Brain-immune interactions generate pathogen-specific sickness states

Zuri A. Sullivan, Bertrand J. Wong, Vikrant Kapoor, Paula Kathleen Vincze, Harris S. Kaplan, Pia Giraudet, Brianna R. Watson, Adel Misherghi, Sebastian Lourido, Jeffrey R. Moffitt, Catherine Dulac
2025 · doi:10.64898/2025.12.06.692770
preprint OA: closed CC-BY-4.0
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The study examined how different types of immune challenges (inflammatory models representing bacterial, viral, allergic, parasitic, or colitis conditions) produce pathogen-specific sickness states by engaging distinct immune-to-brain pathways. Across scales—behavior and physiology, brain-wide neural activity, and single-cell in situ transcriptomics in hypothalamic areas linked to social and homeostatic functions—the authors found that each immune challenge generated a unique repertoire of changes. A major caveat is that the work relies on inflammatory model systems rather than a full range of pathogen exposures in natural infections, which the paper frames as a limitation of prior research based on few mouse models. Relevance to endometriosis: the paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract In nature, animals encounter diverse pathogens that trigger specific peripheral defense programs and elicit sickness behavior, a set of stereotyped physiological and behavioral changes thought to promote host fitness. Most studies to date have relied on one or a few mouse models of infection, limiting insights into pathogen-specific neuroimmune interactions that generate sickness. We hypothesized that different pathogens might elicit distinct sickness states by engaging different cell types and brain circuits. Using inflammatory models representing bacterial, viral, allergic, parasitic or colitis conditions, we assessed sickness across scales: organismal – behavior and physiology; cellular – brain-wide neural activity; and molecular – single-cell in situ transcriptomics in hypothalamus areas associated with social and homeostatic functions affected during sickness. Remarkably, immune challenges elicited unique repertoires of changes across all scales. Our findings reveal pathogen-specific sickness states encoded by the brain across scales, thereby broadening our understanding of how infections make us sick. Competing Interest Statement J.R.M. is an inventor of patents applied for by Harvard University and Boston Childrens Hospital related to MERFISH. J.R.M. is a co-founder and consultant of Vizgen, Inc. The other authors declare no conflict of interest.

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[{'doi': '10.13039/100000055', 'name': 'NIDCD', 'awards': ['R01NS112399']}, {'doi': None, 'name': 'K. Lisa Yang Center for Autism Research at Harvard University', 'awards': []}, {'doi': '10.13039/100000057', 'name': 'NIGMS', 'awards': ['R01GM143277']}, {'doi': None, 'name': 'NIH', 'awards': ['R01AI144369']}, {'doi': None, 'name': 'NIH', 'awards': ['R01AI158501']}, {'doi': '10.13039/100000861', 'name': 'Burroughs Wellcome Fund', 'awards': ['1021330']}, {'doi': None, 'name': 'Jane Coffin Childs Medical Research Awards', 'awards': ['61-1749']}, {'doi': None, 'name': None, 'awards': []}, {'doi': None, 'name': 'National Center for Advancing Translational Sciences, National Institutes of Health', 'awards': ['UL 1TR002541']}]

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License: CC-BY-4.0