Fine particulate matter 2.5 (PM2.5) exposure leads to the progress of pulmonary disease. It has been reported that N6-methyladenosine (m6A) modification was involved in various biological processes and diseases. However, the critical role of m6A modification in pulmonary disease during PM2.5 exposure remains elusive. Here, we revealed that lung inflammation and mucus production caused by PM2.5 were associated with m6A modification. Both in vivo and in vitro assays demonstrated that PM2.5 exposure elevated the total level of m6A modification as well as the methyltransferase like 3 (METTL3) expression. Integration analysis of m6A RNA immunoprecipitation-seq (meRIP-seq) and RNA-seq discovered that METTL3 up-regulated the expression level and the m6A modification of Interleukin 24 (IL24). Importantly, we explored that the stability of IL24 mRNA was enhanced due to the increased m6A modification. Moreover, the data from qRT-PCR showed that PM2.5 also increased YTH N6-Methyladenosine RNA Binding Protein 1 (YTHDF1) expression, and the up-regulated YTHDF1 augmented IL24 mRNA translation efficiency. Down-regulation of Mettl3 reduced Il24 expression and ameliorated the pulmonary inflammation and mucus secretion in mice exposed to PM2.5. Taken together, our finding provided a comprehensive insight for revealing the significant role of m6A regulators in the lung injury via METTL3/YTHDF1-coupled epitranscriptomal regulation of IL24.

Swift degradation of the coral reef ecosystems urges the need to identify the reef decline drivers. Due to their widespread use, bioaccumulative and toxic characteristics, chlorinated organic compounds, such as chlorinated paraffins (CPs), are regarded as specific pollutants of concern. Yet little is known about the occurrence of CPs in the coral reef ecosystems. This study focuses on the short-chain chlorinated paraffins (SCCPs) and medium-chain chlorinated paraffins (MCCPs). Their distribution and congener pattern were investigated in the water-SPM-sediment system and in the corals of the Larak coral reef for the first time. Chlorinated paraffins were detected in all the coral species. Their total loadings ranged from 42.1 to 178 ng g⁻¹ dw in coral tissue, from 6.0 to 144 ng g⁻¹dw in the skeleton, and from 55.0 to 240 ng g⁻¹dw in zooxanthellae. Soft corals were found to accumulate more CPs than Scleractinian corals. Zooxanthellae and mucus accumulated more CPs than tissue and skeleton. In most cases, congener group patterns were dominated by C₁₃ (for SCCPs) and C₁₇ (MCCPs) groups, respectively. The congener patterns of CPs altered to some extent between mucus and the remaining coral compartments. High loadings of CPs were detected in the skeleton of the bleached corals. Moreover, a significant negative correlation between the levels of CPs and the symbiodinium density was observed.

We investigated physiological responses including calcification, photosynthesis and alterations to polar metabolites, in the scleractinian coral Stylophora pistillata exposed to different concentrations of polyethylene microplastics. Results showed that at high plastic concentrations (50 particles/mL nominal concentration) the photosynthetic efficiency of photosystem II in the coral symbiont was affected after 4 weeks of exposure. Both moderate and high (5 and 50 particles/mL nominal) concentrations of microplastics caused subtle but significant alterations to metabolite profiles of coral, as determined by Nuclear Magnetic Resonance (NMR) spectroscopy. Specifically, exposed corals were found to have increased levels of phosphorylated sugars and pyrimidine nucleobases that make up nucleotides, scyllo-inositol and a region containing overlapping proline and glutamate signals, compared to control animals. Together with the photo-physiological stress response observed and previously published literature, these findings support the hypothesis that microplastics disrupt host-symbiont signaling and that corals respond to this interference by increasing signaling and chemical support to the symbiotic zooxanthellae algae. These findings are also consistent with increased mucus production in corals exposed to microplastics described in previous studies. Considering the importance of coral reefs to marine ecosystems and their sensitivity to anthropogenic stressors, more research is needed to elucidate coral response mechanisms to microplastics under realistic exposure conditions.

