Novel non-invasive broad-spectrum infrared treatment of ulcerative colitis by modulating T cell relocation

Novel non-invasive broad-spectrum infrared treatment of ulcerative colitis by modulating T cell relocation | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL Energy & Environmental Materials This is a preprint and has not been peer reviewed. Data may be preliminary. 24 February 2026 V1 Latest version Share on Novel non-invasive broad-spectrum infrared treatment of ulcerative colitis by modulating T cell relocation Authors : Siyu CHEN 0009-0002-8159-6004 [email protected] , Jiangtao Zhao , Bohan Jia , Zhigang Ren 0000-0003-0798-3444 , Ranran Sun , Liwen Liu , Ding Zhang , … Show All … , Yanqiu Fu , Jia Yu , Shen Shen , Fujun Miao , Zaimei Huang , Ruixia Guo 0000-0002-8847-2488 , Peng Zhang , Zujiang Yu , and Guosheng Shao 0000-0003-1498-7929 Show Fewer Authors Info & Affiliations https://doi.org/10.22541/au.177195977.75346549/v1 239 views 98 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Ulcerative colitis (UC) is an incurable inflammatory bowel disease characterized by chronic mucosal inflammation, with a continuously increasing global prevalence. Although infrared (IR) therapy has demonstrated anti-inflammatory potential, conventional devices which can only emit single-wavelength IR often exhibit limited tissue penetration and suboptimal spectral overlap with mammalian absorption. Herein, we develop a broad-spectrum IR (BSIR) device enabled with an almost defect-free graphene (DFG) based radiator to deliver high output IR aligned with mammalian IR absorption spectra. In a mouse model of UC, BSIR treatment significantly alleviated disease symptoms and promoted mucosal recovery. Crucially, this study shows that BSIR radiation induces the relocation of T lymphocytes to the spleen, leading to reduced immune cell infiltration and inflammation in the colon. Gene expression analysis further reveals enhanced innate immune activity and cell regeneration in colonic tissue. Collectively, these findings demonstrate that BSIR represents a safe, non-invasive therapeutic strategy for UC. More broadly, this study highlights spectrum-matched IR irradiation as a novel modality for immune modulation, with potential translational relevance for other deep-tissue inflammatory diseases. 1. Introduction Ulcerative colitis (UC) is a chronic inflammatory disorder with rising global prevalence, imposing an increasing healthcare burden worldwide (Figure S1). [1-3] Despite advances in understanding its multifactorial etiology, including environmental triggers, genetic susceptibility, and aberrant immune activation, current therapeutic strategies remain largely dependent on systemic immunosuppression. [4, 5] These pharmacological treatments are noncurative and are frequently associated with significant adverse effects, impaired host defense, and considerable economic burden. [6-8] These limitations underscore the urgent need for safe, non-pharmacological approaches capable of restoring immune homeostasis without broadly compromising systemic immunity. Recent advances in bio-interactive energy materials have sparked growing interest in non-invasive physical therapy for immune disorder. [9-11] Among these, infrared (IR) radiation, particularly near-IR, has demonstrated therapeutic potential in inflammatory and autoimmune diseases through photobiomodulation (PBM). [12-15] However, conventional near-IR technologies are predominantly based on semiconductor emitters with fixed band gaps, resulting in monochromatic near-infrared light. [16] Such spectral constraints inherently limit tissue penetration efficiency, thereby largely restricting their therapeutic applications to superficial or dermatological conditions. [17-20] Moreover, short-wavelength lights tend to be absorbed or diffusely scattered/reflected by semiconducting molecules or solid particles, further compromises energy delivery to deeper tissues. These intrinsic limitations highlight the need for broadband, spectrally tunable IR sources that can overcome semiconductor band-gap constraints and enable more effective deep tissue modulation. To overcome these limitations, we developed an innovative broad-spectrum infrared (BSIR) generator capable of emitting high output IR radiation across a wide spectral range (1–24 µm), covering near-, mid-, and far-infrared regions. This device is constructed from DFG crystals that preserve the intrinsic Dirac energy band structure, characterized by linear energy momentum dispersion and near zero direct bandgap characteristics. Such unique electronic properties enable continuous spectrum