Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Behavioral immune system”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2025

Mouse Testing Methods in Psychoneuroimmunology: Measuring Behavioral Responses.

The field of psychoneuroimmunology (PNI) aims to uncover the processes and consequences of nervous, immune, and endocrine system relationships. Behavior is a consequence of such interactions and manifests from a complex interweave of factors including immune-to-neural and neural-to-immune communication. Often the signaling molecules involved during a particular episode of neuroimmune activation are not known, but behavioral response provides evidence that bioactives such as neurotransmitters and cytokines are perturbed. Immunobehavioral phenotyping is a first-line approach when examining the neuroimmune system and its reaction to immune stimulation or suppression. Behavioral response is significantly more sensitive than direct measurement of a single specific bioactive and can quickly and efficiently rule in or out relevance of a particular immune challenge or therapeutic to neuroimmunity. Classically, immunobehavioral research was focused on sickness symptoms related to bacterial infection, but neuroimmune activation is now a recognized complication of diseases and disorders ranging from cancer to diabesity to Alzheimer's. Immunobehaviors include lethargy, loss of appetite, and disinterest in social activity/surrounding environment. In addition, neuroimmune activation can diminish physical activity, precipitate feelings of depression and anxiety, and impair cognitive and executive function. Provided is a detailed overview of behavioral tests frequently used to examine neuroimmune activation in mice with a special emphasis on pre-experimental conditions that can confound or prevent successful immunobehavioral experimentation.

Animals↗
PubMed2026

Disentangling host genetic variation for avoidance and resistance to pathogens.

BACKGROUND: Hosts can use avoidance (e.g., behavior) to reduce their contact rates with pathogens; after contact, they can use resistance (e.g., immunity) to reduce the establishment and proliferation of an infection. Because both defenses preserve host fitness and reduce pathogen fitness, we expect that their epidemiological and evolutionary effects will be interdependent. This study used a two-locus model to understand the evolution of allelic associations (i.e., linkage disequilibrium or LD) between genes determining levels of avoidance and resistance in the presence of an infectious disease or a parasite. RESULTS: We found that polymorphism in both avoidance and resistance was possible, but only for a limited range of parameter values. At equilibrium within these polymorphic populations, avoidance and resistance alleles were negatively associated (i.e., in negative LD). However, most commonly, polymorphism was only stably maintained at one defense locus, and the other locus became fixed for one allele. CONCLUSIONS: The model shows that avoidance and resistance are likely to influence each other's evolution because of their joint effects on infection and their costs; however, predictions about their relationship are not necessarily straightforward or intuitive. For example, avoidance and resistance may be more likely to covary across than within populations.

Animals↗
PubMed2026

Kmt2c and Kmt2d histone methyltransferase deficiencies compromise macrophage function.

Methylation of histone (H) 3 lysine (K) 4 (H3K4) has a well-established role in innate immune responses, but the contribution of H3K4 methyltransferases Kmt2c and Kmt2d in innate immunity is incompletely understood. Using conditional knockout mouse models, we investigated how Kmt2c- and Kmt2d-deficiencies affect innate immune cell function. Through functional, transcriptomic, and metabolic analyses, we delineate the consequences of disrupted epigenetic regulation on macrophage biology. Our findings reveal that loss of Kmt2c or Kmt2d in macrophages leads to impaired pro-inflammatory cytokine response and phagocytotic capacity, as well as skewed energy metabolism toward glycolysis, highlighting the critical role of H3K4 methylation-dependent chromatin regulation in shaping innate immune cell behavior. This study provides the first comprehensive characterization of innate immune system dysfunction in mouse models with conditional Kmt2c and Kmt2d deletions and offers mechanistic insight into how epigenetic regulators control fundamental immune processes.

Animals↗
PubMed2025

Innate immune sensing and signaling: Co-opted for genome surveillance? Implications for tumorigenesis.

