Ferroptosis in cancer immunity and immunotherapy: Multifaceted interplay and clinical implications.

Ferroptosis is a type of cell death characterized by iron-dependent phospholipid peroxidation and reactive oxygen species overproduction. Ferroptosis induces immunogenic cell death and elicits anti-tumor immune responses, playing an important role in cancer immunotherapy. Ferroptosis suppression in cancer cells impairs its immunotherapeutic efficacy. To overcome this issue, ferroptosis inducers (FINs) have been combined with other cancer therapies to create an anti-tumor immune microenvironment. However, the ferroptosis-based crosstalk between immune and tumor cells is complex because oxidative products released by ferroptotic tumor cells impair the functions of anti-tumor immune cells, resulting in immunotherapeutic resistance. In the present article, we have reviewed ferroptosis in tumor and immune cells and summarized the crosstalk between ferroptotic tumor cells and the immune microenvironment. Based on the existing literature, we have further discussed future perspectives on opportunities for combining ferroptosis-targeted therapies with cancer immunotherapies.

The Role of Thoracic Vertebral Body Dosimetry in Minimizing Acute Hematologic Toxicities of Patients With Non-Small Cell Lung Cancer Receiving Lung Radiation Therapy and Immunotherapy.

PURPOSE: Hematologic toxicities (HTs) are among the most common toxicities of combined immunotherapy and radiation therapy (RT). It remains essential to prevent RT-induced HTs because they can cause treatment discontinuation (influencing antitumoral effects) and because lymphopenia might dampen the effects of immunotherapy. To date, there are no studies examining the effect of thoracic vertebral body (TVB) RT dose on HTs in patients with non-small cell lung cancer receiving combined lung RT and programmed cell death (ligand) 1 immunotherapy. METHODS AND MATERIALS: For standardization, all doses were reported as 2-Gy equivalents (EQD2). Mirroring publications before the immunotherapy era, TVB volumes referred to T1-T10, and specific dosimetric parameters (DmeanEQD2, V5EQD2-V60EQD2) were analyzed. Logistic regression estimated associations between grade ≥3 HTs (HT3+) and dosimetric/clinical parameters. Normal tissue complication probability (NTCP) models were constructed by logistic regression analysis modeling for HT3+. Receiver operating characteristic (ROC) analysis delineated TVB dosimetric thresholds, the stratification of which was able to evaluate post-RT absolute lymphocyte count and immunotherapy responses. Areas under the curve (AUCs) for NTCP models were corroborated by bootstrapping (optimism-corrected) methodology. RESULTS: In 132 patients, there were 26 (19.7%) instances of HT3+. On multivariate analysis, DmeanEQD2 and V5EQD2 to V20EQD2 were associated with HT3+ (P < .05 for all). The NTCP models illustrated a 50% probability of HT3+ at a DmeanEQD2 = 39.8 Gy, V5EQD2 = 87.4%, V10EQD2 = 77.0%, and V20EQD2 = 68.4%. ROC analysis delineated optimal thresholds of HT3+ with DmeanEQD2 ± 30.2 Gy, V5EQD2 ± 69.1%, V10EQD2 ± 64.6%, and V20EQD2 ± 53.5%. Patients treated with values above those cutoffs had over double the risk of HT3+, with significant differences in post-RT absolute lymphocyte count and immunotherapy responses (P < .05 for all). AUCs for each individual parameter ranged from 0.743 to 0.798, and combining all 4 aforementioned cutoffs into a ROC curve resulted in a qualitatively higher AUC (0.836). CONCLUSIONS: This hypothesis-generating work suggests that TVB dosimetry may equate with HT3+ in patients with non-small cell lung cancer undergoing combined lung RT/immunotherapy. Applying TVB dose constraints in this population could reduce HT3+ and avoid dampening of immunotherapy responses, but prospective validation is required.

Disfunction of communication among immune cells in minimal-deviation adenocarcinoma of the cervix as an immunotherapeutic opportunity.