emission. Importantly, the emission spectrum of BSIR substantially overlaps with the intrinsic infrared radiation window of human biological tissues (approximately 1.33-16.67 µm), which corresponds to the endogenous thermal emission range shaped through long-term biological adaptation. This spectral concordance may contribute to enhanced biocompatibility and underlie both its therapeutic efficacy and safety. Using a dextran sulfate sodium (DSS)-induced mouse model of UC, we demonstrate that BSIR radiation significantly alleviates disease severity and accelerates mucosal recovery. Mechanistically, BSIR modulates systemic immune cell trafficking by promoting the redistribution of T lymphocytes toward the spleen, thereby reducing inflammatory infiltration in the colon. By bridging advanced energy material engineering with inflammatory disease therapy, this work establishes BSIR as a safe, effective, and economically favorable strategy with translational potential for UC and other deep tissue immune-mediated disorders. 2. Results and Discussions 2.1. The high output BSIR radiator based on DFG. The BSIR radiator was fabricated by coating DFG onto the inner surface of fused-silica tubes using a facile slurry-coating strategy. [21] Raman spectroscopy confirmed the high crystalline quality of the graphene, as evidenced by a negligible D peak together with a sharp, symmetric and intense 2D peak (Figure 1A) , indicative of an almost defect-free few-layer crystalline structure. Transmission electron microscopy (TEM) revealed remarkably transparent graphene film (Figure 1B) with clearly resolved three-layer feature at high resolution (Figure 1C). Figure 1D shows the IR emission spectra of the graphene tube at different applied voltages. The graphene radiator exhibits broad IR emission, and the intensity and spectral distribution were continuously tunable. Increasing electric power results in enhanced emission intensity accompanied by a blue shift of the peak wavelength. Figure 1E displays the time evolution of apparent temperature for graphene radiator under different voltages. The apparent temperature rapidly reached stable saturation at each power input until the heating power was turned off, demonstrating the rapid electrothermal response and stable radiative performance. Compared with conventional carbon-fiber and halogenated tungsten tube heaters, the graphene-coated radiator exhibited markedly higher emission intensity and improved heating efficiency under identical power and operating voltage conditions (Figure 1F, Figure S2A and 2B). These results demonstrate that the graphene-coated BSIR radiator represents a tunable, cost-effective and large-area - platform for the generation of high-flux of broadband infrared radiation. 2.2. BSIR radiation reduces the incidence of DSS-induced UC UC was induced by providing mice with 2.5% dextran sulfate sodium (DSS). [22] Body weight, body temperature, and fecal blood were monitored every two days (Figure 2A). Infrared irradiation was applied at 550 W for 60 minutes twice daily. These parameters were selected to achieve high radiation flux while avoiding considerable thermal effects on body temperature (Figure S3A). Compared with the normal control (NC) group, DSS-treated mice exhibited significant weight loss, with marked differences observed on Day 8 and Day 10. In contrast, mice receiving DSS + IR showed only a slight decrease in body weight on Day 8 and no significant difference by Day 10 (Figure 2B). Consistently, the disease activity index (DAI) was significantly reduced in the DSS + IR group relative to the DSS group (Figure 2C). At study termination, colonic pathology was assessed, including colon length, mucosal edema, lymphocyte infiltration, and epithelial continuity (Figure 2D). Colon shortening was evident in DSS-treated mice, whereas colon length was largely preserved in the DSS + IR group (Figure 2E). Histological and quantitative analyses demonstrated reduced lymphocyte infiltration (Figure 2F and 2G) and submucosal edema (Figure 2H and 2I) in DSS + IR mice compared with DSS controls. Immunohistochemical (IHC) analysis further revealed improved epithelial integrity and reduced inflammatory signaling. Expression of epithelial cell adhesion molecule (Epcam), a marker of epithelial tight junctions, was better preserved in the DSS + IR group (Figure 2J). [23] Additionally, the inflammatory transcription factor NF-κB was downregulated following IR treatment (Figure 2K), indicating suppression of inflammatory activation. [24] Together, these results provide evidences that BSIR radiation treatment can significantly prevent DSS-induced UC (Figure 2L). 