Our scientific focus is on the interaction between the brain or its pathologies and the immune system and how this can be influenced with the aim of treatment/neuroprotection. We are particularly concerned with:

1.  The identification of molecular biomarkers to assess the growth and rupture risk of unruptured intracranial aneurysms and to predict the clinical course of subarachnoid haemorrhage after aneurysm rupture, with our main focus on the development of vasospasm with associated delayed cerebral ischaemia (DCI) and brain injury.
2. The identification and testing of new immunomodulatory cellular and molecular therapeutic options aimed at reducing the growth and rupture risk of unruptured intracranial aneurysms and the treatment of complications of ruptured aneurysms, the latter being largely due to pathological inflammatory responses.

To this end, we have established both cellular and animal models in our laboratory, but are also increasingly working with intraoperatively obtained patient tissue and patient fluid samples. In this context, we have set up a biobank in Düsseldorf with liquid and solid tissue samples from patients with neurovascular diseases.

Our envisaged approach is fundamentally translational – by going from bench – to bedside and back, intending to translate our scientific findings into relevant clinical applications as quickly as possible. For the experimental investigation of these aspects, we utilise all current methods of cell and molecular biology and are also in the process of adapting methods for investigations at the single cell level.

1. Chaudhry SR, Kahlert UD, Kinfe TM, Endl E, Dolf A, Niemelä M,Daniel Hänggi D, Muhammad S. Differential polarization and activation dynamics of systemic T helper cell subsets after aneurysmal subarachnoid hemorrhage (SAH) and during post-SAH complications. Sci Rep. 2021 Jul 9;11(1):14226. doi: 10.1038/s41598-021-92873-x. PubMed

2. Muhammad S, Chaudhry SR, Kahlert UD, Lehecka M, Korja M, Mika Niemelä M, Hänggi D, Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review: Int J Mol Sci. 2020 Apr 14;21(8):2709. doi: 10.3390/ijms21082709. PubMed

3. Chaudhary SR, Kahlert UD, Kinfe TM, Lamprecht A, Niemelä M, Hänggi D, Muhammad S. Elevated systemic IL-10 is a sign of immunodepression leading to nosocomial infections after aneurysmal subarachnoidal hemorrhage. Int J Mol Sci. 2020 Feb 25;21(5):1569. doi: 10.3390/ijms21051569. PubMed

4. Chaudhry SR, Güresir A, Stoffel-Wagner B, Fimmers R, Kinfe TM, Dietrich D, Lamprecht A, Vatter H, Güresir E, Muhammad S. Systemic HMGB1, a novel predictive biomarker for cerebral vasospasm in aneurysmal Subarachnoid Hemorrhage. Crit Care Med.2018 Nov;46(11):e1023-e1028. doi: 10.1097/CCM.0000000000003319. PubMed

5. Chaudhry SR, Hafez A, Rezai Jahromi B, Kinfe TM, Lamprecht A, Niemelä M, Muhammad S. Role of Damage Associated Molecular Pattern Molecules (DAMPs) in Aneurysmal Subarachnoid Hemorrhage (aSAH). Int J Mol Sci. 2018 Jul 13;19(7):2035. doi: 10.3390/ijms19072035. PubMed

6. Chaudhry SR, Stoffel-Wagner B, Kinfe TM, Güresir E, Vatter H, Dietrich D, Lamprecht A, Muhammad S. Elevated Systemic IL-6 Levels in Patients with Aneurysmal Subarachnoid Hemorrhage Is an Unspecific Marker for Post-SAH Complications. Int J Mol Sci. 2017 Dec 1;18(12):2580. doi: 10.3390/ijms18122580. PubMed

7. Chaudhry SR, Güresir E, Vatter H, Kinfe TM, Dietrich D, Lamprecht A, Muhammad S. Aneurysmal subarachnoid hemorrhage lead to systemic upregulation of IL-23/IL-17 inflammatory axis. Cytokine. 2017 Sep;97:96-103. doi: 10.1016/j.cyto.2017.05.025. Epub 2017 Jun 10. PubMed

8. Rahman M*, Muhammad S*, Khan M*, Chen H, Ridder DA, Müller-Fielitz H, Pokorna B,  Vollbrandt T, Stötling I, Nadrowitz R, Okun JG, Offermanns S, Schwaninger M. The β-hydroxybutyrate receptor HCA2 induces a neuroprotective phenotype of macrophages. Nature. Commun; 2014 May 21;5:3944. doi: 10.1038/ncomms4944. (* Equally contributed) PubMed

9. Muhammad S, Haasbach E, Kotchourko M, Strigli A, Krenz A, Ridder DA, Vogel AB, Marti HH, Al-Abed Y, Planz O, Schwaninger M; Influenza virus infection aggravates stroke outcome through cytokine release. 2011 Mar;42(3):783-91. doi: 10.1161/STROKEAHA.110.596783. Epub 2011 Feb 3. PubMed

10. Muhammad S, Barakat W, Stoyanov S, Murikinati S, Yang H, Tracey KJ, Bendszus M, Rossetti G, Nawroth PP, Bierhaus A, Schwaninger M.; The HMGB1 receptor RAGE mediates ischemic brain damage. J Neurosci. 2008 Nov 12;28(46):12023-12031. doi: 10.1523/JNEUROSCI.2435-08.2008. PubMed