The scale of insect consumption worldwide is staggering. More than 3,000 ethnic groups eat insects, and 2,205 species have been documented as food across 128 countries. In Africa alone, 464 edible species have been reported from 48 countries, with termites, caterpillars, crickets, and grasshoppers among the most widely consumed. Yet while insects deliver high-quality protein, lipids, vitamins, and minerals, the safety landscape surrounding them has remained surprisingly underexplored—particularly when they are incorporated into foods for the most vulnerable consumers: infants and young children.

To fill this gap, the research team analyzed 30 material types: 11 edible-insect products, seven food ingredients, seven insect-enriched formulations, and five commercial complementary flours. The insects included winged termites (Macrotermes subhyalinus), lake-flies (Chaoborus sp.), crickets (Gryllus bimaculatus and Scapsipedus icipe), desert locusts (Schistocerca gregaria), grasshoppers (Ruspolia differens), silkworm pupae (Bombyx mori), wild silk moth caterpillars (Anaphe panda), mopane worms (Gynanisa maja and Gonimbrasia belina), Bunaea alcinoe, and Gonimbrasia zambesina. Fungal isolation comprised 1,080 inoculated culture observations across three independent batches per material type, from which 798 fungal isolates were recovered and identified by culture, microscopy, and internal transcribed spacer (ITS) sequencing.

The results paint a striking picture of fungal prevalence. Aspergillus accounted for 70.7 percent of isolates recovered from insect products, followed by Penicillium at 18.6 percent and Fusarium at 7.4 percent. Penicillium was detected in all 11 insect products, while Fusarium appeared in eight of them. Across all material categories, Aspergillus dominated at 55.3 percent of the 798 recovered isolates, followed by Penicillium at 26.1 percent and Fusarium at 14.5 percent. The distribution of fungal genera differed significantly between material types, with Aspergillus predominating in insects, ingredients, and enriched formulations, while Penicillium was more common in commercial complementary flours.

Beyond mere presence, the researchers probed the toxigenic potential of the recovered fungi using endpoint PCR. Among 44 Aspergillus flavus-like morphotypes, the aflatoxin-biosynthesis genes aflD and aflQ were detected in 32 and 23 isolates, respectively. Among 22 Fusarium-like isolates, the fumonisin-biosynthesis gene FUM1 was detected in 19, and the VERTF intergenic-spacer profile associated with potentially fumonisin-producing Fusarium verticillioides strains appeared in 10. The authors are careful to note that marker detection does not establish gene expression or actual mycotoxin production—but it does provide biological context for the chemical findings that followed.

Using liquid chromatography–tandem mass spectrometry (LC–MS/MS), the team screened 23 mycotoxins in five complementary-food formulations—four insect-fortified and one non-insect control—over three months of storage at approximately 22 degrees Celsius. Six mycotoxins were confirmed: 3-acetyldeoxynivalenol, aflatoxin G1, sterigmatocystin, and fumonisins B1, B2, and B3. Only aflatoxin G1 and fumonisin B1 were quantified above their limits of quantification, at 4.20 µg/kg and 20.31–86.88 µg/kg, respectively. Quantifiable fumonisin B1 occurred more frequently at later storage points and peaked after three months, although the temporal pattern was not uniformly monotonic across formulations. The aflatoxin G1 point estimate fell below the Kenyan total-aflatoxin maximum for processed cereal-based foods for older infants and young children, and the European Union maize-based infant-food fumonisin value was used only as a contextual benchmark, since the formulations were grain-amaranth-based and contained no maize. Neither comparison established compliance or safety.

Notably, fumonisin B1 was detected in all five formulations, including the non-insect control, while the aflatoxin G1 and fumonisin B3 detections occurred only in the control formulation. The findings therefore do not support attribution of the detected mycotoxins specifically to the insect ingredients. Grain amaranth, common to all formulations, may have contributed to the widespread fumonisin occurrence, but the source cannot be assigned because individual ingredient batches were not analyzed separately for mycotoxins. This nuance underscores a broader challenge in multi-ingredient foods: contamination can flow from any component, and pinpointing origins requires ingredient-level surveillance.