2.3. BSIR radiation accelerates recovery from DSS-induced UC by promoting basal cells generation and reducing inflammation To further explore the therapeutic effects of IR on UC, DSS-induced mouse model was established (Figure 3A). By Day 6, both DSS and IR after DSS groups exhibited significant weight loss compared with NC, with no difference between the two groups, confirming equivalent disease induction (validated by H&E staining, Figure S3B). After DSS withdrawal, body weight continued to decline transiently before gradual recovery. Notably, mice receiving BSIR treatment during the recovery phase demonstrated significantly greater weight regain by Days 16 and 18 compared with DSS controls (Figure 3B), accompanied by a marked reduction in disease activity index (Figure 3C). Histological analysis revealed reduced inflammatory cell infiltration in BSIR treated mice compared with DSS controls (Figure 3E and 3F), despite partial intestinal narrowing persisting in both groups (Figure 3D). IHC staining demonstrated increased Ki-67 expression (a cell proliferation marker) in the BSIR treated group (Figure 3G and 3H), indicating enhanced basal cell proliferation. Consistently, improved epithelial continuity (Epcam, Figure 3I) and decreased NF-κB expression (Figure 3J) suggest coordinated epithelial regeneration and suppression of inflammatory signaling (Figure 3K). These observations are consistent with prior studies reporting that near-infrared irradiation enhances tissue repair and wound healing through modulation of cellular proliferation and inflammatory responses. [25, 26] 2.4. BSIR radiation induces reversible white pulp enlargement in the spleen through T cell homing Given that BSIR radiation both prevents colitis onset and accelerates recovery, its systemic impact was further examined. Serological analyses and H&E staining showed no significant structural or functional alterations in major visceral organs following BSIR treatment (Figure S4A–F), indicating BSIR systemic safety. Interestingly, histological examination revealed a significant increase in splenic white pulp volume after two weeks of BSIR exposure (Figure 4A and 4B). This expansion plateaued after three weeks (Figure S5A) and returned to baseline one week following cessation of IBSIR treatment (Figure S5B and 5C), indicating that the IBSIR induced immune modulation is reversible. To determine the cellular basis of white pulp enlargement, IHC analyses were performed using markers for T cells (CD3), B cells (CD19), and macrophages (CD86, CD168). White pulp expansion was primarily associated with accumulation of CD3-positive T cells (Figure 4C and 4D), whereas no significant changes were observed in B cell or macrophage populations (Figure S5D-5G). Immunofluorescence (IF) confirmed pronounced aggregation of CD3-positive T cells within the enlarged white pulp (Figure 4E and 4F). To distinguish between local proliferation and peripheral recruitment, co-localization analysis of CD3 and Ki-67 was conducted. Accumulated T cells exhibited minimal proliferative activity (Figure 4G), suggesting that white pulp expansion was not driven by in situ proliferation. Moreover, expression of lymphocyte homing associated factors CCR5 and CD18 was significantly upregulated (Figure 4H, P = 0.0072 and P = 0.0305), supporting enhanced recruitment from circulation. [27, 28] Peripheral blood analysis further revealed increased white blood cell counts, particularly neutrophils and lymphocytes (Figure S5H), while relative lymphocyte proportions declined (Figure 4I), consistent with trafficking toward secondary lymphoid organs. Interestingly, DSS-induced colitis also resulted in splenic white pulp enlargement (Figure S5I); however, in this context, T cells exhibited clear proliferative activity, as indicated by Ki-67 co-localization (Figure S5J). These findings indicate that BSIR induced white pulp expansion is mechanistically distinct from inflammation driven splenic activation and is characterized by reversible T cell homing rather than pathological proliferation. 