Neurodegenerative diseases associated with aging are often accompanied by cognitive decline and gut microbiota disorder. But the impact of gut microbiota on these cognitive disturbances remains incompletely understood. Short chain fatty acids (SCFAs) are major metabolites produced by gut microbiota during the digestion of dietary fiber, serving as an energy source for gut epithelial cells and/or circulating to other organs, such as the liver and brain, through the bloodstream. SCFAs have been shown to cross the blood-brain barrier and played crucial roles in brain metabolism, with potential implications in mediating Alzheimer's disease (AD) and Parkinson's disease (PD). However, the underlying mechanisms that SCFAs might influence psychological functioning, including affective and cognitive processes and their neural basis, have not been fully elucidated. Furthermore, the dietary sources which determine these SCFAs production was not thoroughly evaluated yet. This comprehensive review explores the production of SCFAs by gut microbiota, their transportation through the gut-brain axis, and the potential mechanisms by which they influence age-related neurodegenerative disorders. Also, the review discusses the importance of dietary fiber sources and the challenges associated with harnessing dietary-derived SCFAs as promoters of neurological health in elderly individuals. Overall, this study suggests that gut microbiota-derived SCFAs and/or dietary fibers hold promise as potential targets and strategies for addressing age-related neurodegenerative disorders.

Gut microbiota-derived short chain fatty acids act as mediators of the gut-brain axis targeting age-related neurodegenerative disorders: a narrative review.

Abstract Aedes aegypti (Linnaeus) are rapidly spreading across the globe. Evidence suggests that a Type I hypersensitivity reaction, characterized by IgE-mediated mast cell degranulation, may enhance the blood-feeding behavior of Ae. aegypti. Chymases, the mast cell-specific proteases, may play a critical role in this process. To investigate the role of mouse chymase mast cell protease-4 (mMCP-4) on mosquito blood feeding, we incubated bone marrow-derived mast cells with serum from mice sensitized by female Ae. aegypti bites and subsequently challenged the cells with salivary gland proteins (SGPs) from female mosquito. And the degradation of SGPs by mMCP-4 was assessed. Then, the MCP-4 deficient mice were sensitized twice by Ae. aegypti, the first bite on day 0 and the second on day 3. Throughout these experiments, we recorded the total blood meal duration, probing time, and blood feeding of the mosquitoes and analyzed the cutaneous microbiota. We discovered that serum from sensitized mice enhanced mast cell degranulation and chymase release. And mMCP-4 degraded some SGPs, in particular, potentially cleaving the blood-feeding-related salivary protein D7. Mcpt-4 deficiency resulted in prolonged blood-feeding duration during the second exposure, without affecting initial probing behavior. Moreover, Mcpt-4-deficient mice exhibited a reduced proportion of mosquitoes achieving rapid engorgement. Skin microbiome profiling revealed that Mcpt-4 deficiency attenuated the bite-induced expansion of potentially harmful bacterial taxa, including the dominant genus Corynebacterium (Mycobacteriales: Corynebacteriaceae). These findings identify mMCP-4 as a critical mediator of mosquito blood-feeding behavior and a modulator of skin microbial ecology in response to Ae. aegypti bites. 

Mouse chymase mast cell protease-4 facilitates blood feeding of Aedes aegypti (Diptera: Culicidae) mosquitoes

Mosquito allergy has been conceived as the cutaneous reactions that appears during and after mosquito biting process; a perception that is supported by several scientific research. Additional data have led to conceive that other manifestations of allergic responses may occur as a cause of the exposure to somatic mosquito allergens. Two main phenotypes of mosquito allergy are identifiable: the cutaneous allergic reactions, induced by salivary allergens, and other manifestations of the allergic responses such as asthma and allergic rhino conjunctivitis that are caused by somatic allergens. The cutaneous reactions have kept the focus of attention of the scientific community. It appears as skin lesions that resembles the phenotype of papular urticaria with a defined natural history of the disease. Although these two phenotypes of mosquito allergy seem to be well differentiated in terms of the allergens that are involved and the routes of exposures, other factors such as geographical distribution, may participate. Mosquitoes have adapted to the host immune response against bites, producing immunomodulatory molecules that counteract such defensive response. The role that the immunomodulatory molecules have on the allergic immune response has not been studied yet and it is still not known if affects all mosquito allergy phenotypes. Only a few studies of allergen specific immunotherapy for cutaneous allergic reactions induced by mosquito bites have been done, and none for respiratory allergic responses. The clinical practice focuses on symptom management and avoiding mosquito bites as much as possible. Avoiding mosquitoes, using different well described methods, is still the best option to limit contact with these insects. The lack of knowledge of mosquito allergy have raised several questions that affects the clinical management of this allergic disease, from its diagnosis, prevention and immunotherapy. 

Mosquito allergy: Immunological aspects and clinical management.