The histamine and allergen-related findings add another layer of complexity. Histamine, which forms through microbial decarboxylation of histidine during inadequate handling or storage, is heat-stable and has caused poisoning outbreaks following insect consumption in Thailand. In this study, quantifiable histamine concentrations in 17 insect preparations ranged from 3,108 to 30,232 µg/kg, with the highest values recorded in raw and pan-fried lake flies (Chaoborus spp.). One oven-dried mopane worm preparation (Gonimbrasia belina) exceeded the assay’s upper quantitative limit and was reported as greater than 40,000 µg/kg. Three preparations fell below the assay’s lower limit of quantification. These values are descriptive rather than evidence of regulatory compliance, since no histamine limits currently exist for edible insects or insect-based complementary foods.

On the allergen front, lysozyme-reactive ELISA signals were below 25 µg/kg in all 17 insect preparations, suggesting minimal reactivity with hen’s-egg lysozyme antibodies. However, crustacean-reactive signals exceeded the assay’s upper quantification limit of 400 µg/kg in 16 of 17 preparations, with the remaining oven-dried Gonimbrasia belina result at 382 µg/kg. These signals represent analytical boundaries rather than health-based safety thresholds, and the reacting proteins were not identified. Tropomyosin and arginine kinase are among the arthropod proteins most frequently implicated in cross-reactivity between crustaceans and insects, and previous studies have demonstrated IgE recognition of cricket and grasshopper proteins by shrimp-allergic patients. The authors stress that the ELISA component was exploratory and that confirmation using multiple independently collected batches within each species and processing category is required before clinical conclusions can be drawn.

The study’s conclusions are clear: edible insects remain a promising, sustainable, and nutrient-rich food source, but their safety depends on species, rearing, processing, and storage. The findings support improved hygienic processing, ingredient control, routine fungal and mycotoxin surveillance, prompt post-harvest temperature control, and continued assessment of allergen-related cross-reactivity—particularly when insects are intended for incorporation into complementary foods for infants and young children. As insect-based nutrition scales up across Africa and beyond, this research provides a critical technical foundation for building safe, trustworthy value chains that can deliver on the promise of insects as food without compromising the health of the most vulnerable consumers.

Subject of Research: Fungal contamination, mycotoxins, histamine, and allergen-related immunoreactivity in edible insects and insect-fortified complementary foods

Article Title: Fungal contamination, mycotoxins, histamine, and allergen-related immunoreactivity in edible insects and insect-fortified complementary foods

Article References: Imbumi, M., Okoth, S., Audenaert, K., De Steur, H., Gellynck, X., Tanga, C. M., De Saeger, S., Kimiywe, J., & Raes, K. (2026). Fungal contamination, mycotoxins, histamine, and allergen-related immunoreactivity in edible insects and insect-fortified complementary foods. Frontiers in Fungal Biology, 7, Article 1798430. https://doi.org/10.3389/ffunb.2026.1798430

Image Credits: AI Generated

DOI: 10.3389/ffunb.2026.1798430

Keywords: edible insects, fungal contamination, mycotoxins, histamine, allergen cross-reactivity, complementary foods, food safety, Aspergillus, Fusarium, infant nutrition, Fungal, contamination

The article, written by Erika Bistran, M. Evelyn Carpenter and Daniel J. Sprague of the Medical University of South Carolina, focuses on bioaminergic signaling, the system of neurotransmitters that includes serotonin, dopamine, histamine, tyramine and octopamine. These molecules have been implicated in flatworm neuromuscular control for decades, but the authors contend that the field has been stuck cataloging which amines are present and which compounds make worms twitch. What is needed, they say, is mechanistic depth: knowing exactly which receptor detects the signal, which second messenger carries it inside the cell, which tissue hosts the signaling, and which parasite behavior changes when the pathway is disrupted.

To organize that effort, the researchers propose a pathway-to-phenotype framework built on six interconnected areas of investigation. These are the bioamine ligand itself, the receptor or transporter that detects or clears it, the downstream signaling pathway it engages, the cell type or tissue where signaling occurs, the experimental perturbation used to test function, and the resulting parasite phenotype. No single experiment needs to cover all six domains, the authors stress, but each experimentally supported connection between them raises the resolution of the pathway model, moving the field from association toward mechanism.