2.5. BSIR treatment reduces T cell infiltration and promotes basal cell proliferation in the colon Given the observed accumulation of T cells in the spleen following IR exposure, their distribution within the colon was subsequently examined. Histological analysis revealed markedly reduced immune cell infiltration in the colon of BSIR treated mice compared with controls (Figure 5A). Consistently, IHC demonstrated a significant decrease in CD3-positive T cells in the BSIR group (Figure 5B and 5C, P < 0.0001). IF analysis further confirmed reduced CD3-positive cell density within the colon (Figure 5D and 5E, P = 0.0032), indicating attenuated T cell infiltration following infrared treatment. Interestingly, colonic CD3-positive T cells in both control and BSIR treated groups exhibited detectable proliferative activity (Figure S5K), whereas splenic T cells showed minimal Ki-67 co-localization. This organ specific difference indicates that T cells adopt distinct functional states across tissues, underscoring the importance of tissue localization in shaping immune cell function. Together, these findings support the concept that targeting immune cell trafficking is a promising therapeutic strategy for inflammatory bowel disease. [29] Moreover, BSIR treatment significantly enhanced basal cell proliferation in the colon. Increased Ki-67 expression was observed in the BSIR treated group by both IHC and IF analyses (Figure 5F-5I). Given the critical role of basal epithelial cells in mucosal regeneration, their activation likely contributes to improved barrier restoration and tissue repair. Collectively, these findings indicate that BSIR radiation simultaneously suppresses colonic T cell infiltration while promoting epithelial regeneration, reinforcing its immunomodulatory and pro-regenerative effects. [30] 2.6. BSIR radiation reshapes innate immune signaling and metabolic programs in the colon To further elucidate the molecular mechanisms underlying BSIR mediated immune modulation and epithelial regeneration, transcriptomic and metabolomic analyses were performed on colonic tissues from control and BSIR treated mice. Although global gene expression profiles remained largely stable (Figure S6A), BSIR exposure resulted in 134 upregulated and 94 downregulated genes (Figure 6A), indicating targeted transcriptional reprogramming rather than widespread perturbation. Gene Ontology (GO) enrichment analysis revealed significant modulation of pathways related to GTP-binding, extracellular matrix organization, and immune responses (Figure 6B). Upregulated genes were predominantly enriched in innate immune activation and GTP binding, whereas downregulated genes were associated with cell adhesion processes (Figure 6C, Figure S6B and 6C). Gene Set Enrichment Analysis (GSEA) further demonstrated coordinated activation of innate immune signaling and ribosome-associated protein synthesis, accompanied by suppression of membrane and intercellular adhesion pathways (Figure 6D). Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway analysis supported these findings, highlighting enrichment in cytokine–cytokine receptor interactions, and protein digestion and absorption pathways (Figure S6D). GSEA-KEGG further confirmed enhanced antigen presentation and translational activity (Figure S6E), indicating simultaneous activation of immune surveillance and biosynthetic capacity. Protein–protein interaction (PPI) network analysis identified TNF-α and STAT1 as central hubs (Figure 6E), both of which play established roles in immune regulation and proliferation. [31, 32] Interestingly, despite previous reports suggesting IBSIR induced ATP production, metabolomics revealed no increase in ATP levels (Figure 6F). [33, 34] Instead, significant elevations were observed in NAD⁺ and fructose-1,6-bisphosphate ( Figure 6F, Figure S6F). Given the established roles of NAD⁺ in Wnt/β-catenin signaling and SIRT-mediated regulation of epithelial renewal, these findings suggest that BSIR induced regeneration may be mediated through metabolic reprogramming rather than direct enhancement of ATP synthesis. [35, 36] 3. Conclusion Broad-spectrum infrared radiation (BSIR) enabled by graphene-based emitters effectively prevents and ameliorates DSS-induced ulcerative colitis in mice. BSIR exposure induces systemic redistribution of T lymphocytes, characterized by reduced colonic infiltration and reversible accumulation within splenic white pulp, indicating modulation of immune cell trafficking rather than global immunosuppression. Transcriptomic and metabolomic analyses further demonstrate coordinated activation of innate immune signaling and protein biosynthesis, accompanied by suppression of intercellular adhesion pathways, suggesting functional remodeling of the mucosal immune microenvironment. Despite these findings, the present study is limited to an acute colitis model. Long-term safety and therapeutic efficacy in chronic or relapsing inflammatory conditions require further investigation, and the molecular mechanisms governing T cell redistribution require deeper mechanistic elucidation. Future studies should also evaluate the applicability of BSIR in other immune mediated diseases. Collectively, these results establish graphene-enabled BSIR as a non-invasive, safe, and cost-efficient immunomodulatory approach with significant translational potential for ulcerative colitis and other deep-tissue inflammatory disorders. Its intrinsic spectral alignment with endogenous human infrared emission further underscores its physiological compatibility and therapeutic potential. 