Production rate estimation of mycosporine-like amino acids in two Arctic melt ponds by stable isotope probing with NAH(13) CO3.

The net carbon uptake rate and net production rate of mycosporine-like amino acids (MAAs) were measured in phytoplankton from 2 different melt ponds (MPs; closed and open type pond) in the western Arctic Ocean using a (13) C stable isotope tracer technique. The Research Vessel Araon visited ice-covered western-central basins situated at 82°N and 173°E in the summer of 2012, when Arctic sea ice declined to a record minimum. The average net carbon uptake rate of the phytoplankton in polycarbonate (PC) bottles in the closed MP was 3.24 mg C · m(-3) · h(-1) (SD = ±1.12 mg C · m(-3) · h(-1) ), while that in the open MP was 1.3 mg C · m(-3) · h(-1) (SD = ±0.05 mg C · m(-3) · h(-1) ). The net production rate of total MAAs in incubated PC bottles was highest (1.44 (SD = ±0.24) ng C · L(-1) · h(-1) ) in the open MP and lowest (0.05 (SD = ±0.003) ng C · L(-1) · h(-1) ) in the closed MP. The net production rate of shinorine and palythine in incubated PC bottles at the open MP presented significantly high values 0.76 (SD = ±0.12) ng C · L(-1) · h(-1) and 0.53 (SD = ±0.06) ng C · L(-1) · h(-1) . Our results showed that high net production rate of MAAs in the open MP was enhanced by a combination of osmotic and UVR stress and that in situ net production rates of individual MAA can be determined using (13) C tracer in MPs in Arctic sea ice.

Lactobacillus helveticus HY7801 ameliorates vulvovaginal candidiasis in mice by inhibiting fungal growth and NF-κB activation.

The anti-inflammatory effects of hydrogen peroxide-producing lactic acid bacteria (LAB) against Candida albicans-induced vulvovaginal candidiasis in ß-estradiol-immunosuppressed mice were examined. Oral and intravaginal treatment with these LABs significantly decreased the level of viable C. albicans within the vaginal cavity as well as the quantitated myeloperoxidase activity in the vaginal tissues when compared with control untreated mice. Out of all of the LABs tested, Lactobacillus helveticus HY7801 (LH) most potently inhibited vulvovaginal candidiasis. LH also inhibited the expression of the pro-inflammatory cytokines including TNF-α, IL-1ß and IL-6, and inflammatory enzymes, COX-2 and iNOS, as well as the activation of NF-κB. However, the addition of LH led to an increase in IL-10 cytokine expression in the vaginal tissues. In addition, the decrease of Lactobacillaceae and the increase of Pasteurellaceae caused by treatment with C. albicans were reversed with oral and intravaginal administration of LH, suggesting a potential shift in the vaginal microflora present. Addition of LH was toxic to C. albicans in vitro when cultured with HeLa cells. Oral administration of LH inhibited lipopolysaccharide (LPS)-induced TNF-α and IL-1ß expressions in ß-estradiol-immunosuppressed mice but reversed the expression of anti-inflammatory cytokine IL-10 in comparison to levels observed in the normal control group. LH also inhibited the expression of the pro-inflammatory cytokines, TNF-α and IL-1ß, and the activation of NF-κB in LPS-stimulated peritoneal macrophages. Based on these findings, LH may ameliorate vulvovaginal candidiasis by suppressing the NF-κB pathway, as well as through inhibition of the growth of C. albicans.

Lactobacillus johnsonii HY7042 ameliorates Gardnerella vaginalis-induced vaginosis by killing Gardnerella vaginalis and inhibiting NF-κB activation.

Hydrogen peroxide-producing lactic acid bacteria (LAB) were isolated from women's vaginas and their anti-inflammatory effects against Gardnerella vaginalis-induced vaginosis were examined in ß-estradiol-immunosuppressed mice. Oral and intravaginal treatment with five LABs significantly decreased viable G. vaginalis numbers in vaginal cavities and myeloperoxidase activity in mouse vaginal tissues. Of the LABs examined, Lactobacillus johnsonii HY7042 (LJ) most potently inhibited G. vaginalis-induced vaginosis. This LAB also inhibited the expressions of IL-1ß, IL-6, TNF-α, COX-2, and iNOS, and the activation of NF-κB in vaginal tissues, but increased IL-10 expression. Orally administered LJ (0.2×10(8) CFU/mouse) also inhibited the expression of TNF-α by 91.7% in ß-estradiol-immunosuppressed mice intraperitoneally injected with LPS. However, it increased IL-10 expression by 63.3% in these mice. Furthermore, LJ inhibited the expressions of the pro-inflammatory cytokines, TNF-α and IL-1ß, and the activation of NF-κB in lipopolysaccharide-stimulated peritoneal macrophages. LJ also killed G. vaginalis attached with and without HeLa cells. These findings suggest that LJ inhibits bacterial vaginosis by inhibiting the expressions of COX-2, iNOS, IL-1ß, and TNF-α by regulating NF-κB activation and by killing G. vaginalis, and that LJ could ameliorate bacterial vaginosis.