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Purpose To investigate the transcriptome of human bronchial epithelial cells (HBEC) in response to serum from patients with different degrees of inflammation. Methods Serum from 19 COVID-19 patients obtained from the Hannover Unified Biobank was used. At the time of sampling, 5 patients had a WHO Clinical Progression Scale (WHO-CPS) score of 9 (severe illness). The remaining 14 patients had a WHO-CPS of below 9 (range 1–7), and lower illness. Multiplex immunoassay was used to assess serum inflammatory markers. The culture medium of HBEC was supplemented with 2% of the patient’s serum, and the cells were cultured at 37 °C, 5% CO 2 for 18 h. Subsequently, cellular RNA was used for RNA-Seq. Results Patients with scores below 9 had significantly lower albumin and serum levels of E-selectin, IL-8, and MCP-1 than patients with scores of 9. Principal component analysis based on 500 “core genes” of RNA-seq segregated cells into two subsets: exposed to serum from 4 (I) and 15 (II) patients. Cells from a subset (I) treated with serum from 4 patients with a score of 9 showed 5566 differentially expressed genes of which 2793 were up- and 2773 downregulated in comparison with cells of subset II treated with serum from 14 patients with scores between 1 and 7 and one with score = 9. In subset I cells, a higher expression of TLR4 and CXCL8 but a lower CDH1 , ACE2 , and HMOX1 , and greater effects on genes involved in metabolic regulation, cytoskeletal organization, and kinase activity pathways were observed. Conclusion This simple model could be useful to characterize patient serum and epithelial cell properties.

Diffuse Large B-Cell Lymphoma (DLBCL) is a heterogeneous malignancy with distinct Germinal Center B-Cell Like (GCB) and non-GCB subtypes. Accurate subtyping is crucial due to differences in prognosis and treatment response. While gene expression profiling is the gold standard, it is often unavailable in low-resource settings. Inflammatory and nutritional biomarkers such as Systemic Immune-Inflammation Index (SII), Prognostic Nutritional Index (PNI), and Advanced Lung Cancer Inflammation Index (ALI) offer a practical alternative. This study aims to evaluate their diagnostic potential in early-stage DLBCL subtypes. A cross-sectional analysis was conducted on 60 early stage DLBCL patients (30 GCB, 30 non-GCB) at Dr Hasan Sadikin General Hospital Bandung. Clinical characteristics, hematological parameters, and inflammation-based indices (SII, PNI, and ALI) were evaluated. Differences between subtypes were analyzed using the Mann-Whitney -test, and Receiver Operating Characteristic (ROC) analysis was used to determine diagnostic performance. The median SII was significantly higher in non-GCB compared with GCB (982,575; IQR: 609,112-2,239,917 vs 575,598; IQR: 454,578-886,426, p = 0.014). Conversely, PNI was higher in GCB compared to non-GCB group (49.18; IQR: 46.38-56.38 vs 45.96; IQR 40.05-52.28, p = 0.011). ALI values were also higher in the GCB than non-GCB (44.14; IQR: 27.69-67.18 vs 24.51; IQR: 14.34-42.47,p=0.003). ROC analysis revealed that ALI had the highest diagnostic accuracy (AUC = 0.724; 95% CI: 0.593-0.831), followed by SII (AUC = 0.685, 95% CI: 0.552-0.799) and PNI (AUC = 0.691 95% CI: 0.558-0.804). Optimal cut-off values were ≤1,234,133 for SII, >43.27 for PNI, and >27.41 for ALI. ALI demonstrated the best balance between sensitivity (76.7%) and specificity (63.3%), making it the most reliable marker for distinguishing DLBCL subtypes. SII, PNI, and ALI differ significantly between DLBCL subtypes. These findings suggest that integrating these indices into a diagnostic model could enhance risk stratification and guide therapeutic decision-making in DLBCL. Further studies with larger cohorts are warranted to validate these findings.

Extracellular vesicles (EVs) have been reported to facilitate cytokine storm, coagulation, vascular dysfunction, and the spread of the virus in COVID-19. The direct role of circulating EVs from severe COVID-19 patients in lung injury remains unrecognized. Our study demonstrated that plasma EVs obtained from severe COVID-19 patients induced lung inflammation and polarization of alveolar macrophages in vivo . In vitro experiments also revealed the proinflammatory effects of COVID-19 EVs. The present study sheds fresh insight into the mechanisms of COVID-19-induced lung injury, highlighting EVs as a potential therapeutic target in combating the disease.

