Julia Kilian, IRTG fellow from April 2015 - March 2016, defended her dissertation on "The influence of circadian rhythms on the development of experimental allergic asthma" successfully on June 07th, 2022.

Congratulations!!!

The academic research portal research.com presented its 2022 edition of top-ranked scientific-researchers from around the world in the field of Immunology. More than 6,300 scientist profiles have been examined with several indicators and metrics reviewed in order to consider each scientist’s inclusion in the ranking. In order to be considered for the ranking, the h-index threshold was set to 40 if most of the publications were in the field of immunology. The h-index was invented by J.E. Hirsch and is often used as a measure of a researcher's scientific quality and impact. Further, profiles and data from the scientific search engines Google Scholar and Microsoft Academic Graph were evaluated.

The aim of this ranking is to increase the visibility and transparency of the influential and innovative contributions of researchers around the world.

Jörg Köhl, Professor and Director of the Institute for Systemic Inflammation Research at the University of Lübeck was ranked #45 in Germany (out of 240 Professors from 35 German universities) with an h-factor of 74, >18,000 citations and 190 publications. Further, he ranked #887 in the world. The University of Lübeck was ranked #11 among all German universities in the field of Immunology.

Top Immunology Scientists – German Ranking

https://research.com/scientists-rankings/immunology/de

https://research.com/u/jorg-kohl

Top Immunology Universities – German Ranking

https://research.com/university-rankings/immunology/de

Perinatal inflammatory stress is associated with early life morbidity and lifelong consequences for pulmonary health. Chorioamnionitis, an inflammatory condition affecting the placenta and fluid surrounding the developing fetus, affects 25 to 40% of preterm births. Severe chorioamnionitis with preterm birth is associated with significantly increased risk of pulmonary disease and secondary infections in childhood, suggesting that fetal inflammation may markedly alter the development of the lung. Here, we used intra-amniotic lipopolysaccharide (LPS) challenge to induce experimental chorioamnionitis in a prenatal rhesus macaque (Macaca mulatta) model that mirrors structural and temporal aspects of human lung development. Inflammatory injury directly disrupted the developing gas exchange surface of the primate lung, with extensive damage to alveolar structure, particularly the close association and coordinated differentiation of alveolar type 1 pneumocytes and specialized alveolar capillary endothelium. Single-cell RNA sequencing analysis defined a multicellular alveolar signaling niche driving alveologenesis that was extensively disrupted by perinatal inflammation, leading to a loss of gas exchange surface and alveolar simplification, with notable resemblance to chronic lung disease in newborns. Blockade of the inflammatory cytokines interleukin-1β and tumor necrosis factor–α ameliorated LPS-induced inflammatory lung injury by blunting stromal responses to inflammation and modulating innate immune activation in myeloid cells, restoring structural integrity and key signaling networks in the developing alveolus. These data provide new insight into the pathophysiology of developmental lung injury and suggest that modulating inflammation is a promising therapeutic approach to prevent fetal consequences of chorioamnionitis. The publication is available here.

In tuberculosis (TB), protective inflammatory immune responses and the pathological sequelae of chronic inflammation significantly depend on a timely balance of cytokine expression. In contrast to other anti-inflammatory cytokines, interleukin (IL)-27 has fundamental effects in experimental Mycobacterium tuberculosis (Mtb) infection: the absence of IL-27-mediated signalling promotes a better control of mycobacterial growth on the one hand side but also leads to a chronic hyperinflammation and immunopathology later during infection. Hence, in the context of novel host-directed therapeutic approaches and vaccination strategies for the management of TB, the timely restricted blockade of IL-27 signalling may represent an advanced treatment option. In contrast, administration of IL-27 itself may allow to treat the immunopathological consequences of chronic TB. In both cases, a better knowledge of the cell typespecific and kinetic effects of IL-27 after Mtb infection is essential. This review summarizes IL-27-mediated mechanisms affecting protection and immunopathology in TB and discusses possible therapeutic applications. The publication is available here.

The complement system has evolved during the past 1.2 billion years, making it one of the oldest parts of the immune system. Since its discovery around 100 years ago, the system has been mainly associated with its role as a first line defense system and guardian of the vascular space. However, several findings published during the past few years suggest that this might be only a small facet of the multiple functions of the system and that we have explored at best the tip of the iceberg.

Recent reports rediscovered complement production within cells, now with a fresh look on activation of complement factors within cells demonstrating novel roles for complement in cell homeostasis, survival and differentiation. The well know mechanisms of canonical pathway activation in response to C1q, MBL or Ficolin sensing, followed by C3 and C5 cleavage through C3 and C5 convertases have been complemented by non-canonical mechanisms, leading to cleavage and activation of complement factors in the circulation and within immune cells. Moreover, it has been shown that the complement system exerts multiple and bidirectional interactions with other sensor and effector systems of innate immunity thereby regulating and controlling responses of both, innate and adaptive immunity. With this plethora of novel functions, playing critical roles in acute and chronic inflammatory diseases, several molecules of the system became attractive therapeutic targets, eventually getting into the spotlight of the pharmaceutical industry.

The July themed issue of the British Journal of Pharmacology highlights in 10 articles recent discoveries that add to the extended view of the complement system with a fresh look on the functions of intracellular complement, thrombosis, trauma, hypertonia, kidney disease and COVID-19.

Canonical and non-canonical functions of the complement system in health and disease, in Wenzel U., Kemper C., Köhl J. (editors). Br. J. Pharmacol. 2021 177 (14) 2749-2907.

Arthritis typically involves recurrence and progressive worsening at specific predilection sites, but the checkpoints between remission and persistence remain unknown. Here,we defined themolecular and cellular mechanisms of this inflammation-mediated tissue priming. Re-exposure to inflammatory stimuli caused aggravated arthritis in rodent models. Tissue priming developed locally and independently of adaptive immunity. Repeatedly stimulated primed synovial fibroblasts (SFs) exhibited enhanced metabolic activity inducing functional changes with intensifiedmigration, invasiveness and osteoclastogenesis.Meanwhile, human SF frompatients with established arthritis displayed a similar primed phenotype. Transcriptomic and epigenomic analyses as well as genetic and pharmacological targeting demonstrated that inflammatory tissue priming relies on intracellular
complement C3- and C3a receptor-activation and downstream mammalian target of rapamycin- and hypoxia-inducible factor 1a-mediatedmetabolic SF invigoration that prevents activation-induced senescence, enhances NLRP3 inflammasome activity, and in consequence sensitizes tissue for inflammation. Our study suggests possibilities for therapeutic intervention abrogating tissue priming without immunosuppression. The Publication is available here.