In recent years, pollution of antibiotics and heavy metal has often been reported in organic wastes. Saprophytic insects have been recorded as biological control agents in organic waste management. During organic waste conversion, the intestinal bacteria of the saprophytic insects play an important role in digestion, physiology, immunity and prevention of pathogen colonization. Black soldier fly (BSF) Hermetia illucens has been widely used as saprophytic insects and showed tolerance to sulfonamides (SAs) and cadmium (Cd). Diversity and changes in gut microbiota of black soldier fly larvae (BSFL) were evaluated through 16S rRNA high-throughput sequencing, and a decrease in diversity of gut microbiota along with an increase in SAs stress was recorded. Major members identified were Actinomycetaceae, Enterobacteriaceae, and Enterococcaceae. And fourteen multi-resistance Klebsiella pneumoniae strains were isolated. Two strains BSFL7-B-5 (from middle midgut of 7-day BSFL) and BSFL11-C-1 (from posterior midgut of 11-day BSFL) were found to be low-toxic and multi-resistance. The adsorption rate of SAs in 5 mg/kg solutions by these two strains reached 65.2% and 61.6%, respectively. Adsorption rate of Cd in 20 mg/L solutions was 77.2% for BSFL7-B-5. The strain BSFL11-C-1 showed higher than 70% adsorption rates of Cd in 20, 30 and 40 mg/L solutions. This study revealed that the presence of multi-resistance bacterial strains in the gut of BSFL helped the larvae against SAs or Cd stress. After determining how and where they are used, selected BSFL gut bacterial strains might be utilized in managing SAs or Cd contamination at suitable concentrations in the future.

While polychlorinated biphenyl (PCB)-related risks have been reported at the cellular, organ, and individual levels in some marine mammals, studies quantifying the PCB-associated population-level effects are limited. Here, we combined chemical analysis and individual-based model simulation to investigate the impact of PCBs on the Indo-Pacific humpback dolphin (sub)population from the Pearl River Estuary (PRE). An annual PCB accumulation rate of 0.29 ± 0.07 mg/kg lipid per year was estimated based on the measured age-specific male data as males continue to accumulate PCBs throughout their lifetime, without depurating contaminant loads. Using the Taiwan Strait dolphin population with low PCBs as a baseline, we compare our model simulations in PRE population to estimate relative population impacts of PCBs and other stressors. When using the current vital rates of the PRE dolphins which have been affected by PCBs and other stressors (e.g., underwater noise, prey limitation, etc.), our simulations revealed a substantial decline (8.1%) in the annual population growth rate (λ) of PRE metapopulation compared to baseline over the next 100 years. At the estimated PCB accumulation rate, the PCB-mediated effects on calf survival and immunity would cause a slight decline (0.9%) in λ relative to baseline. Our findings suggest a relatively limited impact of PCBs on the long-term survival of PRE dolphins among all stressors. However, it should be noted that even under model simulations where dietary PCBs were eliminated, humpback dolphins would still need a long time to reduce their PCB burdens to a relatively “safe” level through biological cycling. Considering that the baseline vital rates might also have been affected by PCBs and other stressors, our results are considered relative rather than absolute. This study provides a starting point for quantifying population-level consequences of contaminant exposure on humpback dolphins, although more efforts are needed to perfect this type of analysis.

It is necessary to understand the interactions between different pesticides in ecotoxicology because pesticides never appear as individual compounds but rather in combinations with other compounds. In this study, we planned to explicate the combined toxic effect of myclobutanil (MYC) and thiamethoxam (THI) on the zebrafish (Danio rerio) by adopting multiple biomarkers. Results unraveled that the 96-h LC₅₀ values of MYC to D. rerio at various life phases ranged from 5.2 to 10.3 mg L⁻¹, which were lower than those of THI ranging from 147 to 246 mg L⁻¹. Combinations of MYC and THI exhibited synergetic toxicity to zebrafish embryos. The activities of antioxidative enzymes (T-SOD, Cu/Zn-SOD and POD) and detoxification enzyme (GST) were obviously varied in most of the MYC, THI and combined exposures compared to the control. The mRNA expressions of eight genes (Cu-sod, cas3, il-8, cxcl, erα, crh, cyp17 and dio1) involved in antioxidation, apoptosis, immunity and endocrine were obviously altered in the combined exposure of MYC and THI compared to their individual exposures. Our findings hinted the threats when YMC and THI co-existed, which would be beneficial for the risk assessments of pesticide mixtures.