Innate immune signaling is traditionally associated with the response to pathogenic infection. However, emerging evidence suggests that nuclear innate immune sensors and their downstream pathways may also serve as a critical mechanism for genome surveillance. This review explores a model in which DNA sensors such as mouse IFI204 and IFI205 (IFI16 in humans) localize to replication forks, where they detect endogenous aberrant DNA structures and initiate an interferon-stimulated gene (ISG) transcriptional program. A key output of this transcriptional program is ISG15, which we find conjugated to fork-associated proteins and facilitates recruitment of the replication fork protection complex, thereby stabilizing replication forks under physiological conditions. We discuss how nuclear innate immune sensors mediate replication stress sensing and examine the broad consequences of downstream ISG transcription across diverse contexts-including its impact on genome stability and its dual roles in modulating tumor cell behavior and the tumor microenvironment. These findings suggest that the innate immune system, through its nuclear DNA sensing arm, may be evolutionarily co-opted for genome surveillance and may influence tumor initiation and therapy resistance. Understanding how innate immune signaling intersects with replication stress could offer mechanistic insights into tumor development and reveal novel therapeutic targets.

Humans↗
PubMed1978

A multivariate analysis of the likelihood and volume of preventive visit demand in a prepaid group practice.

An economic framework for the investigation of the demand for preventive medical care services is suggested and empirical models for the likelihood and volume of preventive physician visits are specified. These are tested using data on 3,892 individuals enrolled in the Kaiser Foundation Prepaid Health Plan of Portland, Oregon. Preventive visits, delineated by the Kaiser Clinical Behavioral Classification System, included general medical examinations, eye examinations, well-child care and immunization services. Multiple regression is used to estimate the likelihood of preventive visits for all persons and the volume of preventive visits for users. Income and coinsurance were the most significant economic variables in the likelihood equation, possessing the expected positive and negative signs, respectively. The usual findings of a positive education effect and negative family size effect were supported by the results. The economic variables were less significant in the volume equations than in the likelihood equations, suggesting that system and physician effects may neutralize these factors. Females were more likely to make a preventive visit than were males and the relatively young and old were the heaviest age-group users of preventive care. Perceived helath status did not appear to significantly affect preventive care demand.

Adult↗
PubMed1975

Multiple sclerosis: some epidemiological clues to etiology.

The diagnosis of multiple sclerosis is frequently made with undue haste and without a firm basis. A false positive diagnosis is made in about 20 to 30% of the cases originally labeled as multiple sclerosis. The proportion of false positive diagnosis is probably still higher in countries where this disease is less frequent. An exhaustive investigation (neurological, clinical, neurorradiological, isotopic, etc.) is necessary before accepting such a diagnosis. This is particularly important because many of the lesions which can masquerade as multiple sclerosis are amenable to medical or surgical treatment. The prevalence of multiple sclerosis varies widely throughout the world, with a very definite preference for the white race. This difference seems to be caused, at least in part, by dietary habits. Lack of breastfeeding and excessive consumption of cow's milk during infancy is postulated as an important factor in the appearance of multiple sclerosis later in life. A lack of essential fatty acids (and may be of certain minerals and vitamins) in such a diet during pregnancy and childhood may result in the synthesis of abnormally unstable myelin. This underlying deficiency in myelin composition may be the substrate on which immunological factors act to produce the disease. The breakdown of this unstable myelin may be initiated by a variety of factors; natural decay of abnormally weak bonds in proteolipids, viral infection, immune reactions or even trauma. Immune reactions can explain, at least in part, the onset and the course of the disease, and probably immunodeficiency is the most important factor. Demyelination, once it starts, may continue until all abnormally formed myelin is destroyed, or until the building up of immunological defenses can stop the process. It follows from this that prevention of multiple sclerosis should be based mainly on dietic measures which ensure a sufficient supply of essential fatty acids, minerals and vitamins, during pregnancy and childhood. Breast feeding is probably the most important preventive factor. Skin pigmentation, either natural or from exposition to sunshine also seems to act as a preventive factor, and its mode of action deserves further investigation. Treatment of multiple sclerosis should be based on the improvement of immunological defenses, the elimination of possible allergens and saturated fats from the diet, and on the administration of sufficient amounts of essential fatty acids and of other various elements.

Adolescent↗
PubMed1976

Cell mediated immunity and the inflammatory system.