Lung infection can evoke pulmonary and systemic inflammation, which is associated with systemic severe symptoms, such as skeletal muscle wasting. While N-chlorotaurine (also known as taurine chloramine; TauCl) has anti-inflammatory effects in cells, its effects against pulmonary and systemic inflammation after lung infection has not been elucidated. In the present study, we evaluated the anti-inflammatory effect of the taurine derivative, TauCl against Escherichia coli-derived lipopolysaccharide (LPS)-induced pneumonia in obese mice maintained on a high fat diet. In this study, TauCl was injected intraperitoneally 1 h before intratracheal LPS administration. While body weight was decreased by 7.5% after LPS administration, TauCl treatment suppressed body weight loss. TauCl also attenuated the increase in lung weight due to lung edema. While LPS-induced acute pneumonia caused an increase in cytokine/chemokine mRNA expression, including that of IL-1β, -6, TNF-α, MCP-1, TauCl treatment attenuated IL-6, and TNF-alpha expression, but not IL-1β and MCP-1. TauCl treatment partly attenuated the elevation of the serum cytokines. Furthermore, TauCl treatment alleviated skeletal muscle wasting. Importantly, LPS-induced expression of Atrogin-1, MuRF1 and IκB, direct or indirect targets for NFκB, were suppressed by TauCl treatment. These findings suggest that intraperitoneal TauCl treatment attenuates acute pneumonia-related pulmonary and systemic inflammation, including muscle wasting, in vivo.

In the neonatal lung, exposure to both prenatal and early postnatal risk factors converge into the development of injury and ultimately chronic disease, also known as bronchopulmonary dysplasia (BPD). The focus of many studies has been the characteristic inflammatory responses provoked by these exposures. Here, we review the relationship between immaturity and prenatal conditions, as well as postnatal exposure to mechanical ventilation and oxygen toxicity, with the imbalance of pro- and anti-inflammatory regulatory networks. In these conditions, cytokine release, protease activity, and sustained presence of innate immune cells in the lung result in pathologic processes contributing to lung injury. We highlight the recruitment and function of myeloid innate immune cells, in particular, neutrophils and monocyte/macrophages in the BPD lung in human patients and animal models. We also discuss dissimilarities between the infant and adult immune system as a basis for the development of novel therapeutic strategies.

Inflammation is an essential mechanism of various diseases. The development and resolution of inflammation are complex immune-modulation processes which induce the involvement of various types of immune cells. Specialized pro-resolving lipid mediators (SPMs) have been demonstrated to be signaling molecules in inflammation. SPMs are involved in the pathophysiology of different diseases, especially respiratory diseases, including asthma, pneumonia, and chronic obstructive pulmonary disease. All of these diseases are related to the inflammatory response and its persistence. Therefore, a deeper understanding of the mechanisms and development of inflammation in respiratory disease, and the roles of the SPM family in the resolution process, might be useful in the quest for novel therapies and preventive measures for pulmonary diseases.

Background： An acute respiratory distress syndrome （ARDS） is still one of the major challenges in critically ill patients. This study aimed to investigate the effect of inhibiting c-Jun N-terminal kinase （JNK） on ARDS in a lipopolysaccharide （LPS）-induced ARDS rat model. Methods： Thirty-six rats were randomized into three groups： control, LPS, and LPS ＋ JNK inhibitor Rats were sacrificed 8 h alter LPS treatment. The lung edema was observed by measuring the wet-to-dry weight （W/D） ratio of the lung. The severity of ptdmonary inflammation was observed by measuring myeloperoxidase （MPO） activity of lung tissue. Moreover, the neutrophils in bronchoalveolar lavage fluid （BALF） were cotinted to observe the airway inflammation. In addition, lung collagen accumulation was quantified by Sircol Collagen Assay. At the same time, the pulmonary histologic examination was perlbrmed, and lung injury score was achieved in all three groups. Results： MPO activity in lung tissue was found increased in rats treated with LPS comparing with that in control （I.26 ＋ 0.15 U in LPS vs. 0.77 ± 0.27 U in control, P 〈 0.05）. Inhibiting ,INK attenuated LPS-induced MPO activity upregulation （0.52 ± 0. 12 U in LPS ＋ JNK inhibitor vs. 1.26 ± 0.15 U in LPS, P 〈 0.05）. Neutrophils in BALF were also found to be increased with LPS treatment, and inhibiting ,INK attenuated LPS-induced neutrophils increase in BALF （255.0 ± 164.4 in LPS vs. 53 （44.5-103） in control vs. 127.0 ± 44.3 in LPS JNK inhibitor, P 〈 0.05）. At the same time, the lung injury score showed a reduction in LPS ＋ JNK inhibitor group comparing with that in LPS group （ 13.42 ± 4.82 vs. 7.00 ± 1.83, P 0.001 ）. However, the lung W/D ratio and the collagen in BALF did not show any difl＇erences between LPS and LPS ＋ JNK inhibitor group.Conclusions： Inhibiting JNK alleviated LPS-induced acute lung inflammation and had no effects on pulmonary edema and fibrosis..INK inhibitor might be a potential therapeutic medication in ARDS, in the context of reducing lung inflammatory.