Trichloropropyl phosphate (TCPP) is a halogenated organophosphate ester that is widely used as flame retardants and plasticizers. In this study, gender-specific accumulation and responses in mussel Mytilus galloprovincialis to TCPP exposure were focused and highlighted. After TCPP (100 nmol L⁻¹) exposure for 42 days, male mussels showed similar average bioaccumulation (37.14 ± 6.09 nmol g⁻¹ fat weight (fw)) of TCPP with that in female mussels (32.28 ± 4.49 nmol g⁻¹ fw). Proteomic analysis identified 219 differentially expressed proteins (DEPs) between male and female mussels in control group. There were 52 and 54 DEPs induced by TCPP in male and female mussels, respectively. Interestingly, gender-specific DEPs included 37 and 41 DEPs induced by TCPP in male and female mussels, respectively. The proteomic differences between male and female mussels were related to protein synthesis and degradation, energy metabolism, and functions of cytoskeleton and motor proteins. TCPP influenced protein synthesis, energy metabolism, cytoskeleton functions, immunity, and reproduction in both male and female mussels. Protein-protein interaction (PPI) networks indicated that protein synthesis and energy metabolism were the main biological processes influenced by TCPP. However, DEPs involved in these processes and their interaction patterns were quite different between male and female mussels. Basically, twelve ribosome DEPs which directly or indirectly interacted were found in protein synthesis in TCPP-exposed male mussels, while only 3 ribosome DEPs (not interacted) in TCPP-exposed female mussels. In energy metabolism, only 4 DEPs (with the relatively simple interaction pattern) mainly resided in fatty acid metabolism, butanoate/propanoate metabolism and glucose metabolism were discovered in TCPP-exposed male mussels, and more DEPs (with multiple interactions) functioned in TCA cycle and pyruvate/glyoxylate/dicarboxylate metabolism were found in TCCP-exposed female mussels. Taken together, TCPP induced gender-specific toxicological effects in mussels, which may shed new lights on further understanding the toxicological mechanisms of TCPP in aquatic organisms.

Recently, environmental risk and toxicity of neonicotinoid insecticides to honey bees have attracted extensive attention. However, toxicological understanding of neonicotinoid insecticides on gut microbiota is limited. In the present study, honey bees (Apis mellifera L.) were exposed to a series of nitenpyram for 14 days. Results indicated that nitenpyram exposure decreased the survival and food consumption of honey bees. Furthermore, 16S rRNA gene sequencing revealed that nitenpyram caused significant alterations in the relative abundance of several key gut microbiotas, which contribute to metabolic homeostasis and immunity. Using high-throughput RNA-Seq transcriptomic analysis, we identified a total of 526 differentially expressed genes (DEGs) that were significantly altered between nitenpyram-treated and control honey bee gut, including several genes related to metabolic, detoxification and immunity. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed nitenpyram affected several biological processes, of which most were related to metabolism. Collectively, our study demonstrates that the dysbiosis of gut microbiota in honey bee caused by nitenpyram may influence metabolic homeostasis and immunity of bees, and further decrease food consumption and survival of bees.

Microplastic (MP) pollution is potentially a major threat to many aquatic organisms. Yet we currently know very little about the mechanisms responsible for the effects of small MPs on phenotypes, and the extent to which effects of MPs are modified by genetic and environmental factors. Using a multivariate approach, we studied the effects of 500 nm polystyrene microspheres on the life history and immunity of eight clones of the freshwater cladoceran Daphnia magna reared at two temperatures (18 °C/24 °C). MP exposure altered multivariate phenotypes in half of the clones we studied but had no effect on others. In the clones that were affected, individuals exposed to MPs had smaller offspring at both temperatures, and more offspring at high temperature. Differences in response to MP exposure were unrelated to differences in particle uptake, but were instead linked to an upregulation of haemocytes, particularly at high temperature. The clone-specific, context-dependent nature of our results demonstrates the importance of incorporating genetic variation and environmental context into assessments of the impact of plastic particle exposure. Our results identify immunity as an important mechanism underpinning genetically variable responses to MP pollution and may have major implications for predicting consequences of MP pollution.

Osteoporosis or enhanced bone loss is one of the most commonly occurring bone conditions in the world, responsible for higher incidence of fractures leading to increased morbidity and mortality in adults. Bone loss is affected by various environmental factors including diet, age, drugs, toxins etc. Microcystins are toxins produced by cyanobacteria with microcystin-LR being the most abundantly found around the world effecting both human and animal health. The present study demonstrates that MC-LR treatment induces bone loss and impairs both trabecular and cortical bone microarchitecture along with decreasing the mineral density and heterogeneity of bones in mice. This effect of MC-LR was found due to its immunomodulatory effects on the host immune system, wherein MC-LR skews both T cell (CD4+ and CD8+ T cells) and B cell populations in various lymphoid tissues. MC-LR further was found to significantly enhance the levels of osteoclastogenic cytokines (IL-6, IL-17 and TNF-α) along with simultaneously decreasing the levels of anti-osteoclastogenic cytokines (IL-10 and IFN-γ). Taken together, our study for the first time establishes a direct link between MC-LR intake and enhanced bone loss thereby giving a strong impetus to the naïve field of “osteo-toxicology”, to delineate the effects of various toxins (including cyanotoxins) on bone health.

