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Ulcerative colitis (UC) is a chronic, nonspecific inflammatory disorder characterized by symptoms such as abdominal pain, diarrhea, hematochezia, and urgency during defecation. While the primary site of involvement is the colon, UC can extend to encompass the entire rectum and colon. The causes and development mechanisms of UC are still not well understood; nonetheless, it is currently held that factors including environmental influences, genetic predispositions, intestinal mucosal integrity, gut microbiota composition, and immune dysregulation contribute to its development. Dysregulated immune responses are pivotal in the pathophysiology of UC, and these aberrant responses are considered key contributors to the disease onset. In patients with UC, immune cells become hyperactive and erroneously target normal intestinal tissue, resulting in inflammatory cascades and damage to the intestinal mucosa. The therapeutic strategies currently employed for UC include immunosuppressive agents such as aminosalicylates and corticosteroids. However, these treatments often prove costly and carry significant adverse effects — imposing a considerable burden on patients. Traditional Chinese Medicine (TCM) has attracted worldwide attention because of its multi-target approach, minimal side effects, cost-effectiveness, and favorable efficacy profiles. In this review, the ways in which TCM modulates inflammatory responses in the treatment of ulcerative colitis have been outlined. Research into TCM modalities for modulating inflammatory pathways in the treatment of UC, which has yielded promising advancements, including individual herbs, herbal formulations, and their derivatives, has been summarized. TCM has been utilized to treat UC and the immune system plays a key role in regulating intestinal homeostasis. It is imperative to facilitate large-scale evidence-based medical research and promote the clinical application of TCM in the management of UC.

Davallia bilabiata (D. bilabiata) is also called GuSuiBu in Taiwan and is used as a substitute for Drynaria fortunei J. Sm. It is often used for trauma and bone repair. The inhibitory effect of D. bilabiata on inflammatory activity has not been reported. In the present study, we aimed to study the mechanism of anti-inflammation of D. bilabiata on the adhesion of leukocytes to vascular endothelial cells. The results showed that D. bilabiata, at concentrations without cytotoxic effect, inhibited the adhesion of monocytes (THP-1) to the TNF-α-stimulated human umbilical vascular endothelial cells (HUVECs). D. bilabiata suppressed the expression of the adhesion molecules ICAM, VCAM, and E-selectin at both the mRNA and protein level. In addition, both of the TNF-α-induced mRNA and protein expression of chemokines including fractalkine/CX₃CL1, MCP-1 and RANTES as well as the level of secreted soluble fractalkine were decreased by D. bilabiata. We also verified that D. bilabiata inhibited the TNF-α-induced nuclear translocation of NF-κB through the inhibitory process on the TNF-α-activated phosphorylation of IKKα, IKKβ, IκB and NF-κB. All together, we concluded that the D. bilabiata affected the canonical pathway of TNF-α-induced NF-κB activation and down-regulated cell adhesion molecules and chemokine expression through inhibition of the NF-κB/IκBα/IKK signaling pathway. These findings strongly indicated that D. bilabiata might be a promising alternative/adjunct treatment for inflammatory diseases, such as rheumatoid arthritis and osteoarthritis.

Pulmonary fibrosis (PF) is a highly confounding and fatal pathological process with finite treatment options. Multiple factors such as oxidative and immune/inflammation involve key pathological processes in chronic lung disease, and their intimate interactions mediate chronic lung damage, denudation of the alveolar epithelium, hyperproliferation of type II alveolar epithelial cells (AECIIs), proliferation and differentiation of fibroblasts, and the permeability of microvessels. We reviewed the classic mechanism of PF and highlighted a few emerging mechanisms for studying complex networks in lung disease pathology. Polyphenols, as a multi-target drug, has excellent potential in the treatment of pulmonary fibrosis. We then reviewed recent advances in discovering phenolic compounds from fruits, tea, and medical herbs with the bioactivities of simultaneously regulating multiple factors (e.g., oxidative stress, inflammation, autophagy, apoptosis, pyroptosis) for minimizing pulmonary fibrosis injury. These compounds include resveratrol, curcumin, salvianolic acid B, epigallocatechin-3-gallate, gallic acid, corilagin. Each phenolic compound can exert its anti-PF effect through various mechanisms, and the signaling pathways involved in different phenolic compounds are not the same. This review summarized the available evidence on phenolic compounds’ effectiveness in pulmonary diseases and explored the molecular mechanisms and therapeutic targets of phenolic compounds from Chinese herbal medicine with the properties of inhibition of ongoing fibrogenesis and resolution of existing fibrosis.

Biological data is inherently heterogeneous and high-dimensional. Single-cell sequencing of transcripts in a tissue sample generates data for thousands of cells, each of which is characterized by upwards of tens of thousands of genes. How to identify the subsets of cells and genes that are associated with a label of interest remains an open question. In this paper, we integrate a signal-extractive neural network architecture with axiomatic feature attribution to classify tissue samples based on single-cell gene expression profiles. This approach is not only interpretable but also robust to noise, requiring just 5% of genes and 23% of cells in an in silico tissue sample to encode signal in order to distinguish signal from noise with greater than 70% accuracy. We demonstrate its applicability in two real-world settings for discovering cell type-specific chemokine correlates: predicting response to immune checkpoint inhibitors in multiple tissue types and classifying DNA mismatch repair status in colorectal cancer. Our approach not only significantly outperforms traditional machine learning classifiers but also presents actionable biological hypotheses of chemokinemediated tumor immunogenicity.

A detailed understanding of the pathophysiologic mechanisms of severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) infection and Coronavirus disease 2019 (COVID-19) is vital for improving patient management — to facilitate prompt recognition of progression to severe disease and effective therapeutic strategies. This chapter summarizes the underlying pathophysiology in the lungs and other organs of COVID-19 patients. The roles of the cytokine storm culminating in exaggerated inflammatory responses and formation of neutrophil extracellular traps (NETs) are discussed. Pathological features of the various stages from the onset of COVID-19 are outlined — progressing from early mild infection to severe clinical illness to the critically ill phase.

Pulmonary fibrosis (PF) is a highly confounding and fatal pathological process with finite treatment options. Multiple factors such as oxidative and immune/inflammation involve key pathological processes in chronic lung disease, and their intimate interactions mediate chronic lung damage, denudation of the alveolar epithelium, hyperproliferation of type II alveolar epithelial cells (AECIIs), proliferation and differentiation of fibroblasts, and the permeability of microvessels. We reviewed the classic mechanism of PF and highlighted a few emerging mechanisms for studying complex networks in lung disease pathology. Polyphenols, as a multi-target drug, has excellent potential in the treatment of pulmonary fibrosis. We then reviewed recent advances in discovering phenolic compounds from fruits, tea, and medical herbs with the bioactivities of simultaneously regulating multiple factors (e.g., oxidative stress, inflammation, autophagy, apoptosis, pyroptosis) for minimizing pulmonary fibrosis injury. These compounds include resveratrol, curcumin, salvianolic acid B, epigallocatechin-3-gallate, gallic acid, corilagin. Each phenolic compound can exert its anti-PF effect through various mechanisms, and the signaling pathways involved in different phenolic compounds are not the same. This review summarized the available evidence on phenolic compounds’ effectiveness in pulmonary diseases and explored the molecular mechanisms and therapeutic targets of phenolic compounds from Chinese herbal medicine with the properties of inhibition of ongoing fibrogenesis and resolution of existing fibrosis.