Immunometabolic dysregulation at the interface of infectious and non-communicable diseases

Non-communicable diseases such as diabetes, obesity, and metabolic syndrome are rising globally, while infectious diseases, particularly bacterial pathogens like Mycobacterium tuberculosis, continue to pose a major public health burden. These overlapping epidemics create complex syndemic interactions, particularly in low- and middle-income countries. Metabolic disturbances can profoundly influence immune development, activation, and effector functions, thereby shaping host susceptibility to microbial infections and the outcomes of pathogen exposure. Despite extensive clinical observation, the molecular and cellular mechanisms by which metabolic dysfunction modifies host-microbe interactions remain incompletely understood. This Research Topic aims to focus on the molecular immunological pathways linking metabolic dysregulation to altered innate and adaptive immune responses during microbial infections, providing mechanistic insights into how metabolic states influence host defense.Immunometabolism, which examines the interplay between immune responses and cellular metabolic pathways, has emerged as a critical determinant of host-microbe interactions. Hyperglycemia, insulin resistance, chronic inflammation, and metabolic stress can remodel innate immune cell signaling, cytokine production, and pathogen sensing, thereby influencing infection outcomes. In tuberculosis, for example, diabetes is a strong risk factor for progression from latent infection to active disease, yet the innate and adaptive immune pathways that mediate this risk are not fully defined. Across microbial infections, integrating metabolic profiling with immune signaling studies—including cytokine networks, innate cell activation, and T cell functional responses—can elucidate how metabolic perturbations alter host-pathogen interactions. This approach is also relevant to HIV-related immunometabolic changes and to understanding immune responses during pregnancy, which involve substantial shifts in both host metabolism and immunity.This Research Topic seeks to assemble research that dissects how metabolic dysregulation shapes host-microbe interactions, including innate immune signaling, pathogen recognition, and downstream adaptive responses. Contributions may address, but are not limited to:-Innate and adaptive immune mechanisms affected by metabolic stress: macrophage function, inflammasome activation, T cell exhaustion, and regulatory T cell dynamics during infection.-Molecular interactions between microbial products and host sensors: effects of metabolic state on pattern recognition receptor signaling, cytokine responses, and pathogen sensing.-Immunometabolic pathways and molecular mechanisms: metabolic rewiring in immune cells, including mTOR, AMPK, HIF-1α signaling, glucose and lipid metabolism, and their impact on microbial immunity.-Translational approaches and therapeutic interventions: host-directed therapies or metabolic modulators that improve microbial clearance, restore immune function, or modulate inflammation.By integrating immune, metabolic, and molecular profiling, this Research Topic will advance understanding of how metabolic dysfunction influences host-microbe interactions, innate and adaptive immunity, and susceptibility to infectious diseases.We welcome original research articles, comprehensive reviews, and perspective pieces that provide mechanistic, systems-level, or translational insights into immunometabolic regulation during infection. Manuscripts integrating experimental, computational, or clinical approaches are particularly encouraged, as are studies linking fundamental immunometabolic mechanisms to therapeutic or translational applications. The topic editors declare no conflict of interest Topic editors: Hygon Mutavhatsindi, Muki Shey, Léanie Kleynhans, Maria Laura Gennaro Source: https://www.frontiersin.org/research-topics/77841/immunometabolic-dysregulation-at-the-interface-of-infectious-and-non-communicable-diseases