Airborne particulate matter (PM) has become a serious health issue causing pulmonary diseases such as asthma. Due to the side effects and non-specificity of conventional drugs, there is a need to develop natural-product-based alternative treatments. Sargassum horneri is a brown alga shown to have anti-oxidant, anti-inflammatory, and anti-allergic effects. Thus, we sought to determine whether ethanol extract of Sargassum horneri (SHE) mitigates the effect of PM exposure on asthma development. To establish a mouse model of asthma, BALB/c mice were sensitized with ovalbumin (OVA, 10 μg) and challenged with PM (5 mg/m³) for 7 days consecutively. SHE (200, 400 mg/kg), Prednisone (5 mg/kg), or PBS was daily administrated orally before PM exposure. SHE mitigated PM exacerbated dendritic cell activation. More importantly, SHE restrained Th2 polarization by attenuating transcription factors GATA3 and STAT5, which further mitigated the expression of Th2 cytokines interleukin (IL)-4, IL-5, and IL-13 in the lung homogenates of PM-exacerbated asthmatic mice. SHE further attenuated PM-exacerbated eosinophil infiltration in the lung, trachea, and BALF. In addition, SHE markedly mitigated the activation of mast cells and the IgE level in serum. Concomitantly, SHE further restrained the Th17 cell response in PM-exposed allergic mice through attenuating expression of transcription factors RORγT, STAT3 and expression of relevant effector cytokines IL-17a. This resulted in mitigated neutrophil infiltration in the lung. Taken together, SHE significantly suppressed PM-exacerbated hypersecretion of mucus in asthmatic mice. These results suggest that SHE has therapeutic potential for treating PM-exacerbated allergic asthma through concomitantly inhibiting Th2/Th17 responses.

F-53B (6:2 chlorinated polyfluorinated ether sulfonate) is currently recognized as a safe alternative to long-chain PFASs in China. However, an increasing number of studies have recently authenticated its biotoxicological effects. In this study, for evaluating the gut toxicity of F-53B in mammals, both female and male mice were orally exposed to 0, 1, 3, or 10 μg/L F-53B for 10 weeks. Our results showed that F-53B significantly accumulated in the colon, ileum and serum when exposed to 10 μg/L F-53B for 10 weeks. F-53B exposure not only increased the transcriptional levels of ion transport-related genes but could also interact with the CFTR protein directly. Interestingly, subchronic F-53B exposure also increased the transcription of mucus secretion-related genes, but the protein level of Muc2 decreased after F-53B exposure, indicating that there was a compensatory phenomenon after mucus barrier injury. Furthermore, F-53B exposure also induced colonic inflammation associated with gut microbiota dysbiosis in the colon. Taken together, our results indicated that the potential gut toxicity of F-53B and almost all of the changed parameters were significantly affected in both female and male mice, suggesting that F-53B could disturb the gut barrier without sex dependence in mice.

Pollution of marine environments with microplastic particles (i.e. plastic fragments <5 mm) has increased rapidly during the last decades. As these particles are mainly of terrestrial origin, coastal ecosystems such as coral reefs are particularly threatened. Recent studies revealed that microplastic ingestion can have adverse effects on marine invertebrates. However, little is known about its effects on small-polyp stony corals that are the main framework builders in coral reefs. The goal of this study is to characterise how different coral species I) respond to microplastic particles and whether the exposure might II) lead to health effects. Therefore, six small-polyp stony coral species belonging to the genera Acropora, Pocillopora, and Porites were exposed to microplastics (polyethylene, size 37–163 μm, concentration ca. 4000 particles L−1) over four weeks, and responses and effects on health were documented.The study showed that the corals responded differentially to microplastics. Cleaning mechanisms (direct interaction, mucus production) but also feeding interactions (i.e. interaction with mesenterial filaments, ingestion, and egestion) were observed. Additionally, passive contact through overgrowth was documented. In five of the six studied species, negative effects on health (i.e. bleaching and tissue necrosis) were reported.We here provide preliminary knowledge about coral-microplastic-interactions. The results call for further investigations of the effects of realistic microplastic concentrations on growth, reproduction, and survival of stony corals. This might lead to a better understanding of resilience capacities in coral reef ecosystems.

