An ideal vaccine not only attenuates virus growth and disease in infected individuals but also reduces the spread of infections in the population, thereby generating herd immunity. While this strategy has proven successful by generating humoral immunity to measles, yellow fever and polio, many respiratory viruses evolve to evade pre-existing antibodies ¹. One approach for improving the breadth of antiviral immunity against escape variants is through the generation of memory T cells in the respiratory tract, which are positioned to rapidly respond to respiratory virus infections ^2-6. However, it is unknown whether memory T cells alone can effectively surveil the respiratory tract to an extent that they eliminate or greatly reduce viral transmission following exposure of an individual to infection. Here, we use a mouse model of natural parainfluenza virus transmission to quantify the extent to which memory CD8 T cells resident in the respiratory tract can provide herd immunity by reducing both the susceptibility of acquiring infection and the extent of transmission, even in the absence of virus-specific antibodies. We demonstrate that protection by resident memory CD8 T cells requires the antiviral cytokine IFN-γ and leads to altered transcriptional programming of epithelial cells within the respiratory tract. These results suggest that tissue-resident CD8 T cells in the respiratory tract can play important roles in both protecting the host against viral disease and in limiting viral spread throughout the population.

Indole-chalcone hybrids have burst into prominence as potent weapons in the battle against pain and inflammation due to their unique features, allowing these ligands to form pivotal interactions with biological targets. In this context, the base-catalyzed Claisen–Schmidt condensation of 3′,4′-(methylenedioxy)acetophenone with heteroaromatic aldehydes carrying an indole scaffold yielded new chalcones (1–7). The central and peripheral antinociceptive activities of all chalcones (compounds 1–7) at the dose of 10 mg/kg (i.p.) were evaluated by hot plate (supraspinal response), tail immersion (spinal response), and acetic acid-induced writhing tests in mice. The anti-inflammatory activities of compounds 1–7 were also investigated by means of a carrageenan-induced mouse paw edema model. The results revealed that compounds 1–7 extended the latency of response to thermal stimulus significantly in a hot-plate test similar to dipyrone (300 mg/kg; i.p.), the positive control drug. However, only compounds 2–7 were found to be significantly effective in the tail-immersion test. Compounds 1–7 also significantly showed analgesic effect by reducing the number of writhes and anti-inflammatory activity by inhibiting edema formation at different time intervals and levels. 1-(1,3-Benzodioxol-5-yl)-3-(1-methyl-1H-indol-2-yl)prop-2-en-1-one (4) drew attention by providing the highest efficacy results in both acute analgesia and inflammation models. Based on the in silico data acquired from the QikProp module, compound 4 was predicted to possess favorable oral bioavailability and drug-like properties. Taken together, it can be concluded that chalcones (1–7), especially compound 4, are outstanding candidates for further research to investigate their potential use in the management of pain and inflammation.

The gut–brain axis (GBA) refers to the biochemical bidirectional communication between the central nervous system (CNS) and the gastrointestinal tract, linking brain and gut functions. It comprises a complex network of interactions involving the endocrine, immune, autonomic, and enteric nervous systems. The balance of this bidirectional pathway depends on the composition of the gut microbiome and its metabolites. While the causes of neurodegenerative diseases (NDDs) vary, the gut microbiome plays a crucial role in their development and prognosis. NDDs are often associated with an inflammation-related gut microbiome. However, restoring balance to the gut microbiome and reducing inflammation may have therapeutic benefits. In particular, introducing short-chain fatty acid-producing bacteria, key metabolites that support gut homeostasis, can help counteract the inflammatory microbiome. This strong pathological link between the gut and NDDs underscores the gut–brain axis (GBA) as a promising target for therapeutic intervention. This review, by scrutinizing the more recent original research articles published in PubMed (MEDLINE) database, emphasizes the emerging notion that GBA is an equally important pathological marker for neurological movement disorders, particularly in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington’s disease and neurotraumatic disorders such as traumatic brain injury and spinal cord injury. Additionally, the GBA presents a promising therapeutic target for managing these diseases.

The term “inflammatory bowel disease” (IBD) describes a class of relapse-remitting conditions that affect the gastrointestinal (GI) tract. Among these, Crohn’s disease (CD) and ulcerative colitis (UC) are two of the most globally prevalent and debilitating conditions. Several articles have brought attention to the significant role that inflammation and oxidative stress cooperatively play in the development of IBD, offering a different viewpoint both on its etiopathogenesis and on strategies for the effective treatment of these conditions. Marine ecosystems may be a significant source of physiologically active substances, supporting the search for new potential clinical therapeutics. Based on this evidence, this review aims to comprehensively evaluate the activity of marine algae and deriving biomolecules in decreasing pathological features of CD and UC. To match this purpose, a deep search of the literature on PubMed (MEDLINE) and Google Scholar was performed to highlight primary biological mechanisms, the modulation of inflammatory and oxidative stress biochemical parameters, and potential clinical benefits deriving from marine species. From our findings, both macroalgae and microalgae have shown potential as therapeutic solutions for IBD due to their bioactive compounds and their anti-inflammatory and antioxidant activities which are capable of modulating markers such as cytokines, the NF-κB pathway, reactive oxidative and nitrosative species (ROS and RNS), trefoil factor 3 (TFF3), lactoferrin, SIRT1, etc. However, while we found promising preclinical evidence, more extensive and long-term clinical studies are necessary to establish the efficacy and safety of marine algae for IBD treatment.

Spinal cord injury (SCI) involves complex pathological processes that often result in significant and long-term neurological deficits. Increasingly, research has identified microRNA-21 (miR-21) as a pivotal regulator in SCI, with studies focusing on its roles in inflammation, apoptosis, and tissue repair. This review synthesizes current findings on miR-21’s involvement in post-injury molecular events, emphasizing its interactions with regulatory targets such as Phosphatase and Tensin Homolog (PTEN) and Programmed Cell Death Protein 4 (PDCD4), as well as its broader effects on inflammatory and apoptotic signaling pathways. Evidence from both in vitro and in vivo studies suggests that modulating miR-21 influences lesion size, cellular dynamics, and functional recovery, highlighting its potential as a therapeutic target for SCI. Nonetheless, the clinical translation of miR-21-based therapies poses significant challenges, including the need to optimize dosages, delivery mechanisms, and long-term safety profiles. Further research is crucial to fully delineate miR-21’s therapeutic potential and determine its feasibility for integration into SCI treatment protocols. This review aims to provide a comprehensive overview of miR-21’s roles in SCI pathology, offering insights into the molecular mechanisms underlying recovery and the emerging potential of miR-21 in SCI management to enhance outcomes and quality of life for affected patients.