Cadmium (Cd) is a highly toxic metal that is distributed worldwide. Exposure to it is correlated with a vast number of diseases and organism malfunctions. Exopolysaccharides (EPS) derived from Lactiplantibacillus plantarum BGAN8, EPS-AN8, previously showed great potential for the in vitro protection of intestinal cells from this metal. Here, we investigated the potential of food supplemented with EPS-AN8 to protect rats from the hazardous effects of Cd exposure. After thirty days of exposure to lower (5 ppm) and higher (50 ppm)-Cd doses, the administration of EPS-AN8 led to decreased Cd content in the kidneys, liver, and blood compared to only Cd-treated groups, whereas the fecal Cd content was strongly enriched. In addition, EPS-AN8 reversed Cd-provoked effects on the most significant parameters of oxidative stress (MDA, CAT, GST, and GSH) and inflammation (IL-1β, TNF-α, and IFN-γ) in the duodenum. Moreover, micrographs of the duodenum were in line with these findings. As the gut microbiota has an important role in maintaining homeostasis, we used 16S rRNA amplicon sequencing and investigated the effects of Cd and EPS-AN8 on one part of the microbiota presented in the duodenum. Although Cd decreased the growth of lactobacilli and mostly favored the blooming of opportunistic pathogen bacteria, parallel intake of EPS-AN8 reversed those changes. Therefore, our results imply that EPS-AN8 might be extremely noteworthy in combatting this toxic environmental pollutant.

The skin is a direct target of the air pollutant benzo[a]pyrene (BaP). While its carcinogenic qualities are well-studied, the immunotoxicity of BaP after dermal exposure is less understood. This study examines the immunomodulatory effects of a 10-day epicutaneous BaP application, in environmentally/occupationally relevant doses, by analyzing ex vivo skin immune response (skin explant, epidermal cells and draining lymph node/DLN cell activity), alongside the skin’s reaction to sensitization with experimental hapten dinitrochlorobenzene (DNCB). The results show that BaP application disrupts the structure of the epidermal layer and promotes immune cell infiltration in the dermis. BaP exposure led to oxidative stress in epidermal cells, characterized by decreased reduced glutathione and increased AHR and Cyp1A1 expression. Production and gene expression of proinflammatory cytokines (TNF, IL-1β) by epidermal cells decreased, while IL-10 response increased. Decreased spontaneous production of IFN-γ and IL-17, along with unchanged IL-10, was observed in DLC cells, whereas ConA-stimulated production of these cytokines was elevated. Local immunosuppression caused by BaP application seems to reduce the skin’s response to an additional stimulus, evidenced by decreased effector activity of DLN cells three days after sensitization with DNCB. These findings provide new insight into the immunomodulatory effects and health risks associated with skin exposure to BaP.

Although obesity and metabolic syndrome (comprising at least three of the following traits—abdominal obesity, elevated blood pressure, triglycerides and glucose/insulin resistance, and reduced high-density lipoprotein cholesterol in serum) are known to impact immune system activity, these conditions are often not considered when immune response characteristics are investigated in various rodent strains. In this work, metabolic syndrome indices are compared in 3 month-old (young) and 6 month-old (adult) rats of Dark Agouti (DA) and Albino Oxford (AO) strains, while parameters of coagulation, inflammation and oxidative stress were determined in young animals. Study reveals that both young and adult AO rats are obese, intolerant to glucose with higher levels of triglycerides and lower levels of high-density lipoprotein cholesterol when compared to age-matched DA rats. Parameters of coagulation, inflammation and oxidative stress that may contribute to the worsening of metabolic syndrome during aging are also higher in young AO rats. Metabolic syndrome observed in young and intensified in adult AO rats should be taken into consideration when analyzing alterations in immune reactivity during aging in this rat strain.

Background: Antibiotic-associated gut dysbiosis affects lung health and contributes to disease progression, but the individual response to antibiotics, which leads to host-specific reactions to the same respiratory insult, is not fully understood. Methods: Before infection with Aspergillus fumigatus, Albino Oxford (AO) and Dark Agouti (DA) rats received a mixture of antibiotics with poor systemic absorption to induce microbial perturbation only in the gut, and lung and gut tissue and colonic contents were analyzed. Results: Treatment with antibiotics induced gut inflammation in both rat strains, which was more pronounced in AO rats, and a disturbance in lung immunity was observed only in DA rats. Antibiotic-associated gut microbiota disturbance revealed rat strain-specific bacterial profiles (increased Gammaproteobacteria in DA and decreased Coriobacteriia in AO rats). Although gut dysbiosis increased the risk of lung A. fumigatus infection in both rat strains, a higher fungal burden was detected in the lungs of AO rats, whereas lymph node cell activation and lung tissue inflammation were observed in DA rats. Conclusions: Rat strain differences in response to antibiotic- and/or infection-induced gut dysbiosis suggest that basal gut microbiota may influence the lung immune response during A. fumigatus disease, highlighting the importance of the interplay of genotype-specific host gut microbial community with the environmental constraints in shaping individual immune makeup.