The clearest proof that this approach works is the serotonin receptor Sm5HTR in Schistosoma mansoni, the blood fluke responsible for schistosomiasis, a disease that afflicts hundreds of millions of people. Serotonin has long been known to excite schistosome movement and potentiate body wall muscle contraction. The characterization of Sm5HTR turned that observation into a complete molecular story. The receptor is a serotonin-responsive G protein-coupled receptor distantly related to human 5-HT7 receptors. When expressed in heterologous systems, it responds to serotonin by raising intracellular cAMP, consistent with a Gαs-coupled mechanism. Immunolocalization places it throughout the parasite nervous system, including the cerebral ganglia, the longitudinal nerve cords and the peripheral innervation of body wall muscle. Crucially, knocking the receptor down with RNA interference in larvae and adults causes marked hypoactivity and blunted responses to exogenous serotonin.

Sm5HTR has also proven pharmaceutically fruitful. Screening campaigns have identified novel agonists and antagonists, including parasite-selective inhibitor classes, and efforts have been made to distinguish schistosome-specific from human-specific ligands. For the authors, this makes Sm5HTR the benchmark against which every other aminergic system in flatworms should be judged: ligand, receptor, second messenger, anatomy, perturbation and phenotype all connected in one system.

Other aminergic pathways in schistosomes are promising but incomplete. Two dopamine-responsive GPCRs, SmD2 and SmGPR-3, are associated with the parasite neuromusculature, yet the full chain from receptor activation to parasite phenotype has not been closed. The dopamine system also delivers a cautionary lesson about assuming that parasite receptors behave like their mammalian counterparts. SmGPR-3 shows a mixed pharmacological profile in which a mammalian dopamine receptor antagonist acts as an agonist. SmD2, meanwhile, resembles human D2 receptors by sequence, but while the mammalian D2 family couples to inhibitory Gαi/o proteins, SmD2 appears to couple to Gαs instead. Such divergences are exactly what the authors argue could create parasite-selective drug targets.

Histamine adds a further twist: not all flatworm aminergic receptors converge on cAMP. A histamine-responsive receptor called SmGPR-1, expressed mainly in body wall muscles, is linked to intracellular calcium mobilization rather than cAMP accumulation, suggesting a Gαq-like pathway. This matters practically, because receptor screens built solely on cAMP readouts will miss or misclassify calcium-linked receptors. A second histamine receptor, SmGPR-2, is upregulated in schistosomula and expressed in the subtegumental nerve plexus, and it carries a striking molecular anomaly. The conserved aspartate residue at position 3.32 in transmembrane helix 3, a linchpin of ligand activation in most Class A GPCRs, is replaced by an asparagine, and many mammalian histamine antagonists are ineffective against it. Histamine is also conceptually intriguing because parasites may encounter it both as their own signal and as a host-derived inflammatory cue, raising the possibility that some aminergic pathways serve in host sensing rather than classical neurotransmission.

Octopamine and tyramine may offer the largest selectivity window of all, because these tyrosine-derived amines are prominent in invertebrate neuromodulation but peripheral to mammalian neurobiology. Anatomical, phenotypic and pharmacological evidence supports octopamine signaling in S. mansoni, and octopamine-related compounds alter schistosomulum motility and length. But no octopamine or tyramine receptor has yet been functionally profiled, leaving the field unable to say whether these signals travel through cAMP, calcium, inhibitory G proteins or biased pathways. Until the receptors are deorphanized and compared with host targets, the authors note, parasite selectivity remains a hypothesis rather than a fact.

The perspective also warns against a schistosome-centric view. Serotonin-responsive GPCRs have been cloned and characterized from tapeworms such as Echinococcus and Mesocestoides, including a set of 5-HT7-like receptors that stimulate cAMP production and a novel class of 5-HT1-like receptors deorphanized through a promiscuous Gα15 effector and calcium-flux assays. Serotonin boosts larval motility in cestodes, and receptor localization near the suckers of Echinococcus granulosus larvae hints that the same signaling may influence attachment as well as movement. In liver flukes, recent work in Fasciola hepatica has localized serotonin receptors and transporters and used RNAi to probe their function, while dopaminergic antagonists disrupt bile chemotaxis and egg production in the carcinogenic fluke Clonorchis sinensis, even though no aminergic receptor from that parasite has been cloned. Comparing these lineages, the authors argue, will reveal which signaling features are broadly conserved targets and which are lineage-specific opportunities.