In this review we have considered the evidence for the existence of lymphokines and have focused on the specific mechanisms by which lymphokines modify the behavior of the various inflammatory cells. These mechanisms are based for the most part on in vitro observations. We have therefore discussed in detail data that document an in vivo role for various lymphokines. This evidence is based on experiments falling into two broad categories: the identification of lymphokines in tissue extracts and serum, and the demonstration of various biologic activities of exogenous lymphokines administered locally or systemically. The details of these kinds of experiments have been presented throughout the preceding discussion. The demonstration of lymphokines in vivo adds a new dimension to our ability to study human disease. The detection of migration inhibition factor in serum, for example, is technically simpler than studies of lymphocyte reactivity in patients with altered cellular immunity. Migration inhibition factor has already been found in the serum in several clinical settings, as described. The capacity of exogenous lymphokines for suppressing manifestations of delayed hypersensitivity may provide an explanation for the altered immunoreactivity often observed in some of those diseases. A final comment is in order regarding the significance of lymphokine production in the overall biologic scheme of things. In previous sections we noted that although activation of lymphocytes for lymphokine production by specific antigen is a property of T cells, B cells may be so activated nonspecifically by certain mitogens. Moreover, it has been shown that migration inhibition factor, or substances with similar biologic and physicochemical properties, may be found in certain replicating cultures of nonlymphoid cells. Also, we have recently shown that migration inhibitory activity, as well as certain other lymphokine-like activities such as macrophage and lymphocyte chemotaxis, may appear following the in vitro or in vivo infection of nonlymphoid as well as lymphoid cells by certain viruses. All these results suggest that lymphokine production, rather than "merely" representing an effector mechanism for cell mediated immunity and for certain kinds of helper functions in antibody synthesis, represents a general biologic phenomenon that may play a role in various aspects of host defense. Thus, such mediator substances should be more properly called "cytokines." Lymphokines represent a restricted set of cytokines made by one class of cells (lymphocytes) activated in certain unique ways. In this view the lmyphocyte has acquired some specialized means for triggering such production, not available to other cells.

Animals↗
PubMed2026

The role of HIL1 in strain-level adhesion and immune recognition in Debaryomyces hansenii.

UNLABELLED: Strains of food-derived microbes can become facultative pathogens in susceptible human hosts. Surprisingly, we previously isolated Debaryomyces hansenii, a yeast common in fermented foods, from Crohn disease (CD) ulcers, raising questions about its strain-specific traits that influence host interactions. Here, we further developed the genetic tractability of D. hansenii and identified a single adhesin, Hil1, as a major determinant of colony morphology, biofilm formation, and immune targeting in CD patients. We used Agrobacterium tumefaciens-mediated transformation to perform a forward genetic screen in a food-derived reference strain. We isolated mutants that converted from a wrinkled, biofilm-forming phenotype to a smooth, non-adherent phenotype characteristic of CD patient isolates. Mapping of multiple insertion sites showed a disrupted subtelomeric Hyr/Iff-like adhesin gene, herein referred to as HIL1. CRISPR-Cas9-mediated deletion of HIL1 recapitulated the mutant phenotype, demonstrating that HIL1 was necessary for biofilm formation and high cell-surface hydrophobicity phenotypes. To contextualize these findings, we performed comparative genomics on a D. hansenii strain collection to assess allelic variation in the number of HIL1 tandem repeats. Longer alleles in food strains correlated with increased biofilm formation, while CD-isolated strains contained shorter HIL1 alleles and reduced binding to surfaces. Serology profiling showed that HIL1 was a direct antigenic target of circulating immunoglobulin G (IgG) in CD patients. Together, these results suggest Hil1 is a key, strain-variable adhesin shaping fungal surface properties and host immune recognition. This work establishes D. hansenii as a genetically tractable system and shows how adhesin polymorphisms may influence fungal behavior in food and disease contexts. IMPORTANCE: Debaryomyces hansenii is a yeast that is common in food and is generally recognized as safe for human consumption, though recently it has been identified within diseased regions of the intestine in Crohn disease patients. A current need is to determine the genetic and phenotypic differences between safe food isolates and isolates from human Crohn disease patient ulcers. Here, we used a loss-of-function genetic screen and identified HIL1, an adhesin that we found mediates cellular adhesion in many food strains but not in patient strains. We identified circulating HIL1-reactive antibodies in patients with Crohn disease, indicating that food strains can be a target of host immune responses through Hil1.

Humans↗
PubMed1977

Virological and immunological studies in experimental SSPE.