4. Experimental Section Characterizations The graphene microstructures were characterized by field-emission scanning electron microscopy (SEM, ZEISS SIGMA 500) and transmission electron microscopy (TEM, FEI Tecnai G20). Raman spectroscopy was conducted using a LabRAM HR Evolution instrument with a laser wavelength of 532 nm. The infrared emission spectra were acquired using a Fourier transform infrared (FTIR) spectrometer (Nicolet iS50, Thermo Fisher Scientific) over the wavelength range of 1.3–24.95 μm. The tubes under test were driven by a direct-current power source under ambient conditions. The surface temperature was monitored using an infrared thermal camera (Fluke Ti10). The emissivity was calibrated in the camera settings to ensure accurate temperature determination. Animal Experiment Female C57BL/6 mice, six weeks old and weighing 20 ± 2 g, were obtained from the Skebes Biotechnology (Henan). The mice were housed under standard laboratory conditions with a 12-hour light/dark cycle and had free access to food and water. After a three-day acclimatization period, the mice were randomly assigned to different groups. The DSS groups were administered 2.5% DSS, prepared by dissolving 25 g of DSS powder in 1 L of sterile water, via oral administration in drinking water. Euthanasia was performed by isoflurane inhalation followed by cervical dislocation in accordance with institutional animal care guidelines. Post-mortem, colon and other organs were collected for further analysis. Animal studies were approved by the Animal Research Ethics Committee of Henan Shuangyun Biotechnology Co.,Ltd. All animal experiments were strictly implemented in compliance with the NIH Guide for the Care and Use of Laboratory Animals. Assessment of Disease Activity Index (DAI) Clinical progression of ulcerative colitis was assessed every two days throughout the experiment using the Disease Activity Index (DAI), which is based on changes in body weight, stool consistency, and rectal bleeding. The DAI scoring criteria were as follows: Body weight loss: 0 (no loss), 1 (1-5%), 2 (5-10%), 3 (10-20%), 4 (>20%); Stool consistency: 0 (normal), 2 (loose stool), 4 (diarrhea); Bleeding: 0 (no blood), 1 (Hemoccult positive), 2 (Hemoccult positive with visible bleeding), 4 (gross bleeding around the anus). Hematoxylin and Eosin (H&E) Staining Colon tissues were fixed in 10% neutral-buffered formalin for 24 hours, dehydrated, embedded in paraffin, sectioned at 5 μm thickness, and mounted on slides. The sections were deparaffinized using xylene in two rounds of 20 minutes each, followed by rehydration through a graded ethanol series (100%, 95%, 90%, 80%, and 70%) and a final rinse in distilled water. Hematoxylin staining was carried out for 5 minutes to visualize nuclei, after which the sections were rinsed with running water. Differentiation was performed using 1% hydrochloric acid ethanol solution for 2-5 seconds to remove excess stain from the cytoplasm, followed by a rinse in water. Bluing was achieved by immersing sections in 0.5% ammonia water for 30 seconds and then rinsing with water for 5 minutes. The sections were then stained with eosin for 5 minutes, providing contrast for cytoplasmic components. After staining, the sections were dehydrated through graded ethanol, cleared with two rounds of xylene, briefly air-dried, and mounted with neutral resin. Stained sections were capturing by the Olympus CX21 (Japan). For IHC, tissue fixation, sectioning, and rehydration were performed as described in the H&E protocol. Antigen retrieval was carried out by heating the sections in 0.01M citrate buffer (pH 6.0) in a microwave for 10 minutes, followed by cooling to room temperature. To quench endogenous peroxidase activity, sections were incubated with 3% hydrogen peroxide for 15 minutes and then rinsed with PBS. To block non-specific binding, 10% goat serum was applied for 30 minutes. Primary antibodies were added and incubated overnight at 4°C. The next day, after washing, sections were incubated with an HRP-conjugated secondary antibody (1:200, ZSGB-Bio,China) for 30 minutes. For color development, DAB (Cell Signaling Technology, MA) was applied, and the reaction was