Transporters form the underdeveloped half of the story. By clearing serotonin, dopamine and other amines from the extracellular space, transporters control signal duration and receptor desensitization, and inhibiting them could disrupt multiple receptor pathways at once. Candidate and characterized transporters exist in schistosomes, F. hepatica and C. sinensis, but their substrate specificity, inhibitor sensitivity, expression patterns and whole-parasite consequences remain poorly mapped. Any transporter-directed strategy will demand careful selectivity profiling, since host monoamine transporters are the pharmacologically sensitive targets of drugs such as antidepressants. Looking forward, the authors highlight three unresolved questions: what intracellular signaling machinery parasite receptors actually use outside heterologous systems, whether the worms are sensing their own neurotransmitters or host-derived chemical cues, and how aminergic pathways crosstalk with neuropeptidergic and cholinergic networks. The most promising future drug targets, they conclude, will combine functional importance, parasite-selective pharmacology and measurable whole-parasite consequences, and the Sm5HTR story provides the template for finding them.

Subject of Research: Bioaminergic GPCR signaling pathways and drug discovery in parasitic flatworms

Article Title: Bioaminergic signaling in parasitic flatworms: a perspective for linking GPCRs to behavior and drug discovery

Article References: Bistran, E., Carpenter, M. E., & Sprague, D. J. (2026). Bioaminergic signaling in parasitic flatworms: a perspective for linking GPCRs to behavior and drug discovery. Frontiers in Parasitology, 5, Article 1933406. https://doi.org/10.3389/fpara.2026.1933406

Image Credits: AI Generated

DOI: 10.3389/fpara.2026.1933406

Keywords: parasitic flatworms, schistosomiasis, G protein-coupled receptors, serotonin, dopamine, histamine, octopamine, neurotransmitter transporters, anthelmintics, drug discovery, Schistosoma mansoni, trematodes

The team turned to a well-established animal model in which mice are treated with β,β′-iminodipropionitrile, commonly abbreviated IDPN. This compound, when administered systemically, reliably produces stereotyped, repetitive movements in rodents that closely mirror the phenomenology of human tics. Researchers have used the IDPN model for decades to probe the basal ganglia circuits and neurotransmitter systems implicated in movement disorders, but the contribution of histaminergic signaling and neuroinflammation to the phenotype had not been fully characterized. The new work set out to fill that gap by measuring histamine dynamics, receptor expression, and microglial activation in the brains of IDPN-treated animals.

The first key finding concerned the hypothalamus, the brain region that contains the majority of the brain’s histamine-producing neurons. When the researchers quantified histamine levels and H1 receptor expression in this region, they found that both were significantly reduced in IDPN-treated mice compared with controls. This depletion of the central histaminergic tone is notable because histamine released from the tuberomammillary nucleus of the hypothalamus projects widely across the brain, influencing arousal, motor control, and immune signaling. A deficit in this system, the authors suggest, could plausibly disturb the circuit balance that governs the initiation and suppression of movements, creating conditions favorable to the emergence of tic-like stereotypies.

To test whether the loss of H1 receptor signaling is not merely a correlate but a potential driver of the behavior, the investigators administered diphenhydramine, a classic first-generation antihistamine that readily crosses the blood-brain barrier and blocks the H1 receptor. When wild-type mice, animals with no prior IDPN exposure, received intraperitoneal injections of diphenhydramine, they began to display tic-like stereotyped behaviors of their own. This pharmacological mimicry is a striking result: simply silencing H1 receptor signaling in otherwise healthy brains was sufficient to elicit a behavioral phenotype resembling that produced by IDPN. The observation aligns with clinical reports that have associated exposure to H1 receptor antagonists with increased risk and severity of tic disorders in children, lending translational weight to the animal data.

The second half of the study shifted focus to the striatum, a key component of the basal ganglia motor circuitry and a region long implicated in tic pathophysiology. In the IDPN-treated mice, the researchers observed increased immunoreactivity for Iba-1, a calcium-binding protein expressed specifically in microglia and macrophages that serves as a standard marker of microglial activation. Elevated Iba-1 staining indicates that the resident immune cells of the striatum had shifted into a reactive state, a phenomenon often associated with neuroinflammatory processes. Because microglia are the central phagocytic and immune-surveying cells of the central nervous system, their reactivity can influence synaptic pruning, neuronal excitability, and circuit function, all of which are plausible mechanistic links to abnormal movement patterns.

