1.
High-Dose Probiotic Supplementation Containing Lactobacillus casei for 7 Days Does Not Enhance Salivary Antimicrobial Protein Responses to Exertional Heat Stress Compared With Placebo.
Gill, SK, Teixeira, AM, Rosado, F, Cox, M, Costa, RJ
International journal of sport nutrition and exercise metabolism. 2016;(2):150-60
Abstract
The study aimed to determine whether high-dose probiotic supplementation containing Lactobacillus casei (L. casei) for 7 consecutive days enhances salivary antimicrobial protein (S-AMP) responses to exertional-heat stress (EHS). Eight endurance-trained male volunteers (age 26 ± 6 years, nude body mass 70.2 ± 8.8 kg, height 1.75 ± 0.05 m, VO2max 59 ± 5 ml·kg-1·min-1 [M ± SD]) completed a blinded randomized and counterbalanced crossover design. Oral supplementation of the probiotic beverage (PRO; L. casei . 1011 colony-forming units·day-1) or placebo (PLA) was consumed for 7 consecutive days before 2 hr running exercise at 60% VO2max in hot ambient conditions (34.0° C and 32% RH). Body mass and unstimulated saliva and venous blood samples were collected at baseline (7 days before EHS), pre-EHS, post-EHS (1 hr, 2 hr, and 4 hr), and at 24 hr. Saliva samples were analyzed for salivary (S) IgA, α-amylase, lysozyme, and cortisol. Plasma samples were analyzed for plasma osmolality. Body mass and plasma osmolality did not differ between trials. Saliva flow rate remained relatively constant throughout the experimental design in PRO (overall M ± SD = 601 ± 284 μl/min) and PLA (557 ± 296 μl/min). PRO did not induce significant changes in resting S-AMP responses compared with PLA (p > .05). Increases in S-IgA, S-α-amylase, and S-cortisol responses, but not S-lysozyme responses, were observed after EHS (p < .05). No main effects of trial or Time x Trial interaction were observed for S-AMP and S-cortisol responses. Supplementation of a probiotic beverage containing L. casei for 7 days before EHS does not provide any further oral-respiratory mucosal immune protection, with respect to S-AMP, over PLA.
2.
A cross sectional analysis of the role of the antimicrobial peptide cathelicidin in lung function impairment within the ALIVE cohort.
Lambert, AA, Kirk, GD, Astemborski, J, Neptune, ER, Mehta, SH, Wise, RA, Drummond, MB
PloS one. 2014;(4):e95099
Abstract
BACKGROUND Vitamin D deficiency is associated with reduced lung function. Cathelicidin, an antimicrobial peptide regulated by vitamin D, plays a role within the innate immune system. The association of cathelicidin with lung function decrement and respiratory infection is undefined. We determined the independent relationship of cathelicidin with lung function. METHODS In a cross-sectional analysis of 650 participants in an urban observational cohort with high smoking prevalence, plasma 25(OH)-vitamin D and cathelicidin levels were measured from stored samples obtained within 6 months of spirometry study visits. Multivariable linear regression was used to determine the independent association between low cathelicidin (defined as the lowest quartile of the cohort) and absolute forced expiratory volume in 1 second (FEV1). RESULTS The mean age of the cohort was 49 years; 91% were black, 35% female and 41% HIV-infected. Participants with low cathelicidin had a 183 mL lower FEV1 compared to higher cathelicidin (p = 0.009); this relationship was maintained (115 ml lower; p = 0.035) after adjusting for demographics, BMI, and smoking. Neither HIV serostatus, heavy smoking history, nor 25(OH)-vitamin D levels were associated with cathelicidin levels. Participants with low cathelicidin had a greater prevalence of prior bacterial pneumonia (21% versus 14%; p = 0.047). Inclusion of pneumonia in adjusted models did not substantially reduce the FEV1 decrement observed with low cathelicidin (104 mL lower FEV1; p = 0.05). Lung function decrements associated with low cathelicidin were greatest among individuals with lower 25(OH)-vitamin D levels. CONCLUSIONS In a cohort at risk for airflow obstruction, low cathelicidin was independently associated with lower FEV1. These clinical data support a mechanistic link between 25(OH)-vitamin D deficiency and lung function impairment, independent of pneumonia risk.