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pdf/interplay-between-innate-immune-cells-and-inflammatory-zt9dhtc2kqxp.pdf

Interplay between Innate Immune cells and Inflammatory Mediators in Dengue Infection: An Evolving Therapeutic paradigm

Neurological and psychiatric patients have increased dramatically in number in the past few decades. However, effective treatments for these diseases and disorders are limited due to heterogeneous and unclear pathogenic mechanisms. Therefore, further exploration of the biological aspects of the disease, and the identification of novel targets to develop alternative treatment strategies, is urgently required. Systems-level investigations have indicated the potential involvement of the brain–gut axis and intestinal microbiota in the pathogenesis and regulation of neurological and psychiatric disorders. While intestinal microbiota is crucial for maintaining host physiology, some important sensory and regulatory cells in the host should not be overlooked. Intestinal epithelial enteroendocrine cells (EECs) residing in the epithelium throughout intestine are the key regulators orchestrating the communication along the brain-gut-microbiota axis. On one hand, EECs sense changes in luminal microorganisms via microbial metabolites; on the other hand, they communicate with host body systems via neuroendocrine molecules. Therefore, EECs are believed to play important roles in neurological and psychiatric disorders. This review highlights the involvement of EECs and subtype cells, via secretion of endocrine molecules, in the development and regulation of neurological and psychiatric disorders, including Parkinson’s disease (PD), schizophrenia, visceral pain, neuropathic pain, and depression. Moreover, the current paper summarizes the potential mechanism of EECs in contributing to disease pathogenesis. Examination of these mechanisms may inspire and lead to the development of new aspects of treatment strategies for neurological and psychiatric disorders in the future.

/pdf/involvement-of-intestinal-enteroendocrine-cells-in-hhawjs8z.pdf

Involvement of Intestinal Enteroendocrine Cells in Neurological and Psychiatric Disorders

ABSTRACT Peptide YY (PYY) 3–36, the main circulatory form of PYY, plays important roles in gastrointestinal motility, secretion, and absorption. However, it is unknown whether PYY 3–36 has underlying functions in colitis. The Crohn’s disease (CD)-like mouse model in which CD is induced by trinitrobenzene sulfonic acid (TNBS) was established and utilized to investigate this potential role for PYY 3–36. The results showed that the expression of colonic mucosal PYY and PYY receptors Y1, Y2, Y4 were significantly increased in mice with TNBS-induced colitis. In vitro, PYY 3–36 remarkably inhibited the production of proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) from lipopolysaccharide (LPS)-induced macrophages. In vivo, a high concentration of PYY 3–36 robustly decreased the weight loss and death rate and attenuated the pathological colon tissue damage observed in mice with TNBS-induced colitis. Further studies uncovered that PYY 3–36 treatment reduced the levels of colon myeloperoxidase (MPO) and both colonic and systemic TNF-α and IL-6 observed in murine colitis. Furthermore, flow cytometric analysis showed PYY 3–36 altered the proportion of Th1/Th2 splenocytes in the disease model of colitis. Collectively, these results suggest that PYY 3–36 may be a promising candidate for the improvement of colitis, reflected by the attenuation of colon inflammatory responses observed in experimental murine colitis. Graphical Abstract

https://www.tandfonline.com/doi/pdf/10.1080/21655979.2022.2064147?needAccess=true

Peptide YY 3–36 attenuates trinitrobenzene sulfonic acid-induced colitis in mice by modulating Th1/Th2 differentiation

The deficiency of chymase mast cell protease 4 exacerbates dextran sulfate sodium salt-induced colitis in mice and is associated with altered microbiota and metabolome profiles

ABSTRACT When mosquitoes probe to feed blood, they inoculate a mixture of salivary molecules into vertebrate hosts’ skin causing acute inflammatory reactions where mast cell-derived mediators are involved. Mosquito saliva contains many proteins with largely unknown biological functions. Here, two Aedes albopictus salivary proteins – adenosine deaminase (alADA) and al34k2 – were investigated for their immunological impact on mast cells and two mast cell-specific proteases, the tryptase and the chymase. Mouse bone marrow-derived mast cells were challenged with increased concentrations of recombinant alADA or al34k2 for 1, 3, and 6 h, and to measure mast cell activation, the activity levels of β-hexosaminidase and tryptase and secretion of IL-6 were evaluated. In addition, a direct interaction between alADA or al34k2 with tryptase or chymase was investigated. Results show that bone marrow-derived mast cells challenged with 10 μg/ml of alADA secreted significant levels of β-hexosaminidase, tryptase, and IL-6. Furthermore, both al34k2 and alADA are cut by human tryptase and chymase. Interestingly, al34k2 dose-dependently enhance enzymatic activity of both tryptase and chymase. In contrast, while alADA enhances the enzymatic activity of tryptase, chymase activity was inhibited. Our finding suggests that alADA and al34k2 via interaction with mast cell-specific proteases tryptase and chymase modulate mast cell-driven immune response in the local skin microenvironment. alADA- and al34k2-mediated modulation of tryptase and chymase may also recruit more inflammatory cells and induce vascular leakage, which may contribute to the inflammatory responses at the mosquito bite site. GRAPHICAL ABSTRACT

https://www.tandfonline.com/doi/pdf/10.1080/21655979.2022.2081652?needAccess=true

Aedes albopictus salivary proteins adenosine deaminase and 34k2 interact with human mast cell specific proteases tryptase and chymase

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Peptide YY 3–36 attenuates trinitrobenzene sulfonic acid-induced colitis in mice by modulating Th1/Th2 differentiation

The deficiency of chymase mast cell protease 4 exacerbates dextran sulfate sodium salt-induced colitis in mice and is associated with altered microbiota and metabolome profiles

Aedes albopictus salivary proteins adenosine deaminase and 34k2 interact with human mast cell specific proteases tryptase and chymase