closely monitored under a microscope to ensure optimal brown staining of positive signals. Nuclear counterstaining was performed with hematoxylin before the sections were dehydrated, cleared in xylene, and mounted with neutral gum. Brown staining indicated positive antigen expression, and the intensity and percentage of positive cells were evaluated for statistical analysis. Immunofluorescent staining Tissues were processed similarly to the H&E staining protocol for fixation, deparaffinization, and rehydration. Following rehydration, sections were permeabilized with 0.1% Triton-X 100 (Solarbio, Shanghai, China) for 5 minutes. Afterward, blocking was performed using 10% normal goat serum in PBST for 1 hour at room temperature. Primary antibodies were then incubated at 4°C overnight, followed by the appropriate secondary antibodies (servicebio, China) for 30 minutes at room temperature. After washing with PBST, the nuclei were stained with DAPI (servicebio, China) for 10 minutes at room temperature. Fluorescent images were captured using a Zeiss Axio microscope (3DHISTECH, Hungary). Detailed information on the antibodies used in this study is provided in Table S. Blood specimen analysis Whole blood specimens were allowed to stand at room temperature for 2 hours, then centrifuged at 3000 rpm for 15 minutes at 4℃ to collect the supernatant. Biochemical analysis of serum samples was performed using the Chemray 240 automatic biochemical analyzer from Wuhan Servicebio Technology Co., Ltd., and hematological analysis was conducted with the veterinary-use Mindray BC-2800vet automatic hematology analyzer. Quantitative Real-Time PCR (qRT-PCR) Total RNA was extracted from colon tissues using Trizol reagent (Thermo Scientific). The RNA was reverse-transcribed to cDNA using an RNA reverse transcription kit according to the manufacturer’s instructions (Roche, Switzerland). qRT-PCR was performed with SYBR QPCR mixture using a LightCycler 96 (Roche, Switzerland) connect Real-time System. The amplification protocol included an initial denaturation step at 95 °C for 2 minutes, followed by 40 cycles at 95 °C for 15 seconds and 60 °C for 30 seconds. Primer sequences are listed in Supplementary Table. Relative gene expression was quantified using the 2 (−ΔΔCt) method. Bulk RNA Sequencing and Analysis Total RNA extraction was performed using Trizol reagent (Invitrogen Life Technologies). RNA purity and concentration were assessed using a NanoDrop spectrophotometer (Thermo Scientific) and Qubit 4.0, while integrity was verified with the Agilent 2100/4200 system. For library preparation, 3 µg of RNA was utilized. mRNA was isolated using poly-T oligo-attached magnetic beads, then fragmented under high temperatures with divalent cations. First-strand cDNA synthesis was initiated with random hexamers, and second-strand synthesis used buffer, dNTPs, RNase H, and DNA polymerase I. The double-stranded cDNA was subjected to end repair and the addition of an ’A’ base to the 3’ end. Purification and fragment selection were performed with Hieff NGS® DNA Selection Beads, followed by PCR amplification. The target region library was denatured, cycled, and digested to produce single-stranded circular DNA, which was amplified via rolling circle amplification (RCA) to create DNA nano balls (DNBs). Final library quantification was performed using Qubit. Sequencing was executed on a DNBSEQ-T7 with a PE150 model at Bioyi Biotechnology Co., Ltd. (Wuhan, China). Sequencing data were converted to FASTQ format and filtered with fastp (v0.21.0) to obtain high-quality clean data. Cleaned reads were aligned to the reference genome using HISAT2 (v2.1.0). Gene expression was quantified with StringTie (v2.1.5) and normalized with FPKM. Differential expression analysis was conducted using DESeq2 (v1.30.1) with criteria of |log2FoldChange| > 1 and padj ≤ 0.05. Bidirectional clustering for visualizing gene expression patterns was performed using R’s Pheatmap (1.0.8). