Recent Advances in Inflammation & Allergy Drug Discovery - Current Issue

The landscape of wound management has undergone a revolutionary transformation with the integration of nanomaterials-based therapeutics. This abstract explores the profound impact of nanotechnology on wound care, highlighting the unique properties of nanomaterials and their role in advancing therapeutic interventions. Nanomaterials, characterized by their dimensions at the nanoscale, have emerged as versatile tools in wound management. The review focuses on various types of nanomaterials, including nanoparticles, nanofibers, and nanocomposites, which offer tailored solutions for optimizing wound healing processes to facilitate controlled drug delivery, developing a novel approach on account of achieving controlled transport of bioactive agents, such as growth factors, antimicrobial compounds, and anti-inflammatory drugs. This precision in drug delivery enhances therapeutic efficacy, promoting optimal wound healing outcomes. One of the pivotal contributions of nanomaterials to wound management is their engineered antimicrobial properties. Nanoparticles also exhibit effective antibacterial characteristics, addressing concerns related to wound infections. Nanomaterials integrated into dressings and scaffolds enhance mechanical strength and provide a conducive environment for cellular processes, fostering tissue regeneration, angiogenesis, and extracellular matrix synthesis. Nanoparticles with anti-inflammatory and antioxidant functionalities create a balanced microenvironment, reduce chronic inflammation, and promote a pro-regenerative milieu. In conclusion, integrating nanomaterials into wound management strategies represents a paradigm shift in therapeutic approaches.

The Toll-like Receptors (TLRs) family has significantly enhanced the understanding of innate immune responses by identifying and responding to various microbes or host-derived organisms. TLRs contribute to these responses by increasing the levels of cytokines, interleukins, and other inflammatory mediators through multiple pathways. Located both intracellularly and on the surface of various cells and tissues, including vascular smooth muscles (VSMs) and myocardium cells, TLRs play distinct roles in innate immune activation, such as recognizing pathogen-associated molecular patterns (PAMPs) and activating downstream signaling pathways. In the context of COVID-19, TLRs are critically involved in the pathophysiology by mediating excessive inflammatory responses that exacerbate disease severity, influencing both the acute phase and long-term outcomes. It has been observed that inflammatory diseases such as atherosclerosis, viral myocarditis, and other comorbidities associated with the spread of COVID-19 have increased, although the exact mechanisms remain not fully understood. Nonetheless, there is evidence of TLR-mediated increased pro-inflammatory signaling by different mechanisms in these diseases. This review explains the role of TLRs in various inflammatory diseases related to COVID-19, including viral myocarditis, acute lung infections, and atherosclerosis. Furthermore, the review discusses various herbal drugs, such as Platycodon grandiflorum, Acanthopanax senticosus, Scutellaria baicalensis Georgi, and Engelhardia roxburghiana, and their mechanisms of action on TLRs, including NF-κB, MyD88-dependent, MyD88-independent pathways, and Plasmacytoid DCs. Enhanced clarity on TLRs' specific contributions to COVID-19 pathophysiology and stronger evidence supporting herbal interventions targeting TLRs could improve the impact and applicability of these findings in clinical settings.

Tiliroside, a natural polyphenolic compound found in several plant sources, has garnered attention for its potential to mitigate inflammation and its associated diseases. The current review explores the multifaceted functions of Tiliroside in inflammation-related diseases, delving into the underlying mechanisms and prospects for therapeutic applications. Tiliroside exerts its anti-inflammatory effects through a variety of mechanisms, such as the inhibition of inflammatory mediators’ cytokines and chemokines, as well as the suppression of nuclear factor-kappa B (NF-κB) signaling pathways. Additionally, it demonstrates potent antioxidant properties, which further contribute to its anti-inflammatory activity by reducing oxidative stress. In preclinical studies, Tiliroside has shown promising results in ameliorating inflammation in conditions like rheumatoid arthritis, inflammatory bowel disease, and atherosclerosis. Furthermore, Tiliroside's ability to modulate immune responses and stimulate tissue regeneration contributes to its potential as a multimodal agent in treating inflammation-associated disorders. In conclusion, Tiliroside emerges as a promising natural compound with a multifaceted role in inflammation-related diseases with understanding the underlying mechanisms of its therapeutic prospects may pave the way for novel treatments.

