We report comprehensive X-ray diffraction and NMR studies of potassium-induced dimerization of heteroleptic triple-decker crown-phthalocyaninates [(15C5)4Pc]­M­(Pc)­M­(Pc) (1M, M = Y and Tb). Characterization of the crystalline dimer 2­(1Y)·4KBPh 4 ·12CH 3 CN·10CHCl 3 gave the first structural evidence of the formation of a six-decker structure with four rare earth metal ions perfectly aligned near the symmetry axis. NMR studies of soluble supramolecular dimers 2­(1M)·4KOAc provided a spectral–structural model that allowed us to assign the NMR spectra of related complexes with paramagnetic lanthanides and to further evaluate their structure and long-range interaction between the Ln­(III) centers in multinuclear tetrapyrrolic complexes. The obtained results are promising for elaboration of new supramolecular magnetic materials.

Herein we report single-crystal X-ray diffraction characterization and complementary solution studies of supramolecular interaction between potassium salts and heteroleptic homo- and heteronuclear triple-decker crown phthalocyaninates [(15C5)4Pc]­M*­[(15C5)4Pc]­M­(Pc) or [M*,M], where M* and M = Y and/or Tb. Our results evidence that, in contrast to the previously studied crown-substituted phthalocyanines, the interaction of K+ cations with [M*,M] does not induce their intermolecular aggregation. Instead, the cations reversibly intercalate between the crown-substituted phthalocyanine ligands, resulting in switching of the coordination polyhedron of the metal center M* from square-antiprismatic to square-prismatic. In the case of terbium­(III) complexes, such a switching alters their magnetic properties, which can be read-out by 1H NMR spectroscopy. For [Tb*,Y], such a switching causes an almost 25% increase in the axial component of the magnetic susceptibility tensor. Even though the polyhedron of the paramagnetic center in [Y*,Tb] is not switched, minor structural perturbations associated with the overall reorganization of the receptor also cause smaller, but nevertheless appreciable, growth of the axial anisotropy. The observed effects render the studied complexes as molecular switches with tunable magnetic properties.

The complex manifestations of COVID-19 are still not fully decoded on the molecular level. We combined quantitative the nuclear magnetic resonance (NMR) spectroscopy serum analysis of metabolites, lipoproteins and inflammation markers with clinical parameters and a targeted cytokine panel to characterize COVID-19 in a large (534 patient samples, 305 controls) outpatient cohort of recently tested PCR-positive patients. The COVID-19 cohort consisted of patients who were predominantly in the initial phase of the disease and mostly exhibited a milder disease course. Concerning the metabolic profiles of SARS-CoV-2-infected patients, we identified markers of oxidative stress and a severe dysregulation of energy metabolism. NMR markers, such as phenylalanine, inflammatory glycoproteins (Glyc) and their ratio with the previously reported supramolecular phospholipid composite (Glyc/SPC), showed a predictive power comparable to laboratory parameters such as C-reactive protein (CRP) or ferritin. We demonstrated interfaces between the metabolism and the immune system, e.g., we could trace an interleukin (IL-6)-induced transformation of a high-density lipoprotein (HDL) to a pro-inflammatory actor. Finally, we showed that metadata such as age, sex and constitution (e.g., body mass index, BMI) need to be considered when exploring new biomarkers and that adding NMR parameters to existing diagnoses expands the diagnostic toolbox for patient stratification and personalized medicine.

The SARS-CoV-2 virus is the causative agent of the global COVID-19 infectious disease outbreak, which can lead to acute respiratory distress syndrome (ARDS). However, it is still unclear how the virus interferes with immune cell and metabolic functions in the human body. In this study, we investigated the immune response in acute or convalescent COVID-19 patients. We characterized the peripheral blood mononuclear cells (PBMCs) using flow cytometry and found that CD8 þ T cells were significantly subsided in moderate COVID-19 and convalescent patients. Furthermore, characterization of CD8 þ T cells suggested that convalescent patients have significantly diminished expression of both perforin and granzyme A. Using 1 H-NMR spectroscopy, we characterized the metabolic status of their autologous PBMCs. We found that fructose, lactate and taurine levels were elevated in infected (mild and moderate) patients compared with control and convalescent patients. Glucose, glutamate, formate and acetate levels were attenuated in COVID-19 (mild and moderate) patients. In summary, our report suggests that SARS-CoV-2 infection leads to disrupted CD8 þ T cytotoxic functions and changes the overall metabolic functions of immune cells.