Having established that microglial reactivity accompanies the tic-like phenotype, the team then asked whether boosting histamine signaling in the striatum could reverse it. They performed intrastriatal injections of histamine directly into the brains of IDPN-treated mice. The result was twofold: the animals showed a reduction in their stereotyped behaviors, and the heightened Iba-1 immunoreactivity in the striatum was attenuated. In other words, replenishing histamine locally appeared to calm both the behavior and the immune activation simultaneously. This parallel effect strengthens the hypothesis that the behavioral and neuroimmune changes are mechanistically connected rather than independent byproducts of the IDPN treatment.

Crucially, the protective effect of histamine was not absolute. When the mice were pretreated with diphenhydramine before receiving the intrastriatal histamine, both the behavioral improvement and the reduction in microglial reactivity were blunted. This antagonist-attenuation experiment provides the strongest causal inference available within the study’s design: the benefits of histamine appear to depend on intact H1 receptor signaling, since blocking the receptor abolished the effect. Taken together, the data sketch a coherent pathway in which histamine acts through H1 receptors to restrain microglial reactivity in the striatum, and disruption of this signaling, whether by IDPN-induced depletion or by pharmacological antagonism, promotes tic-like stereotypies.

The authors are careful to frame their conclusions with appropriate scientific caution. Because the study relied on a pharmacological antagonist approach rather than genetic manipulation of the H1 receptor, and because it did not include microglia-specific interventions such as conditional knockout or depletion strategies, the findings should be interpreted as hypothesis-generating rather than definitive proof of mechanism. Diphenhydramine has pharmacological actions beyond H1 receptor blockade, including anticholinergic effects, and systemic administration cannot exclude contributions from peripheral immune signaling. Nonetheless, the convergence of multiple lines of evidence, reduced hypothalamic histamine and H1R in the model, induction of tic-like behavior by antagonist in wild-type animals, and rescue of both behavior and microglial activation by striatal histamine that is reversed by antagonist pretreatment, forms a compelling pattern.

The clinical implications are intriguing but require careful handling. Antihistamines are among the most widely used medications in pediatric populations, found in allergy remedies, cold preparations, and sleep aids. If H1 receptor blockade indeed exacerbates tic vulnerability, as both this animal work and prior clinical associations suggest, it may prompt clinicians to weigh tic risk more deliberately when prescribing brain-penetrant first-generation antihistamines to children, particularly those with a family history or early signs of tic disorders. Conversely, strategies that enhance central histaminergic tone or support H1 receptor signaling could represent a novel therapeutic direction, though any such approach would need to navigate histamine’s broad involvement in sleep, appetite, cognition, and other physiological functions.

Beyond tics, the study contributes to a rapidly growing appreciation of neuroimmunology in developmental neuropsychiatric conditions. Microglial reactivity has been implicated in conditions ranging from autism spectrum disorder to obsessive-compulsive disorder, conditions that share phenomenological and neurobiological overlap with tic disorders. The idea that a classical neurotransmitter system like histamine can serve as a modulatory bridge between neuronal circuits and glial immune responses opens a conceptual avenue that extends well beyond a single disease. The work was supported by the Joint Funds for the Innovation of Science and Technology of Fujian Province and the Fujian Provincial Natural Science Foundation of China, and all animal experiments were approved by the Experimental Animal Ethics Committee of Fujian Medical University. As the field moves forward, genetic models and microglia-specific tools will be essential to confirm whether the histamine-H1R-microglia axis can be safely and effectively targeted to help patients whose lives are disrupted by persistent tics.

Subject of Research: Histamine-H1 receptor regulation of microglial reactivity in an IDPN-induced mouse model of tic-like behaviors

Article Title: Histamine and H1R regulate microglia in an IDPN-Induced Mouse Model of Tic-like behaviors

Article References: Lin, D., Tang, Y., Li, Q., Lu, Y., Xie, J., & Liu, X. (2026). Histamine and H1R regulate microglia in an IDPN-Induced Mouse Model of Tic-like behaviors. BMC Neuroscience. https://doi.org/10.1186/s12868-026-01039-w

Image Credits: AI Generated

DOI: 10.1186/s12868-026-01039-w

Keywords: tic disorder, histamine, H1 receptor, microglia, IDPN, diphenhydramine, neuroinflammation, striatum, basal ganglia, hypothalamus, neuroimmunology, movement disorders