Response and Inflammation
  • Antibiotic Resistance in Bacteria
  • Blood disorders and treatments
  • Neonatal and Maternal Infections
  • Influenza Virus Research Studies
  • Blood groups and transfusion
  • Complement system in diseases
  • Bacterial Genetics and Biotechnology
  • Helicobacter pylori-related gastroenterology studies
  • Erythrocyte Function and Pathophysiology
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Nanopore and Nanochannel Transport Studies
  • Inflammasome and immune disorders
  • T-cell and B-cell Immunology

Universität Greifswald
2016-2025

Institute of Ecology and Genetics of Microorganisms
2013

Institute of Medical Microbiology and Hygiene
2009-2010

University of Tübingen
2007-2010

Staphylococcal cell separation depends largely on the bifunctional autolysin Atl that is processed to amidase-R(1,2) and R(3)-glucosaminidase. These murein hydrolases are targeted via repeat domains (R) septal region of surface, thereby allowing localized peptidoglycan hydrolysis dividing cells. Here we show targeting amidase repeats based an exclusion strategy mediated by wall teichoic acid (WTA). In Staphylococcus aureus wild-type, externally applied (R(1,2)) or endogenously expressed were...

10.1111/j.1365-2958.2009.07007.x article EN Molecular Microbiology 2010-01-26

Summary Many Gram‐positive bacteria produce lipoteichoic acid (LTA) polymers whose physiological roles have remained a matter of debate because the lack LTA‐deficient mutants. The ypfP gene responsible for biosynthesis glycolipid found in LTA was deleted Staphylococcus aureus SA113, causing 87% reduction content. Mass spectrometry and nuclear magnetic resonance spectroscopy revealed that mutant contained diacylglycerol anchor instead glycolipid, whereas remaining part similar to wild‐type...

10.1111/j.1365-2958.2007.05854.x article EN other-oa Molecular Microbiology 2007-07-19

The human pathogen Staphylococcus aureus successfully colonizes its primary reservoir, the nasal cavity, most likely by regulatory adaptation to nose environment. Cotton rats represent an excellent model for study of bacterial gene expression in initial phases colonization. To gain insight into profile necessary establishment colonization, we performed direct transcript analysis quantitative real-time reverse-transcription polymerase chain reaction on cotton rat noses removed from euthanized...

10.1086/651619 article EN The Journal of Infectious Diseases 2010-03-22

ABSTRACT Skin-colonizing gram-positive bacteria produce wall teichoic acids (WTAs) or related glycopolymers for unclear reasons. Using a WTA-deficient Staphylococcus aureus mutant, we demonstrated that WTA confers resistance to antimicrobial fatty from human sebaceous glands by preventing acid binding. Thus, is probably important bacterial skin colonization.

10.1128/jb.00221-09 article EN Journal of Bacteriology 2009-05-09

Abstract Teichoic acid (TA), a crucial cell wall constituent of the pathobiont Streptococcus pneumoniae , is bound to peptidoglycan (wall teichoic acid, WTA) or membrane glycolipids (lipoteichoic LTA). Both TA polymers share common precursor synthesis pathway, but differ in final transfer chain either glycolipid. Here, we show that LTA exhibits different linkage conformation compared WTA, and identify TacL (previously known as RafX) putative lipoteichoic ligase required for assembly....

10.1038/s41467-017-01720-z article EN cc-by Nature Communications 2017-12-06

The capsular polysaccharide (CPS) of pathogenic bacteria is a critical virulence factor, often evading phagocytosis by host immune cells, while also interfering with the contact pathogen cells and contributing to biofilm formation. Klebsiella pneumoniae, Gram-negative human associated high antimicrobial resistances, produces 77 CPS serotypes. masks proteinaceous factors but protects K. pneumoniae from uptake phagocytic activation complement system. In addition nosocomial, urinary tract...

10.3389/fmicb.2025.1450984 article EN cc-by Frontiers in Microbiology 2025-02-06

ABSTRACT Dermcidin (DCD) is an antimicrobial peptide which constitutively expressed in eccrine sweat glands. By postsecretory proteolytic processing sweat, the DCD protein gives rise to anionic and cationic peptides with a broad spectrum of activity. Many induce membrane permeabilization as part their killing mechanism, accompanied by loss bacterial potential. In this study we show that there time-dependent bactericidal activity DCD-derived followed depolarization. However, do not pore...

10.1128/aac.01679-08 article EN Antimicrobial Agents and Chemotherapy 2009-04-14

Complement is a critical component of antimicrobial immunity. Various complement regulatory proteins prevent host cells from being attacked.