Recent studies suggest an association between particulate matter (PM) air pollution and gastrointestinal (GI) disease. In addition to direct deposition, PM can be indirectly deposited in oropharynx via mucociliary clearance and upon swallowing of saliva and mucus. Within the GI tract, PM may alter the GI epithelium and gut microbiome. Our goal was to determine the effect of PM on gut microbiota in a murine model of PM exposure via inhalation. C57BL/6 mice were exposed via inhalation to either concentrated ambient particles or filtered air for 8-h per day, 5-days a week, for a total of 3-weeks. At exposure's end, GI tract tissues and feces were harvested, and gut microbiota was analyzed. Alpha-diversity was modestly altered with increased richness in PM-exposed mice compared to air-exposed mice in some parts of the GI tract. Most importantly, PM-induced alterations in the microbiota were very apparent in beta-diversity comparisons throughout the GI tract and appeared to increase from the proximal to distal parts. Changes in some genera suggest that distinct bacteria may have the capacity to bloom with PM exposure. Exposure to PM alters the microbiota throughout the GI tract which maybe a potential mechanism that explains PM induced inflammation in the GI tract.

4-Nitrophenol (PNP) is a persistent organic pollutant that was proven to be an environmental endocrine disruptor. The aim of this study was to evaluate the role of the estrogen receptor-α (ER-α) and aryl hydrocarbon receptor (AhR) signaling pathway in regulating the damage response to PNP in the small intestine of rats. Wistar-Imamichi male rats (21 d) were randomly divided into two groups: the control group and PNP group. Each group had three processes that were gavaged with PNP or vehicle daily: single dose (1 d), repeated dose (3 consecutive days) (3 d), and repeated dose with recovery (3 consecutive days and 3 recovery days) (6 d). The weight of the body, the related viscera, and small intestine were examined. Histological parameters of the small intestine and the quantity of mucus proteins secreted by small goblet cells were determined using HE staining and PAS staining. The mRNA expression of AhR, ER-α, CYP1A1, and GST was measured by real-time qPCR. In addition, we also analyzed the AhR, ER-α, and CYP1A1 expression in the small intestine by immunohistochemical staining. The small intestines histologically changed in the PNP-treated rat and the expression of AhR, CYP1A1, and GST was increased. While ER-α was significantly decreased in the small intestine, simultaneously, when rats were exposed to a longer PNP treatment, the damages disappeared. Our results demonstrate that PNP has an effect on the expression of AhR signaling pathway genes, AhR, CYP1A1, and GST, and ER-α in the rat small intestine.

Increasing use of metal and metal oxide nanoparticles [Me(O)NPs] in products means many will inevitably find their way into marine systems. Their likely fate here is sedimentation following hetero-aggregation with natural organic matter and/or free anions, putting benthic, sediment-dwelling and filter feeding organisms most at risk. In marine systems, Me(O)NPs can absorb to micro-organisms with potential for trophic transfer following consumption. Filter feeders, especially bivalves, accumulate Me(O)NPs through trapping them in mucus prior to ingestion. Benthic in-fauna may directly ingest sedimented Me(O)NPs. In fish, uptake is principally via the gut following drinking, whilst Me(O)NPs caught in gill mucus may affect respiratory processes and ion transport. Currently, environmentally-realistic Me(O)NP concentrations are unlikely to cause significant adverse acute health problems, however sub-lethal effects e.g. oxidative stresses have been noted in many organisms, often deriving from dissolution of Ag, Cu or Zn ions, and this could result in chronic health impacts.

The effects on the growth of tomato seedlings and cadmium accumulation of earthworm mucus and a solution of amino acids matching those in earthworm mucus was studied through a hydroponic experiment. The experiment included four treatments: 5 mg Cd L⁻¹ (CC), 5 mg Cd L⁻¹ þ 100 mL L⁻¹ earthworm mucus (CE), 5 mg Cd L⁻¹ þ 100 mL L⁻¹ amino acids solution (CA) and the control (CK). Results showed that, compared with CC treatment, either earthworm mucus or amino acids significantly increased tomato seedling growth and Cd accumulation but the increase was much higher in the CE treatment compared with the CA treatment. This may be due to earthworm mucus and amino acids significantly increasing the chlorophyll content, antioxidative enzyme activities, and essential microelement uptake and transport in the tomato seedlings. The much greater increase in the effect of earthworm mucus compared with amino acid treatments may be due to IAA-like substances in earthworm mucus.