Subacute sclerosing panencephalitis (SSPE) is a progressive, fatal inclusion cell encephalitis of children and adolescents caused by persistent measles virus within the central nervous system (CNS). Because studies in man have failed to elucidate the pathogenesis of this condition, animal studies are necessary. Persistent infection of the hamster CNS can be achieved with a hamster adapted SSPE agent. Animals inoculated intracerebrally with this virus raise antibodies to all known antigens of measles virus and some display clinical signs and pathological changes similar to those noted in human SSPE. Persistent CNS infection occurs only if the hamster is inoculated at a critical age (18 to 25 days of life) or if adults are given transient immunosuppression during acute infection. The biological behavior of the virus isolated from hamster CNS appears to change from a complete to a defective state coincidents with the appearance of serum antibodies to measles virus. Adult hamsters from whom the thymus was removed in the newborn period develop a subacute, uniformly fatal infection when exposed to the SSPE agent. These studies suggest that SSPE may develop in man when measles virus invades the immature CNS at a critical age or when the immune system is uncompletely developed or is inhibited. The finding that transient immunosuppression allows development of persistent CNS infection in adults suggest that immunological malfunction is the significant factor. Of interest, antibody appears to alter viral behavior to a defective, intracellular state thus enhancing viral survival in the host. Once a defective, CNS infection is achieved, lack of, or inhibition of the host cellular immunes response allows it to persist. Methods of therapy in light of these findings will be discussed.

Adolescent↗
PubMed1977

Toxicological properties of lead.

The pathological effects of lead on the renal, nervous, reproductive, endocrine, and immune systems have been reviewed. Emphasis is placed on reported subclinical effects due to chronic, low-level lead exposure. The crucial issue of whether subtle behavioral, intellectual, and developmental impairment occurs in young children, as a result of lead-induced CNS damage is discussed in detail. This issue remains unresolved. Further studies are needed in order to determine the long-term health effects of continuous, low-level lead exposure.

Adult↗
PubMed2026

Analysis of the dual role of amyloid-beta in Alzheimer's disease through multi-omics integration.

Accumulation of amyloid-beta is highly important in the development of Alzheimer's disease. Given the limitations of the amyloid cascade hypothesis and the repeated clinical failures of anti-amyloid-beta therapies, researchers are increasingly exploring the infection hypothesis. This review explores the dual behaviors of amyloid-beta in Alzheimer's disease, with a particular focus on its protective role against infection by microorganisms and its complicated connections with innate immune system. This new opinion holds that amyloid-beta can play an antimicrobial peptide role. During microbial invasion, its original role is to protect neural tissue, but prolonged accumulation leads to chronic deposition and involvement in pathological processes. Evidence from in vitro experiments, animal models, and clinical studies indicates that amyloid-beta may possess antiviral and antibacterial properties, particularly against infections such as herpes simplex virus, human immunodeficiency virus, and Porphyromonas gingivalis . However, excessive accumulation of amyloid beta triggers a neuroinflammatory cascade that impairs neuronal regeneration and cognitive function. Despite substantial research into Alzheimer's disease, current treatments have not yielded significant clinical benefits. Although monoclonal antibodies such as Aducanumab , Lecanemab , and Donanemab have been approved for marketing, their strict indications and high costs pose challenges for widespread promotion. The infection hypothesis of amyloid-beta has spurred clinical trials investigating vaccines targeting specific pathogens to assess their potential in preventing or treating Alzheimer's disease. This highlights the need for further exploring the multifaceted role of amyloid-beta in Alzheimer's disease. In addition, microbial infections can also trigger or regulate genetic and epigenetic factors, accelerating amyloid beta deposition. Among them, the apolipoprotein E epsilon 4 allele is the strongest genetic risk factor for Alzheimer's disease, as it exacerbates the accumulation of amyloid beta and promotes neuroinflammation. Strategies targeting epigenetic regulation may provide novel approaches to inhibit Alzheimer's disease pathology. This review also integrates various technologies such as genomics, proteomics, and metabolomics. This provides a broader system-level understanding of the risk gene loci, protein interaction networks, and metabolic changes associated with amyloid beta under the influence of microbial infections. Such techniques may lead to the identification of new molecular targets, the development of individualized treatment strategies, and the creation of early biomarkers for use in clinical research. In conclusion, this review suggests that amyloid-beta is not merely a pathological by-product but an environmentally responsive molecule with dual functions. A deeper understanding of the dynamic regulation of amyloid-beta, considering infection status and disease stage, can provide new directions for treatment strategies aimed at the prevention and treatment of Alzheimer's disease.

Herpesvirus 1↗