Minimal deviation adenocarcinoma (MDA) of the uterine cervix, also referred to as malignant adenoma, is a rare subtype of cervical adenocarcinoma that exhibits histological characteristics resembling those of benign tumors, resulting in a low diagnostic rate and a lack of effective treatment options. The transcriptomic features of MDA at the single-cell resolution and within the tumor microenvironment (TME) remain unclear. In this study, we conducted single-cell transcriptomic analyses of MDA samples (Ca) and adjacent normal tissues (PCa). The present study reveals the prevalence of dendritic cells (DCs) and T cells in the carcinoma (Ca) of mammary ductal adenocarcinoma (MDA), with DCs undergoing significant metabolic reprogramming and immune stress. Additionally, our findings demonstrate the crucial involvement of DCs and T cells in the pathogenesis and metastatic progression of MDA, as evidenced by single-cell transcriptomic profiling of MDA and HPV samples. This resource provides a more profound understanding of the indolent nature of MDA and may prove useful in the development of MDA immunotherapy.

[Updated Interpretation of the NCCN Clinical Practice Guidelines (Version 3. 2023) 
for Non-small Cell Lung Cancer].

Lung cancer is the malignant tumor with the highest morbidity and mortality in China. Non-small cell lung cancer (NSCLC) is the main pathological subtype of lung cancer. On April 13, 2023, the National Comprehensive Cancer Network (NCCN) released the third edition of the 2023 NCCN Oncology Clinical Practice Guidelines: Non-small Cell Lung Cancer, which reflects the latest advances in international lung cancer research. This article will interpret the main updated contents of the new edition of the guidelines, and compare it with the third edition of the NCCN guidelines in 2022, so as to provide references about the diagnosis and treatment of NSCLC for clinical medical personnel in China.
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Gas6/AXL pathway: immunological landscape and therapeutic potential.

Cancer is a disease with ecological and evolutionary unity, which seriously affects the survival and quality of human beings. Currently, many reports have suggested Gas6 plays an important role in cancer. Binding of gas6 to TAM receptors is associated with the carcinogenetic mechanisms of multiple malignancies, such as in breast cancer, chronic lymphocytic leukemia, non-small cell lung cancer, melanoma, prostate cancer, etc., and shortened overall survival. It is accepted that the Gas6/TAM pathway can promote the malignant transformation of various types of cancer cells. Gas6 has the highest affinity for Axl, an important member of the TAM receptor family. Knockdown of the TAM receptors Axl significantly affects cell cycle progression in tumor cells. Interestingly, Gas6 also has an essential function in the tumor microenvironment. The Gas6/AXL pathway regulates angiogenesis, immune-related molecular markers and the secretion of certain cytokines in the tumor microenvironment, and also modulates the functions of a variety of immune cells. In addition, evidence suggests that the Gas6/AXL pathway is involved in tumor therapy resistance. Recently, multiple studies have begun to explore in depth the importance of the Gas6/AXL pathway as a potential tumor therapeutic target as well as its broad promise in immunotherapy; therefore, a timely review of the characteristics of the Gas6/AXL pathway and its value in tumor treatment strategies is warranted. This comprehensive review assessed the roles of Gas6 and AXL receptors and their associated pathways in carcinogenesis and cancer progression, summarized the impact of Gas6/AXL on the tumor microenvironment, and highlighted the recent research progress on the relationship between Gas6/AXL and cancer drug resistance.

Case report: Complete pathological admission in N3 unresectable locally advanced lung adenocarcinoma with a novel INTS10-ALK and EML4-ALK fusion after neoadjuvant crizotinib.

Background: Although anaplastic lymphoma kinase tyrosine kinase inhibitors (ALK-TKIs) have impressive response in advanced lung adenocarcinoma with anaplastic lymphoma kinase (ALK) fusion, no guidelines point to the potential benefits of neoadjuvant ALK-TKIs for N3 unresectable locally advanced lung cancer. Current ongoing clinical trials mainly focus on the efficacy of neoadjuvant ALK-TKIs in resectable locally advanced lung cancer and ignore the role of neoadjuvant ALK-TKIs in N3 unresectable locally advanced lung cancer. Materials and methods: We report a lung cancer case with a novel INTS10-ALK and EML4-ALK rearrangement that achieved complete pathologic response to neoadjuvant crizotinib. We conducted molecular pathologic analysis by using next-generation sequencing (NGS). Genomic DNA was extracted from formalin-fixed paraffin-embedded (FFPE) samples and profiled using a capture-based targeted sequencing panel consisting of 56 lung cancer-related genes. Results: Our study reported a patient with stage IIIB-N3 lung adenocarcinoma with an unreported dual ALK rearrangement (INTS10-ALK and EML4-ALK) who received 5 months of crizotinib, followed by R0 right upper lobectomy, achieving complete pathological response (ypT0 ypN0). No recurrence of the tumor was found for 3 years postoperatively. Conclusion: The case supports the strategy of neoadjuvant ALK inhibitors for N3 unresectable locally advanced lung cancer, expanding the spectrum of treatment of stage IIIB-N3 lung cancer.