10.1128/iai.00742-18 article EN Infection and Immunity 2018-10-16

Streptococcus pneumoniae is endowed with a variety of surface-exposed proteins representing putative vaccine candidates. Lipoproteins are covalently anchored to the cell membrane and highly conserved among pneumococcal serotypes. Here, we evaluated these lipoproteins for their immunogenicity protective potential against colonisation. A multiplex-based immunoproteomics approach revealed selected lipoproteins. High antibody titres were measured in sera from mice immunised MetQ, PnrA, PsaA,...

10.3389/fimmu.2018.02405 article EN cc-by Frontiers in Immunology 2018-10-18

The human matricellular glycoprotein thrombospondin-1 (hTSP-1) is released by activated platelets and mediates adhesion of Gram-positive bacteria to various host cells. In staphylococci, the adhesins extracellular adherence protein (Eap) autolysin (Atl), both surface-exposed proteins containing repeating structures, were shown be involved in acquisition hTSP-1 bacterial surface. interaction partner(s) on pneumococcal surface was hitherto unknown. Here, we demonstrate for first time that...

10.1074/jbc.m114.623876 article EN cc-by Journal of Biological Chemistry 2015-04-21

Staphylococcus aureus can cause bloodstream infections associated with infective endocarditis (IE) and disseminated intravascular coagulopathy (DIC). Both complications involve platelets. In view of an increasing number antibiotic-resistant strains, new approaches to control systemic S. infection are gaining importance. Using a repertoire 52 recombinant proteins in flow cytometry-based platelet activation aggregation assays, we identified, addition the extracellular adherence protein Eap,...

10.1055/s-0038-1637735 article EN Thrombosis and Haemostasis 2018-03-19

Community-acquired pneumonia by primary or superinfections with Streptococcus pneumoniae can lead to acute respiratory distress requiring mechanical ventilation. The pore-forming toxin pneumolysin alters the alveolar-capillary barrier and causes extravasation of protein-rich fluid into interstitial pulmonary tissue, which impairs gas exchange. Platelets usually prevent endothelial leakage in inflamed tissue sealing inflammation-induced gaps. We not only confirm that S induces CD62P...

10.1182/bloodadvances.2020002372 article EN cc-by-nc-nd Blood Advances 2020-12-18

Toxins are key virulence determinants of pathogens and can impair the function host immune cells, including platelets. Insights into pathogen toxin interference with platelets will be pivotal to improve treatment patients bacterial bloodstream infections.In this study, we deciphered effects Staphylococcus aureus toxins α-hemolysin, LukAB, LukDE, LukSF on human compared pore forming pneumolysin Streptococcus pneumoniae. Activation loss platelet were investigated by flow cytometry,...

10.1111/jth.15703 article EN cc-by-nc-nd Journal of Thrombosis and Haemostasis 2022-03-18

The M protein of Streptococcus canis (SCM) is a virulence factor and serves as surface-associated receptor with particular affinity for mini-plasminogen, cleavage product the broad-spectrum serine protease plasmin. Here, we report that SCM has an additional high-affinity immunoglobulin G (IgG) binding activity. ability S. isolate to bind IgG significantly correlates scm-positive phenotype, suggesting dominant role receptor. Subsequent heterologous expression in non-IgG gordonii Western Blot...

10.3389/fcimb.2017.00080 article EN cc-by Frontiers in Cellular and Infection Microbiology 2017-03-28

Colonization of mucosal respiratory surfaces is a prerequisite for the human pathobiont Streptococcus pneumoniae (the pneumococcus) to cause severe invasive infections. The arsenal pneumococcal adhesins interacts with multitude extracellular matrix proteins. A paradigm pneumococci their interaction adhesive glycoprotein fibronectin, which facilitates bacterial adherence host cells. Here, we deciphered molecular between fibronectin and fibronectin-binding proteins (FnBPs) PavA PavB...

10.1111/mmi.13740 article EN Molecular Microbiology 2017-06-28

Secreted antimicrobial peptides (AMPs) are an important part of the human innate immune system and prevent local systemic infections by inhibiting bacterial growth in a concentration-dependent manner. In respiratory tract, cationic peptide LL-37 is one most abundant AMPs capable building pore complexes usually negatively charged membranes, leading to destruction bacteria. However, adaptation mechanisms several pathogens already described known weaken effect AMP, for instance, repulsion,...

10.3390/microorganisms8030413 article EN cc-by Microorganisms 2020-03-14

Heparin induced thrombocytopenia (HIT) is likely a misdirected bacterial host defense mechanism. Platelet factor 4 (PF4) binds to polyanions on surfaces exposing neo-epitopes which HIT antibodies bind. Platelets are activated by the resulting immune complexes via FcγRIIA, release bactericidal substances, and kill Gram-negative Escherichia coli.To assess role of PF4, anti-PF4/H FcγRIIa in killing Gram-positive bacteria platelets.Binding PF4 protein-A deficient Staphylococcus aureus...

10.1111/jth.14814 article EN cc-by-nc Journal of Thrombosis and Haemostasis 2020-04-01
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