Black Currant Nectar Reduces Muscle Damage and Inflammation Following a Bout of High-Intensity Eccentric Contractions.

This investigation determined the efficacy of black currant nectar (BCN) in reducing symptoms of exercise-induced muscle damage (EIMD). Sixteen college students were randomly assigned to drink either 16 oz of BCN or a placebo (PLA) twice a day for eight consecutive days. A bout of eccentric knee extensions (3 × 10 sets @ 115% of 1RM) was performed on the fourth day. Outcome measures included muscle soreness (subjective scale from 0 to 10) and blood markers of muscle damage (creatine kinase, CK), inflammation (interleukin-6, IL-6), and oxygen radical absorbance capacity (ORAC). Although there were no differences in reported soreness between groups, consumption of BCN reduced CK levels at both 48 (PLA = 82.13% vs. BCN = -6.71%, p = .042) and 96 h post exercise (PLA = 74.96% vs. BCN = -12.11%, p = .030). The change in IL-6 was higher in the PLA group (PLA = 8.84% vs. BCN = -6.54%, p = .023) at 24 h post exercise. The change in ORAC levels was higher in the treatment group (BCN = 2.68% vs. PLA = -6.02%, p = .039) at 48 h post exercise. Our results demonstrate that consumption of BCN prior to and after a bout of eccentric exercise attenuates muscle damage and inflammation.

HIV replication in conjunction with granzyme B production by CCR5+ memory CD4 T cells: Implications for bystander cell and tissue pathologies.

Granzyme B (GrzB) is expressed by activated T cells and mediates cellular apoptosis. GrzB also acts as an extracellular protease involved in tissue degradation. We hypothesized that GrzB production from activated memory CD4 T cells may be associated with HIV pathogenesis. We found that stimulated memory CD4 T cells (via costimulation, cytokines, and TLR ligands) concomitantly produced GrzB and HIV. Both GrzB and HIV expression were mainly restricted to CCR5-expressing memory CD4+CD45RO+ T cells, including Th1 and Th17 subsets. Activated memory CD4 T cells also mediated tissue damage, such as disruption of intestinal epithelial monolayers. In non-human primates, CD4 T cells of rhesus macaques (pathogenic SIV hosts) expressed higher GrzB compared to African green monkeys (non-pathogenic SIV hosts). These results suggest that GrzB from CCR5+ memory CD4 T cells may have a role in cellular and tissue pathologies during HIV infection.

Granzyme B- and Fas ligand-mediated cytotoxic function induced by mitogenic CD28 stimulation of human memory CD4+ T cells.

Some human memory CD4(+) T cells have cytotoxic functions best understood in the context of viral infections; however, their possible role in pathologic processes is understudied. The novel discovery that mitogenic CD28 antibodies induced proliferation and expansion of Tregs offered therapeutic promise for autoimmune disorders. However, the failed TGN1412 trial forced reassessment of this concept. As memory CD4(+) T cells are known to produce toxic molecules, including granzyme B (GrzB) and FasL, we wondered whether mitogenic CD28 was able to induce these cytotoxic molecules. A commercially available mitogenic human CD28 mAb (clone ANC28.1) was used to determine whether mitogenic CD28 induces cytotoxic function from human memory CD4(+) T cells. We found that stimulation of memory CD4(+) T cells by ANC28.1, as well as by conventional costimulation (CD3/CD28 mAb), robustly induced enzymatically active GrzB, along with increased surface expression of FasL. These functional phenotypes were induced in association with increased expression of T cell activation markers CD69 and CD25, and elimination of target cells by ANC28.1-activated memory CD4(+) T cells involved both GrzB and FasL. Additionally, ANC28.1-activated memory CD4(+) T cells caused disruption of epithelial cell monolayer integrity, which was partially mediated by GrzB. These findings reveal functions of memory CD4(+) T cells previously unknown to be induced by mitogenic CD28, and suggest that these pathogenic mechanisms may have been responsible for some of the widespread tissue destruction that occurred in the TGN1412 trial recipients.

Knowledge of carbohydrate consumption does not alter natural killer cell activity following an acute bout of high-intensity aerobic exercise.

Carbohydrate consumption during strenuous aerobic exercise reportedly minimizes post-exercise suppression of the innate immune system. One of the most common measurements of innate immunity is natural killer cell activity (NKCA). It is not known whether actual carbohydrate consumption or merely the knowledge of carbohydrate consumption mediates alteration in NKCA. The purpose of the present investigation was to determine if knowledge of carbohydrate beverage could result in alteration of RPE and NKCA, independent of actual carbohydrate intake. We recruited 11 male and female endurance athletes and randomly assigned them to either a correct or false knowledge of carbohydrate intake, such that in the false group, subjects were informed that they were receiving the carbohydrate beverage (CHO), but actually received a placebo (PLA) beverage. CHO and PLA beverages were matched to be similar in taste and appearance. Subjects completed 60 min of cycle ergometry (74% of VO2 peak). Venous blood samples were collected before (PRE), immediately after (POST), and 2 h after (2H) exercise and used to determine plasma glucose concentration, leukocyte total and differential counts, and NKCA. Data were statistically analyzed using a 3-factor analysis of variance (ANOVA) (p < 0.05). We did not find a significant effect of knowledge of drink type on leukocyte count, leukocyte differential, or NKCA. Drink type did not significantly alter leukocyte total, differential counts, or NKCA. There was a significant effect of exercise on NKCA. Knowledge of drink type does not alter innate immunity following exercise as assessed by leukocyte counts and NKCA.

Inflammatory markers are elevated in overweight Mexican-American children.

OBJECTIVE: The purpose of the present study was to determine the effect of body weight on blood lipid profile, insulin resistance and inflammatory biomarkers in Mexican-American children. METHODS: Children (13.3+/-0.1 year) were recruited from a local school and assigned to one of three groups as a volunteer sample: healthy weight (HW) (> or =10th and <85th BMI percentile; n=42), at risk of overweight (RO) (> or =85th and <95th; n =25) or overweight (OW) (> or =95th; n=42). Plasma concentrations of hsCRP, sCD14, sIL-6R, sTNF-alphaR1, sTNF-alphaR2, IL-6 and TNF-alpha were determined by ELISA. RESULTS: OW children had significantly greater plasma concentrations of hsCRP (P =0.003), sCD14 (P =0.013), sIL-6R (P =0.010), sTNF-alphaR1 (P<0.001), sTNF-alphaR2 (P=0.005), insulin (P=0.001), TC:HDL ratio (P<0.001) and triglycerides (P <0.001) than HW children. Also plasma concentrations of hsCRP, sIL-6R and sTNF-alphaR1 were significantly greater in OW compared with RO children. CONCLUSION: Overweight Mexican-American children had a higher concentration of inflammatory biomarkers than healthy weight children. To our knowledge, this is the first study to report that sCD14 is elevated in overweight compared with healthy weight Mexican-American children.