Combination of STING agonist and CXCR3 antagonist disrupts immune tolerance to overcome anti-PD-L1 resistance in lung adenocarcinoma under oxidative stress.

We investigated the role of the STING1-CXCR3 axis using database data and verified it in a mouse model bearing Lewis lung carcinoma (LLC) cells exposed to hydrogen peroxide (H2O2). Mice were treated with STING agonist liposomes (STING-Lip), anti-programmed death-ligand 1 (PD-L1), or STING-Lip + anti-PD-L1. The database data revealed that immune response pathways were enriched in patients with lung adenocarcinoma with upregulated STING1 signaling. Upregulated STING1 signaling was associated with a high abundance of immunoregulatory and effector molecules, cytokines, activated CD8+ T cells, and M1 macrophages in patients with lung adenocarcinoma. In this study, H2O2-treated LLC cells promoted an immunosuppressive microenvironment and enhanced tumor growth in mice. STING-Lip inhibited distant, untreated, and H2O2-induced LLC growth by activating systemic immunity. STING-Lip + anti-PD-L1 failed to slow distant and untreated LLC growth, whereas STING-Lip + anti-PD-L1 + CXCR3 antagonist inhibited distant tumor growth in mice. The combination of STING1 activation and CXCR3 inhibition may be a novel immunotherapeutic strategy to overcome immune checkpoint inhibitor resistance in lung adenocarcinoma by activating systemic immunity in the tumor microenvironment under oxidative stress.

Classical ALK G1202R resistance mutation was identified in a lung adenocarcinoma patient with rare LOC388942-ALK fusion after sequential treatment with ALK-TKIs and anlotinib: a case report.

Background: Anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC) is a heterogeneous disease. To date, more than ninety ALK fusions in lung cancer have been found. Here, we report for the first time a rare LOC388942-ALK fusion in NSCLC was sensitive to crizotinib but resistant to the sequential ceritinib and alectinib and acquired classical ALK G1202R resistance mutation after long-term treatment with anlotinib. This case highlights dynamic monitoring of gene alteration using next-generation sequencing (NGS) is necessary during the anti-tumor process. Case Description: A 55-year-old male, with no history of smoking history and no family history of cancer, was found malignant pleural effusion and multiple metastasis nodules in the left lung. He was histopathologically diagnosed with ALK-positive cT4N0M1a adenocarcinoma in June 2016. NGS of the tumor identified a rare LOC388942-ALK fusion (L intergenic: A 20, 1.41%). Then, the patient was treated with chemotherapy, crizotinib, ceritinib, alectinib, and anlotinib sequentially. The patient achieved partial response (PR) to chemotherapy and crizotinib. No evidence of a secondary resistant molecular event was found after resistance to crizotinib, ceritinib, or Alectinib. After 8 months of alectinib treatment, the tumor gradually enlarged again. Anlotinib was followed for 13 months. Thirteen months later, new lesions in the lower lobe of the right lung appeared and increased gradually, indicating definite progression of the tumor. Classical ALK G1202R resistance mutations was detected using cfDNA NGS. The patient refused to receive lorlatinib targeting G1202R resistance mutations and continued with anlotinib. He dead in August 2022, achieving 5-year overall survival (OS). Conclusions: Distinct ALK fusions in NSCLC have different cancer biology, leading to different response to ALK tyrosine kinase inhibitors (ALK-TKIs), even developed different resistance mechanism. Reporting the clinical details of rare ALK fusions in NSCLC is necessary to guide the treatment for clinicians and researchers.

A narrative review of COVID-19-related acute respiratory distress syndrome (CARDS): "typical" or "atypical" ARDS?