Background Dysbiosis of the gut microbiome is involved in the pathogenesis of various diseases, but the contribution of gut microbes to the progression of chronic obstructive pulmonary disease (COPD) is still poorly understood. Methods We carried out 16S rRNA gene sequencing and short-chain fatty acid analyses in stool samples from a cohort of 73 healthy controls, 67 patients with COPD of GOLD stages I and II severity, and 32 patients with COPD of GOLD stages III and IV severity. Fecal microbiota from the three groups were then inoculated into recipient mice for a total of 14 times in 28 days to induce pulmonary changes. Furthermore, fecal microbiota from the three groups were inoculated into mice exposed to smoke from biomass fuel to induce COPD-like changes. Results We observed that the gut microbiome of COPD patients varied from that of healthy controls and was characterized by a distinct overall microbial diversity and composition, a Prevotella -dominated gut enterotype and lower levels of short-chain fatty acids. After 28 days of fecal transplantation from COPD patients, recipient mice exhibited elevated lung inflammation. Moreover, when mice were under both fecal transplantation and biomass fuel smoke exposure for a total of 20 weeks, accelerated declines in lung function, severe emphysematous changes, airway remodeling and mucus hypersecretion were observed. Conclusion These data demonstrate that altered gut microbiota in COPD patients is associated with disease progression in mice model.

Background Changes in systemic inflammation, nutritional status and serum vitamin D level are important characteristics of asthma. However, role and importance of nutritional inflammatory indicators or serum vitamin D concentrations in predicting the prognosis of asthma remain unclear. The advanced lung cancer inflammation index (ALI), based on body mass index (BMI), serum albumin and neutrophil–lymphocyte ratio (NLR), is a comprehensive index to assess systemic inflammation and nutrition. This study aimed to evaluate their independent and combined predictive value of mortality in asthma patients. Methods This study analyzed data from the National Health and Nutrition Examination Survey (NHANES) 2001–2018. Cox regression analysis was used to assess the independent or joint effect of ALI and serum vitamin D on mortality risks of asthma. Receiver operator characteristic curve analysis was used to compare the prognostic ability of ALI with its component factors, including NLR, albumin, neutrophil, lymphocyte and BMI. Results A total of 2870 eligible asthma patients were included. After adjustment, higher ALI correlated significantly with reduced all-cause and respiratory disease mortality (adjusted hazard ratio [aHR] = 0.64 and 0.34; P  < 0.05). Meanwhile, vitamin D deficiency correlated significantly with increased all-cause and respiratory disease mortality (aHR = 2.06 and 2.73; P  < 0.05). The area under the curve of ALI in predicting 1-year, 5-year or 10-year all-cause mortality surpassed that of its five component indices. Joint analyses showed that individuals with higher levels of ALI and vitamin D had the lowest risks of all-cause and respiratory disease mortality (aHR = 0.31 and 0.17; P  < 0.05). Conclusions ALI and serum vitamin D are robust independent and combined predictors of mortality in asthma patients. ALI offers superior predictive capability over its components, and sufficient vitamin D levels are beneficial for survival outcomes. The synergistic effect of high ALI and adequate vitamin D highlights the benefit of integrating both metrics into clinical practice for enhanced prognostic accuracy.

The recent exposure of novel coronavirus strain, severe acute respiratory syndrome (SARS-CoV-2) has spread to different countries at an alarming rate. Faster transmission rate and genetic modifications have provoked scientists to search for an immediate solution. With an increasing death rate, it becomes important to throw some light on the life cycle of the virus and its associated pathogenesis in the form of lung inflammation through cytokine storm (CS) production. This paper highlights the different stages of viral-mediated inflammatory responses in the host respiratory system. Previously, known anti-inflammatory drugs and therapeutic strategies that might show potential in controlling the CS of Coronavirus disease-2019 (COVID-19) is also mentioned in this study. Our critical analysis provides insights into the inflammation cycle induced in the lungs by early virus replication, downregulation and shedding of angiotensin-converting enzyme 2 (ACE2), and in the CS production. Identification of suitable targets within the inflammatory pathways for devising the therapeutic strategies useful in controlling the prognosis of COVID-19 finds a special mention in this article. However, antibody-dependent enhancement is the key aspect to consider before testing any drug/compound for therapeutic purposes. Our in-depth analysis would provide similarities and differences between the inflammatory responses induced by SARS-CoV and SARS-CoV-2, providing an excellent avenue to further look at how earlier outbreaks of coronaviruses were controlled and where new steps are required?