Campylobacter jejuni is one of the most common causes of foodborne human gastroenteritis in the developed world. This bacterium colonizes in the ceca of chickens, spreads throughout the poultry production chain, and contaminates poultry products. Despite numerous on farm intervention strategies and developments in post-harvest antimicrobial treatments, C. jejuni is frequently detected on broiler meat products. This indicates that C. jejuni is evolving over time to overcome the stresses/interventions that are present throughout poultry production and processing. The development of aerotolerance has been reported to be a major survival strategy used by C. jejuni in high oxygen environments. Recent studies have indicated that C. jejuni can enter a viable but non-culturable (VBNC) state or develop biofilm in response to environmental stressors such as refrigeration and freezing stress and aerobic stress. This review provides an overview of different stressors that C. jejuni are exposed to throughout the poultry production chain and the genotypic and phenotypic survival mechanisms, with special attention to aerotolerance, biofilm formation, and development of the VBNC state.

The study examined the association between body composition and beverage consumption and the risk of asthma and chronic obstructive pulmonary disease (COPD) and explored the single nucleotide polymorphisms (SNPs) involved in these associations by leveraging summary statistics from genome-wide association studies (GWAS) in nonoverlapping populations. The IEU OpenGWAS project was sourced for exposure datasets: body mass index, body fat percentage, fat-free mass, total body water mass, alcohol intake frequency, and coffee intake, and selected health outcome datasets: asthma and chronic obstructive pulmonary disease. Datasets were assessed and filtered using R, followed by a two-sample Mendelian randomization analysis. The MR Egger, weighted median, inverse variance weighted, simple mode, and weighted mode methods were used to examine the association between exposures and outcomes. Heterogeneity and pleiotropy analyses were used to evaluate the reliability of results. Additionally, SNPnexus was used to ascertain SNPs linked to established phenotypes, while SNP annotation was obtained from the Ensembl BioMart database via the biomaRt package. Genes belonging to overlapping groups were visualized using ComplexHeatmap. Higher body fat percentage (OR = 1.72, 95% CI: 1.23–2.41, p = 0.002), increased BMI (OR = 1.56, CI: 1.23–1.20, p = 2.53 × 10⁻⁴), and more frequent alcohol intake (OR = 1.34, CI: 1.08–1.68, p = 0.009) were associated with elevated COPD risk. Asthma risk was similarly increased with higher body fat percentage (OR = 1.60, CI: 1.23–2.21, p = 0.001), BMI (OR = 1.54, CI: 1.29–1.84, p = 2.23 × 10⁻⁶), fat-free mass (OR = 1.21, CI: 1.02–1.44, p = 0.032), and alcohol intake frequency (OR = 1.19, CI: 1.01–1.40, p = 0.039). Total body water mass and coffee intake were not associated with asthma and COPD. SNP annotation revealed that some genetic variants that influenced the association of the exposure variables with asthma and COPD were missense variants in several genes, including the evolutionarily highly conserved gene, SLC39A8 (rs13107325; C/A/T allele), and POC5 (rs2307111; T/A/C allele), as well as intronic variants in FTO (rs56094641; A/G/T allele) and NRXN3 (rs10146997; A/G allele). The discovery of the missense variants rs13107325 and rs2307111 in SLC39A8 and POC5, respectively, in addition to other intronic and synonymous SNPs suggests that these SNPs may have some roles in the development or progression of asthma and COPD. This may contribute to the identification of molecular signatures or biomarkers that forecast the risk, development, or therapeutic response of chronic lung diseases in persons with metabolic dysregulation, including obesity.

Background: Obesity is a well-documented risk factor for cardiometabolic diseases associated with insulin resistance. However, research on its relationship with alcohol intake and stress markers, such as cortisol and α-amylase, remains limited, particularly among young adults in the general population. Objective: This study investigated the relationship between adiposity measures, alcohol intake, and biological stress biomarkers among college students. Methods: Participants (n = 189) completed the NIH Diet History Questionnaire II. Body composition was measured via bioelectrical impedance analysis. Salivary α-amylase (sAA) activity and cortisol (sCort) were assessed using the Salimetrics α-amylase kinetic enzyme assay and enzyme immunoassay kits, respectively. Multivariable linear regression models were used to determine the association between alcohol consumption and adiposity on biological stress biomarkers. Results: Among students who were overweight and obese, higher alcohol consumption increased sAA activity (β = 1.52, p = 0.030), with a greater effect in females (β = 2.24, p = 0.012). Body fat percentage showed similar patterns with sAA activity (β = 2.20, p = 0.015), with no significant effect in males. There was no significant interaction between BMI or body fat and alcohol consumption on sCort levels. However, significant main effects were observed for African Americans (β = 0.22, p = 0.020) and overweight and obese status (β = −0.19, p = 0.025) on male students’ sCort levels. African Americans (β = 0.21, p = 0.026) and young male adults within the underfat category (β = 0.35, p = 0.022) also exhibited increased sCort levels. Conclusion: Sex-specific patterns in physiological responses between males and females revealed stronger associations in females for sAA activity and distinct patterns in sCort levels among African American males.