Background and Objective: The coronavirus disease of 2019 (COVID-19) is highly infectious and mainly involves the respiratory system, with some patients rapidly progress to acute respiratory distress syndrome (ARDS), which is the leading cause of death in COVID-19 patients. Hence, fully understanding the features of COVID-19-related ARDS (CARDS) and early management of this disease would improve the prognosis and reduce the mortality of severe COVID-19. With the development of recent studies which have focused on CARDS, whether CARDS is "typical" or "atypical" ARDS has become a hotly debated topic. Methods: We searched for relevant literature from 1999 to 2021 published in PubMed by using the following keywords and their combinations: "COVID-19", "CARDS", "ARDS", "pathophysiological mechanism", "clinical manifestations", "prognosis", and "clinical trials". Then, we analyzed, compared and highlighted the differences between classic ARDS and CARDS from all of the aspects above. Key Content and Findings: Classical ARDS commonly occurs within 1 week after a predisposing cause, yet the median time from symptoms onset to CARDS is longer than that of classical ARDS, manifesting within a period of 9.0-12.0 days. Although the lung mechanics exhibited in CARDS grossly match those of classical ARDS, there are some atypical manifestations of CARDS: the severity of hypoxemia seemed not to be proportional to injury of lung mechanics and an increase of thrombogenic processes. Meanwhile, some patients' symptoms do not correspond with the extent of the organic injury: a chest computed tomography (CT) will reveal the severe and diffuse lung injuries, yet the clinical presentations of patients can be mild. Conclusions: Despite the differences between the CARDS and ARDS, in addition to the treatment of antivirals, clinicians should continue to follow the accepted evidence-based framework for managing all ARDS cases, including CARDS.

Demographics, clinical features, and prognosis of rare lymphoepithelioma-like carcinoma across different anatomic sites.

BACKGROUND: Lymphoepithelioma-like carcinoma (LELC) is an unusual histological malignancy type. Due to the rarity of this disease, we used the Surveillance, Epidemiology, and End Results (SEER) database to investigate comprehensively and systematically the prognosis factor of LELC. METHODS: We identified 2079 patients diagnosed with LELC during 1973-2015 from the SEER database. LELC was classified according to the tumor site. We analyzed the clinical characteristics and estimated the hazard ratio (HR) of overall mortality of LELC at each site. RESULTS: The nasopharynx was the most frequent site where LELC (58%) occurred. A large percentage of nasopharyngeal and pulmonary LELC patients were of Asian descent (44.5 and 32.56%, respectively). Furthermore, the majority of LELC patients were rather young when diagnosed. However, urinary bladder LELC and digestive system LELC (mean age: 69.03 and 68.05 years, respectively) were mainly to be found in older patients. Then according to Kaplan-Meier survival analysis, we found that patients with pulmonary LELC had worse survival. After adjusting for clinical tumor characteristics, pulmonary LELC patients were at increased risk of overall mortality compared with nasopharyngeal LELC either at the localized stage (HR 3.12, 95% confidence interval [CI], 1.55-6.26. P < 0.01) or at the regional stage (HR 1.72, 95% CI 1.03-2.88 P = 0.04). CONCLUSIONS: In conclusion, we found that urinary bladder and digestive system LELCs mainly were diagnosed in old people and different from other LELCs. Pulmonary LELC patients might have a bad prognosis. The origination site may represent a predictive factor for determining survival in patients with LELC.

The unique pancreatic stellate cell gene expression signatures are associated with the progression from acute to chronic pancreatitis.

Chronic pancreatitis (CP) is characterized by irreversible fibro-inflammatory changes induced by pancreatic stellate cell (PSC). Unresolved or recurrent injury causes dysregulation of biological process following AP, which would cause CP. Here, we systematically identify genes whose expressions are unique to PSC by comparing transcriptome profiles among total pancreas, pancreatic stellate, acinar, islet and immune cells. We then identified candidate genes and correlated them with the pancreatic disease continuum by performing intersection analysis among total PSC and activated PSC genes, and genes persistently differentially expressed during acute pancreatitis (AP) recovery. Last, we examined the association between candidate genes and AP, and substantiated their potential as biomarkers in experimental AP and recurrent AP (RAP) models. A total of 68 genes were identified as highly and uniquely expressed in PSC. The PSC signatures were highly enriched with extracellular matrix remodeling genes and were significantly enriched in AP pancreas compared to healthy control tissues. Among PSC signature genes that comprised a fibrotic phenotype, 10 were persistently differentially expressed during AP recovery. SPARC was determined as a candidate marker for the pancreatic disease continuum, which was not only persistently differentially expressed even five days after AP injury, but also highly expressed in two clinical datasets of CP. Sparc was also validated as highly elevated in RAP compared to AP mice. This work highlights the unique transcriptional profiles of PSC. These PSC signatures' expression may help to identify patients with high risk of AP progression to CP.

