Sepsis rewires host metabolism, and these changes may be readable in the volatile organic compounds (VOCs) released from the body. Whether whole-body VOC profiles can be mapped onto specific disrupted biochemical pathways has not been tested. In this discovery-phase, single-time-point feasibility study, polymicrobial sepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice (14 CLP, 10 sham controls). Whole-body headspace gases were collected 12 h after surgery and analysed by thermal desorption-gas chromatography-mass spectrometry. After preprocessing, 113 features were tested univariately with Benjamini-Hochberg correction and by orthogonal partial least squares discriminant analysis (OPLS-DA). Candidate VOCs (FDR < 0.1, |log2FC| > 0.26, VIP > 1.0) were annotated against PubChem, KEGG COMPOUND, and the Human Metabolome Database. OPLS-DA separated the groups (R2X = 0.489, R2Y = 0.981, Q2 = 0.777; P = 0.001 by 1,000 permutations), and leave-one-out cross-validation classified 95.8% of animals correctly, though n = 24. Of 54 candidate VOCs, 18 had established endogenous origins; 16 fell and 2 rose in septic mice. Pathway mapping indicated four perturbed domains: lipid peroxidation (12 depleted VOCs), ketone body metabolism (3 decreased), cholesterol/isoprenoid metabolism (isoprene, decreased), and putative gut microbiota-associated metabolism (toluene and carbon disulfide, increased). All 18 endogenous VOCs kept candidate status after environment-derived VOCs were removed. Because whole-body headspace volatiles superimpose tissue metabolism, ventilation, activity, and background, these results suggest the septic volatilome may be mapped onto distinct pathway perturbations; ventilation and activity effects cannot be excluded. These findings generate testable hypotheses for non-invasive metabolic phenotyping in sepsis.

Hemin released from erythrocytes activates platelets through both receptor-dependent and receptor-independent mechanisms. While lower hemin concentrations predominantly activate the immune receptor tyrosine-based activation motif (ITAM) signaling via glycoprotein VI (GPVI) and C-type lectin-like receptor 2 (CLEC-2), higher concentrations induce pronounced receptor-independent cellular alterations, including loss of mitochondrial membrane potential, generation of reactive oxygen species (ROS), lipid peroxidation, and plasma membrane fragmentation. However, the mechanism of receptor-independent effect of hemin is still unclear. To test whether hemin can directly interact with and remodel membranes, we employed giant unilamellar vesicles composed of different lipid compositions as model membrane systems and treated them with unlabeled and fluorescently-labeled hemin. We analyzed how hemin treatment alters membrane biophysical properties using fluorescence microscopy, spectral imaging, fluorescence correlation spectroscopy (FCS), and flow cytometry. We found that fluorophore-labeled hemin can be directly visualized in lipid bilayers. Furthermore, high concentrations of hemin increased membrane order in all lipid compositions tested. The strongest effect was observed in more fluid membranes, whereas highly ordered membranes were less affected. Interestingly, in cholesterol-containing membranes, even the lowest hemin concentration produced changes comparable to those induced by the highest concentration, suggesting that cholesterol enhances the influence of hemin on lipid bilayers. Finally, we observed strong increase in permeability of membranes upon hemin treatment. Overall, our findings demonstrate that hemin can directly accumulate in lipid membranes, increase membrane order, reduce membrane fluidity and alter membrane integrity, resulting in enhanced membrane permeability.

Background: Anxiety and obsessive-compulsive disorders can co-occur with disordered eating behaviors and difficulties in emotional regulation. This article presents the clinical case of a 21-year-old female student whose complex neuropsychiatric profile required the simultaneous consideration of psychological, psychosocial, and somatic factors. The aim of this case report was to examine the coexistence of psychopathological symptoms, eating disturbances, psychosocial experiences, and somatic findings, while considering the potential role of post-infectious factors. Methods: A retrospective analysis of the patient's medical and psychiatric history was conducted, including childhood infections, psychiatric diagnoses, psychosocial experiences, eating behaviors, and available laboratory findings. The assessment also included quantitative electroencephalography (QEEG) brain mapping performed under eyes-open and eyes-closed conditions. Particular attention was given to the retrospective hypothesis of PANDAS/PANS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections/Pediatric Acute-onset Neuropsychiatric Syndrome), while distinguishing documented clinical findings from unconfirmed etiopathogenetic hypotheses. Results: Retrospective history revealed recurrent upper respiratory tract infections and bilateral pneumonia in early childhood, followed by increasing anxiety and social withdrawal from peers. The patient was diagnosed with obsessive-compulsive disorder (OCD) at the age of 13, while psychiatric records from 2023 also documented depressive disorders and social phobia. Within the family system, the patient experienced relational trauma, including systematic verbal and psychological abuse by her father. Blood tests performed on 11 June 2025 revealed an elevated antistreptolysin O (ASO) level of 436 IU/mL, which may indicate previous streptococcal exposure but does not confirm active infection, PANDAS/PANS, or a causal relationship with neuropsychiatric symptoms. The available documentation lacked microbiological confirmation of streptococcal infections or evidence substantiating a PANDAS/PANS diagnosis. QEEG brain mapping revealed elevated fast HiBeta activity in the frontal regions under both recording conditions; however, incomplete methodological documentation precluded definitive interpretation of this finding as evidence of persistent cortical overactivity or specific cognitive deficits. Somatic and metabolic findings included morning cortisol of 7.7 µg/dL, dehydroepiandrosterone sulfate (DHEA-SO4) of 163 µg/dL, prolactin of 513.0 mIU/L, and total cholesterol of 138 mg/dL. A previously recorded glycemic value of 45 mg/dL was also noted, although insufficient information was available to confirm reactive hypoglycemia. The patient reported a dichotomous eating pattern characterized by appetite suppression during acute stress, followed by episodes of increased food intake aimed at regulating emotional tension. However, the absence of standardized assessment prevented confirmation of formal binge-eating episodes. Food avoidance and restriction were associated with contamination fears and obsessive-compulsive rituals. The patient also expressed marked body image dissatisfaction and a desire for an extremely thin physique, although no formal diagnosis of body dysmorphic disorder was documented. Conclusions: This case highlights the complex coexistence of obsessive-compulsive and anxiety symptoms, disordered eating behaviors, psychosocial trauma, and somatic findings. Although retrospective clinical history and elevated ASO levels raise the possibility of a post-infectious contribution, the available evidence does not establish an autoimmune mechanism or confirm PANDAS/PANS. The findings emphasize the importance of distinguishing documented clinical observations from etiopathogenetic hypotheses and support an interdisciplinary approach integrating psychiatric care, psychotherapy, nutritional assessment, and appropriate somatic diagnostics.