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed with ClusterProfiler (v3.18.1), identifying significant terms and pathways (padj ≤ 0.05). Gene Set Enrichment Analysis (GSEA) was executed with ClusterProfiler (v3.8.1), focusing on pathways with p-values < 0.05. The top 20 enriched terms and pathways were visualized with bar and bubble charts, and the top 10 GSEA results were displayed as a network map. Protein-protein interactions were analyzed using STRING, mapping the top 100 interactions. Mass Spectrometry For sample preparation, tissues were thawed on ice and mixed with 80% methanol/water. After vortexing at 2500 rpm for 2 minutes, the samples underwent three freeze-thaw cycles by freezing in liquid nitrogen for 5 minutes and thawing on ice for 5 minutes. Following centrifugation at 12,000 rpm for 10 minutes at 4°C, the supernatant was stored at -20°C for 30 minutes, then re-centrifuged for LC-MS analysis. An Ultra Performance Liquid Chromatography (UPLC) system coupled with a QTRAP® 6500+ mass spectrometer was used, employing an ACQUITY UPLC BEH Amide column. The mobile phases consisted of 10 mM ammonium acetate in water (A) and 90% acetonitrile/water (B). The flow rate was set to 0.40 mL/min, and a gradient elution was performed. Mass spectrometry was conducted with Electrospray Ionization (ESI) in both positive and negative modes, using optimized conditions for detecting ion pairs. Statistical Analysis Results are presented as standard error of the difference (SED). To assess statistical differences between groups, data were analyzed using GraphPad Prism version 10.0 (GraphPad Software, USA). An unpaired two-tailed Student’s t-test was employed for comparisons between two groups. A p-value of less than 0.05 was considered indicative of statistically significant differences. Supporting Information Supporting Information is available from the Wiley Online Library or from the author. Acknowledgements This work was supported by the National Natural Science Foundation of China (Nos. 52472110, U2004172, and 51972287), the Central Plains Science and Technology Innovation Leading Talents Program (No. 254000510052), the National Natural Science Foundation of Henan Province (No. 242300421008), the Program for Science and Technology Innovation Talents in Universities of Henan Province (No. 23HASTIT001), the Joint Construction Project of the Henan Medical Science and Technology Tackling Plan (No. LHGJ20240270), and the China Postdoctoral Science Foundation (No.2025 M771969) References 1. Burisch, J., et al., Lancet Gastroenterol Hepatol 2023, 8, 458-4922. Kaplan, G.G., Nat Rev Gastroenterol Hepatol 2015, 12, 720-73. Coward, S., et al., J Can Assoc Gastroenterol 2023, 6, S9-s154. Du, L. and C. Ha, Gastroenterol Clin North Am 2020, 49, 643-6545. Calvez, V., et al., Biomedicines 2025, 136. Wangchuk, P., K. Yeshi, and A. Loukas, Trends Pharmacol Sci 2024, 45, 892-9037. 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Imai, S., et al., Nature 2000, 403, 795-800 Competing interests The authors declare that they have no competing interests. Data Availability The RNA-seq data are being deposited in the NCBI Sequence Read Archive (SRA). All data needed to evaluate the conclusions in the paper are present in the paper and the Supplementary Materials. Information & Authors Information Version history V1 Version 1 24 February 2026 Copyright This work is licensed under a Non Exclusive No Reuse License. Collection Energy & Environmental Materials Keywords graphene materials immune modulation infrared therapy ulcerative colitis Authors Affiliations Siyu CHEN 0009-0002-8159-6004 [email protected] The First Affiliated Hospital of Zhengzhou University View all articles by this author Jiangtao Zhao Zhengzhou University View all articles by this author Bohan Jia The First Affiliated Hospital of Zhengzhou University View all articles by this author Zhigang Ren 0000-0003-0798-3444 The First Affiliated Hospital of Zhengzhou University View all articles by this author Ranran Sun The First Affiliated Hospital of Zhengzhou University View all articles by this author Liwen Liu The First Affiliated Hospital of Zhengzhou University View all articles by this author Ding Zhang The First Affiliated Hospital of Zhengzhou University View all articles by this author Yanqiu Fu The First Affiliated Hospital of Zhengzhou University View all articles by this author Jia Yu The First Affiliated Hospital of Zhengzhou University View all articles by this author Shen Shen The First Affiliated Hospital of Zhengzhou University View all articles by this author Fujun Miao Zhengzhou University View all articles by this author Zaimei Huang Zhengzhou University View all articles by this author Ruixia Guo 0000-0002-8847-2488 The First Affiliated Hospital of Zhengzhou University View all articles by this author Peng Zhang Zhengzhou University View all articles by this author Zujiang Yu The First Affiliated Hospital of Zhengzhou University View all articles by this author Guosheng Shao 0000-0003-1498-7929 Zhengzhou University View all articles by this author Metrics & Citations Metrics Article Usage 239 views 98 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Siyu CHEN, Jiangtao Zhao, Bohan Jia, et al. 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