Case Report: Re-Sensitization to Gefitinib in Lung Adenocarcinoma Harboring EGFR Mutation and High PD-L1 Expression After Immunotherapy Resistance, Which Finally Transform Into Small Cell Carcinoma.

The treatment sequence of immunotherapy (IO) and epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is of great importance for the survival of non-small cell lung cancer (NSCLC) patients with EGFR sensitive mutation. Here, we reported an advanced lung adenocarcinoma case concurrent with EGFR sensitive mutation and high PD-L1 expression (>50%) that was administrated with gefitinib firstly, and then became resistant to EGFR-TKI. He received the strategy of immunity-combined chemo-radiotherapy and responded significantly. However, the disease re-progressed after 10 months. Surprisingly, the tumor re-sensitized to gefitinib for 13 months. At final, following the treatment pressure of TKI-IO combination therapy-TKI strategy, tumor clone eventually transformed into small cell lung carcinoma (SCLC). For one thing, our study provided novel approach and extended the treatment spectra of overcoming immunotherapy resistance after EGFR resistance in driver oncogene-mutated NSCLC. For another thing, our case is the first time to report that SCLC transformation can be achieved after gefitinib-pembrolizumab-gefitinib resistance in EGFR sensitive mutation NSCLC, providing a new condition for SCLC transformation.

Carbonate assisted lipid extraction and biodiesel production from wet microalgal biomass and recycling waste carbonate for CO2 supply in microalgae cultivation.

High cost of microalgal biofuel is caused by all the steps in current technology, including cultivation, harvesting, lipid extraction, biofuel processing and wastewater and waste treatment. This study aims to systematically reduce these costs with one integrated process, in which carbonate is used for cell rupture, lipid extraction and biodiesel processing, and then recycled for CO2 absorption and carbon supply for a new round of algae cultivation. To reach this goal, carbonate-heating treatment with N, N' - dibutylurea which can enhance cell disruption were used for cell-wall breaking of wet Neochloris oleoabundans (UTEX 1185) biomass. Lipid extraction was fulfilled with carbonate/ethanol aqueous two phase extraction method and residual carbonate with wastewater from bottom phase was recycled to absorb CO2 to generate bicarbonate for algal cultivation with fresh medium. Taking into comprehensive consideration of cell disruption efficiency, partition coefficient, and lipid recovery, the condition of cell disruption and lipid extraction was set at 90 °C, 100 min reaction time, 1:7.5 DBU:H2O (w/w) ratio, 1:3 Na2CO3:H2O (w/w) ratio, and 9% (w/wT) ethanol concentration. The results showed that carbonate-heating treatment of wet N. oleoabundans biomass resulted in up to 90.7% cell disruption efficiency. The lipid recovery rate in carbonate/ethanol system was up to 97.9%, and the final biodiesel production was 1.30 times of that with Soxhlet method. Utilization of the waste broth after CO2 absorption with the content of 4% (v/vT) in the medium for new batch of algae cultivation resulted in biomass concentration of 1.68 g/L. The corresponding total fatty acids production was 0.35 g/L, which was 1.63 fold of that with fresh medium. This study firstly proved the feasibility of using carbonate for lipid extraction and biodiesel production and recycle waste carbonate for carbon re-supply during algae cultivation.

Identification of Immune Subtypes of Lung Squamous Cell Carcinoma by Integrative Genome-Scale Analysis.

BACKGROUND: Characterization of the tumor microenvironment is helpful to understand the tumor immune environment of lung cancer and help predict the prognosis. METHODS: First, immune subtypes were identified by consensus subtype among lung squamous carcinoma (LUSC) patients. Immune cell infiltration was evaluated by CIBERSORT and ESTIMATE analyses. Then, based on differentially expressed genes (DEGs) identified, a risk score model was constructed. Finally, gene FPR1 was validated by using YTMLC-90. FINDINGS: LUSC samples were divided into four heterogeneous immune subtypes, with significantly different prognoses with subtype 4 having the poorest overall survival (OS). The immune infiltration score showed that subtype 4 was characterized as immune enriched and fibrotic, while subtype 3 was tumor enriched. DEG analysis showed that upregulated genes in subtype 4 were enriched of neutrophil and exhausted T cell-related biological processes. Based on a univariate Cox regression model, prognostic 7 immune-related genes were combined to construct a risk score model and able to predict OS rates in the validation datasets. Wound healing and transwell assay were conducted to evaluate the invasion property after activating the gene FPR1. INTERPRETATION: The analysis of tumor immune microenvironments among LUSC subtypes may provide new insights into the strategy of immunotherapy.