Chrysophanol, a naturally occurring anthraquinone compound found in various plants, fungi, and lichens, has garnered increasing attention for its potential therapeutic benefits, particularly in the context of inflammation-related disorders. This review aims to provide a comprehensive overview of the anti-inflammatory properties of chrysophanol and its potential as a therapeutic agent for intervention in inflammatory conditions. In this review, the current understanding of the molecular mechanisms underlying the anti-inflammatory effects of Chrysophanol, including its modulation of key inflammatory signaling pathways, such as NF-κB, MAPK, JAK-STAT, Nrf2, and other NLRP3 inflammasomes. Additionally, we discuss the evidence from in vitro and in vivo studies supporting the anti-inflammatory efficacy of chrysophanol in various experimental models of inflammation, including various inflammatory diseases. Furthermore, we explore the pharmacokinetic profile of Chrysophanol and other nanoformulations to understand its therapeutic potential. Overall, accumulating evidence suggests that chrysophanol holds promise as a novel therapeutic candidate for the management of inflammatory disorders, warranting further investigation and clinical translation.

This extensive analysis explores the dynamic interface between precision medicine and diabetes mellitus treatment, with a specific emphasis on wound healing in diabetic populations. Beginning with an insightful introduction, the article underscores the critical importance of effective wound healing within the broader context of diabetes mellitus, while tracing the evolutionary trajectory of precision medicine in healthcare. By elucidating the pathophysiological intricacies of diabetic wound healing, the review unveils the complex molecular mechanisms that drive this multifaceted process. Subsequently, a meticulous exploration follows into the application of precision medicine paradigms in diabetic wound care, delineating fundamental principles and diverse avenues through which precision medicine strategies can optimize diabetes management. Through a nuanced discussion of targeted therapies and interventions, the review highlights burgeoning approaches tailored to individual patient needs, accentuating the transformative potential of precision medicine in reshaping treatment paradigms. Drawing upon clinical trials and compelling case studies, the article offers valuable insights into the real-world efficacy of precision treatment modalities, elucidating successful applications and their profound implications for diabetic wound healing outcomes. Moreover, the review anticipates and addresses emerging challenges and future trajectories within the field, including the pivotal roles of biomarkers and diagnostic modalities, the integration of telemedicine platforms, and the increasing influence of artificial intelligence on diabetic wound healing endeavours. By synthesizing contemporary knowledge and delineating prospective pathways, this review underscores the catalytic potential of precision medicine in heralding a new era of enhanced outcomes for diabetic patients grappling with impaired wound healing.

In recent years, phenolic acids have garnered considerable interest on account of their diverse biological, practical, and pharmacological effects. Chlorogenic Acid (CGA), presently referred to as 3-CQA, is the most prevalent isomer among caffeoylquinic acid isomers (3-, 4-, and 5-CQA). Among the naturally occurring phenolic acid compounds found in green coffee extracts and tea, it is one of the most readily accessible acids. Recent studies have demonstrated that chlorogenic acid exerts its anti-inflammatory effects via various mechanisms, including the inhibition of inflammatory mediators, demonstration of antioxidant activity, modulation of signaling pathways, and regulation of the immune system. Each of these mechanisms is essential for immune system regulation. Chlorogenic acid mitigates tissue injury and impedes the inflammatory response through mechanisms, including inhibition of pro-inflammatory chemical synthesis and activity, scavenging of free radicals, and modulation of immune cell functionality. Throughout this review article, we have methodically examined the advantageous contributions of CGA in relation to its origin, assimilation, metabolism, molecular mechanisms, mechanistic effects, and impact on various forms of inflammation.

Background: Inflammatory bowel diseases (IBD) necessitate cost-effective biomarkers for efficient management. This study aimed to explore the potential correlations of neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), and platelet-to-lymphocyte ratio (PLR) with IBD disease activity. Additionally, we assessed their associations with other inflammatory markers.

Methods: We recruited 180 IBD patients with over 12 months of disease duration, categorized into two groups: Group 1 (active IBD) with 113 cases and Group 2 (inactive IBD) with 67 cases, alongside 200 group-matched healthy controls (Group 3). Hemogram, NLR, LMR, PLR, hs-CRP, ESR, fecal calprotectin (FC), and relevant parameters were recorded.

Results: NLR and PLR were elevated, while LMR was decreased in active IBD patients compared to those in remission. The cutoff values for active IBD were determined as NLR > 1.98, LMR < 3.01, and PLR > 147, exhibiting sensitivity of 92%, 88%, and 91%, and specificity of 93%, 87%, and 89% respectively. Optimal cutoff values for IBD disease activity were CRP > 9.71, ESR > 24, and FC > 176. Multivariate logistic regression identified NLR, LMR, and PLR as robust parameters for discriminating IBD disease activity after adjusting for WBC, CRP, ESR, and FC markers (p < 0.05). NLR and PLR exhibited proportional increases with IBD severity, while LMR lacked such predictive capability.

Conclusion: NLR, PLR, and LMR emerge as simple, non-invasive, and cost-effective independent markers of IBD disease activity, complementing traditional markers like CRP and ESR.