Tuberculosis (TB) is still a serious public health problem in various countries. One of the long-elusive but critical questions about TB is what the risk factors are and how they contribute for its seasonality. An ecologic study was conducted to examine the association between the variation of outdoor PM2.5 concentration and the TB seasonality based on the monthly TB notification and PM2.5 concentration data of Hong Kong and Beijing. Both descriptive analysis and Poisson regression analysis suggested that the outdoor PM2.5 concentration could be a potential risk factor for the seasonality of TB disease. The significant relationship between the number of TB cases and PM2.5 concentration was not changed when regression models were adjusted by sunshine duration, a potential confounder. The regression analysis showed that a 10 μg/m3 increase in PM2.5 concentrations during winter is significantly associated with a 3% (i.e. 18 and 14 cases for Beijing and Hong Kong, respectively) increase in the number of TB cases notified during the coming spring or summer for both Beijing and Hong Kong. Three potential mechanisms were proposed to explain the significant relationship: (1) increased PM2.5 exposure increases host's susceptibility to TB disease by impairing or modifying the immunology of the human respiratory system; (2) increased indoor activities during high outdoor PM2.5 episodes leads to an increase in human contact and thus the risk of TB transmission; (3) the seasonal change of PM2.5 concentration is correlated with the variation of other potential risk factors of TB seasonality. Preliminary evidence from the analysis of this work favors the first mechanism about the PM2.5 exposure-induced immunity impairment. This work adds new horizons to the explanation of the TB seasonality and improves our understanding of the potential mechanisms affecting TB incidence, which benefits the prevention and control of TB disease.

Ocean acidification may increase the risk of disease outbreaks that would challenge the future persistence of marine organisms if their immune system and capacity to produce vital structures for survival (e.g., byssus threads produced by bivalves) are compromised by acidified seawater. These potential adverse effects may be exacerbated by microplastic pollution, which is forecast to co-occur with ocean acidification in the future. Thus, we evaluated the impact of ocean acidification and microplastics on the health of a mussel species (Mytilus coruscus) by assessing its physiological performance, immunity and byssus properties. We found that ocean acidification and microplastics not only reduced hemocyte concentration and viability due to elevated oxidative stress, but also undermined phagocytic activity of hemocytes due to lowered energy budget of mussels, which was in turn caused by the reduced feeding performance and energy assimilation. Byssus quality (strength and extensibility) and production were also reduced by ocean acidification and microplastics. To increase the chance of survival with these stressors, the mussels prioritized the synthesis of some byssus proteins (Mfp-4 and Mfp-5) to help maintain adhesion to substrata. Nevertheless, our findings suggest that co-occurrence of ocean acidification and microplastic pollution would increase the susceptibility of bivalves to infectious diseases and dislodgement risk, thereby threatening their survival and undermining their ecological contributions to the community.

The homeostasis of gut immunity and microbiota are associated with the health of the gut. Dechlorane 602 (Dec 602) with food web magnification potential has been detected in daily food. People who were orally exposed to Dec 602 may encounter increased risk of health problems in the gut. In order to reveal the influence of short-term exposure of Dec 602 on gut immunity and microbiota, adult female C57BL/6 mice were administered orally with Dec 602 (low/high doses: 1.0/10.0 μg/kg body weight per day) for 7 days. Lymphocytes were examined by flow cytometry. Gut microbiota was measured by 16S rRNA gene sequencing. Results showed that fecal IgA was upregulated after exposure to the high dose of Dec 602, suggesting that there might be inflammation in the gut. Then, changes of immune cells in mesenteric lymph nodes and colonic lamina propria were examined. We found that exposure to the high dose of Dec 602 decreased the percentages of the anti-inflammatory T regulatory cells in mesenteric lymph nodes. In colonic lamina propria, the production of gut protective cytokine interleukin-22 by CD4⁺ T cells was decreased, and a decreased trend of interleukin-22 production was also observed in type 3 innate lymphoid cells in the high dose group. Furthermore, an altered microbiota composition toward inflammation in the gut was observed after exposure to Dec 602. Additionally, the altered microbiota correlated with changes of immune parameters, suggesting that there were interactions between influenced microbiota and immune parameters after exposure to Dec 602. Taken together, short-term exposure to Dec 602 induced gut immunity and microbiota perturbations, and this might be the mechanisms for Dec 602 to elicit inflammation in the gut.