Case Report: A Novel Non-Reciprocal ALK Fusion: ALK-GCA and EML4-ALK Were Identified in Lung Adenocarcinoma, Which May Respond to Alectinib Adjuvant-Targeted Therapy.

Anaplastic lymphoma kinase (ALK)-positive non-small-cell lung cancers (NSCLCs) have favorable and impressive response to ALK tyrosine kinase inhibitors (TKIs). However, ALK rearrangement had approximately 90 distinct fusion partners. Patients with different ALK fusions might have distinct responses to different-generation ALK-TKIs. In this case report, we identified a novel non-reciprocal ALK fusion: ALK-grancalcin (GCA) (A19: intragenic) and EML4-ALK (E20: A20) by next-generation sequencing (NGS) in a male lung adenocarcinoma patient who was staged as IIIB-N2 after surgery. After a multidisciplinary discussion, the patient received alectinib adjuvant targeted therapy and postoperative radiotherapy (PORT). He is currently in good condition, and disease-free survival (DFS) has been 20 months so far, which has been longer than the median survival time of IIIB NSCLC patients. Our study extended the spectrum of ALK fusion partners in ALK + NSCLC, and we reported a new ALK fusion: ALK-GCA and EML4-ALK and its sensitivity to alectinib firstly in lung cancer. It is vital for clinicians to detect fusion mutations of patients and report timely the newfound fusions and their response to guide treatment.

Seawater supplemented with bicarbonate for efficient marine microalgae production in floating photobioreactor on ocean: A case study of Chlorella sp.

Cultivation of microalgae on ocean provides a promising way to produce massive biomass without utilizing limited land space, and using seawater as culture medium can avoid consumption of valuable fresh water. Bicarbonate is proved as a better approach for carbon supply in microalgae cultivation, but Ca2+ and Mg2+ in seawater is subjected to precipitate with carbonate derived from it. In this study, cultivation with this medium for a marine Chlorella sp. resulted in productivity of 0.470 g L-1 day-1, despite of continual precipitation caused by increased pH due to bicarbonate consumption. Actually, this precipitation is favorable, since it can work as a flocculation harvesting method for microalgae. The highest flocculation efficiency of 98.9 ± 0.0% was observed in cultures with 7.0 g L-1 NaHCO3, which was higher than that of cultures without bicarbonate (44.1 ± 0.2%). Additionally, the spent medium after flocculation supported better growth (1.60 ± 0.0 g L-1) than the fresh medium (1.26 ± 0.0 g L-1). Outdoor cultivation with floating photobioreactor on ocean resulted in the productivity of 0.190 g L-1 day-1, which was higher than that in land-based culture systems. The floating system also benefited from better temperature control with range from 20.6 to 37.2 °C, due to solar heating and surrounding water cooling. These results showed feasibility of efficient microalgae biomass production with fully utilizing of ocean resources, including culture medium preparation and temperature control with seawater, as well as wave energy for mixing, holding great potential to produce massive biomass to support sustainable development of human society.

Antibacterial activity of chlorogenic acid-loaded SiO2 nanoparticles caused by accumulation of reactive oxygen species.

Diseases caused by pathogenic bacilli pose an increasing threat to human health. A common feature of these bacteria is a complete cell wall; therefore, drugs that can penetrate this protective barrier could be used as a novel approach for treating these infections. Here we present a simple method for synthesizing a silica mesoporous material loaded with cadmium selenide (CdSe) and chlorogenic acid. Using UV-visible, fluorescence, and infrared imaging in combination with transmission electron microscopy, it was shown that CdSe and chlorogenic acid could be successfully embedded in the mesopores of silica nanoparticles (CSC NPs), and these NPs presented with a strong fluorescence, uniform size, and good dispersion. Additionally, the results of these analyses indicated that the fluorescence of the CSC NPs was localized within the cells of Escherichia coli and Bacillus subtilis, signifying that these NPs could breach the cell wall and enter the cells of these two bacilli. Additional assessments found that these CSC NPs inhibited the proliferation of the bacteria by disrupting the cell wall, and this was most likely due to the overproduction of reactive oxygen species induced by chlorogenic acid. Importantly, histopathology analysis indicated that the CSC NPs had limited side effects and high biocompatibility.