Tumor-infiltrating immune cells (TIICs) play essential roles in cancer development and progression. However, the association of TIICs with prognosis in colorectal cancer (CRC) patients remains elusive. Infiltration of TIICs was assessed using ssGSEA and CIBERSORT tools. The association of TIICs with prognosis was analyzed in 1,802 CRC data downloaded from the GEO (https://www.ncbi.nlm.nih.gov/geo/) and TCGA (https://portal.gdc.cancer.gov/) databases. Three populations of TIICs, including CD66b+ tumor-associated neutrophils (TANs), FoxP3+ Tregs, and CD163+ tumor-associated macrophages (TAMs) were selected for immunohistochemistry (IHC) validation analysis in 1,008 CRC biopsies, and their influence on clinical features and prognosis of CRC patients was analyzed. Prognostic models were constructed based on the training cohort (359 patients). The models were further tested and verified in testing (249 patients) and validation cohorts (400 patients). Based on ssGSEA and CIBERSORT analysis, the correlation between TIICs and CRC prognosis was inconsistent in different datasets. Moreover, the results with disease-free survival (DFS) and overall survival (OS) data in the same dataset also differed. The high abundance of TIICs found by ssGSEA or CIBERSORT tools can be used for prognostic evaluation effectively. IHC results showed that TANs, Tregs, TAMs were significantly correlated with prognosis in CRC patients and were independent prognostic factors (P_DFS ≤ 0.001; P_OS ≤ 0.023). The prognostic predictive models were constructed based on the numbers of TANs, Tregs, TAMs (C-index_DFS&OS = 0.86; AIC_DFS = 448.43; AIC_OS = 184.30) and they were more reliable than traditional indicators for evaluating prognosis in CRC patients. Besides, TIICs may affect the response to chemotherapy. In conclusion, TIICs were correlated with clinical features and prognosis in patients with CRC and thus can be used as markers.

The purpose of this study was to evaluate burn-related variations of inflammation and immunity. Fifty-five mice were divided randomly into sham burn and burn groups. Eighty-seven hospitalized burn patients were also reviewed. In mice, neutrophils and monocytes were elevated significantly on post burn day (PBD 1). Lymphocytes were reduced on PBDs 1 and 3. Levels of serum tumor necrosis factor-α and interleukin-6 were highest on PBD 1. Interleukin-1β levels were the highest on PBD 3. On PBD 3, CD4+CD25+T regulatory cells/CD4+ cells in spleen were higher. On PBDs 1, 3, 7, and 14, percentage of splenic dendritic cells were significantly lower than the sham burn group. In patients, neutrophils and monocytes were significantly elevated on PBD 1. Levels declined but remained elevated at most days to PBD 7. Lymphocytes in burn groups 1 and 2 were reduced on PBDs 1 and 3, respectively. Our results exhibited that severe burn injury initiated a hyperinflammatory response and immunosuppression. PBDs 1 to 3 were important for changes in inflammation and immunosuppression.

Background: Although inflammation is a known predictor for poor prognosis in patients with diabetics, few data report the synergistic association between inflammation, malnutrition, and mortality in patients with diabetics. We aim to explore whether malnutrition modifies the predictor of inflammation on prognosis.Methods: Nutritional status and inflammation were measured in 6,682 patients with diabetics undergoing coronary angiography or percutaneous coronary intervention between January 2007 to December 2018 from Cardiorenal Improvement Registry. Malnutrition was defined as Controlling Nutritional Status (CONUT) score, which was more than 1. High-sensitivity C-reactive protein (hs-CRP) exceeding the median was assessed as a high-risk inflammation. Cox regression models were used to estimate hazard ratios (HR) for mortality across combined hs-CRP and CONUT score categories.Results: During a median follow-up of 5.0 years (interquartile range: 3.0–7.6 years), 759 (11.36%) patients died. The mortality of the four groups (normal nutrition and low hs-CRP level; normal nutrition and high hs-CRP level; malnutrition and low hs-CRP level; and malnutrition and high hs-CRP level) were 7.29, 7.12, 10.71, and 17.31%, respectively. Compared with normal nutrition and low hs-CRP level, an isolated condition of either malnutrition or high hs-CRP level was not associated with any significant risk for all-cause mortality. However, concomitant presence of both high hs-CRP level and malnutrition condition was associated with a significantly increased risk of all-cause mortality (HR: 1.51; 95% CI: 1.20–1.89; p < 0.001). The p-value for interaction between nutritional status and hs-CRP level on all-cause mortality was 0.03.Conclusion: The interplay of inflammation and malnutrition in patients with diabetics significantly amplifies the deleterious effects of each as distinct disease entities. A prospective randomized clinical trial is needed in the future to verify the results.

This study aimed to clarify the role and mechanism of tetrahedral framework nucleic acids (tFNAs) in regulating M2 macrophages to reduce intestinal injury. An intestinal injury model was established by intraperitoneal injection of lipopolysaccharides (LPS) in mice to explore the alleviating effects of tFNAs on intestinal injury. Inflammatory factors were detected by quantitative polymerase chain reaction (qPCR) and enzyme‐linked immunosorbent assay (ELISA). The intestinal barrier and permeability were assessed using western blotting and immunohistochemistry. Macrophages in the gut were localised and quantified using immunofluorescence. Western blotting was used to investigate the role and mechanism of tFNAs in regulating macrophages and alleviating inflammation in the injured intestines. These results show that tFNAs attenuated sepsis‐induced intestinal injury. tFNAs can also promote the intestinal barrier reconstruction and reduce intestinal permeability. In vivo, tFNAs accelerated the aggregation of M2 macrophages at an early stage of injury and reduced the number of M1 macrophages in the intestine. In addition, tFNAs enhanced the clearance ability of intestinal macrophages. They activated the signalling and transcription activating factor 1(STAT1) and cytokine signalling inhibitory factor 1/3 (SOCS1/3) pathways by increasing the expression of the phagocytic receptor Mertk. These findings indicated that tFNAs can alleviate sepsis‐induced intestinal injury by regulating M2 macrophages, providing a new option for treating intestinal injury.