Uptake Of Strains Research Articles

Targeting of DC-SIGN on Human Dendritic Cells by Minor Fimbriated Porphyromonas gingivalis Strains Elicits a Distinct Effector T Cell Response

The oral mucosal pathogen Porphyromonas gingivalis expresses at least two adhesins: the 67-kDa mfa-1 (minor) fimbriae and the 41-kDa fimA (major) fimbriae. In periodontal disease, P. gingivalis associates in situ with dermal dendritic cells (DCs), many of which express DC-SIGN (DC-specific ICAM-3 grabbing nonintegrin; CD209). The cellular receptors present on DCs that are involved in the uptake of minor/major fimbriated P. gingivalis, along with the effector immune response induced, are presently unclear. In this study, stably transfected human DC-SIGN(+/-) Raji cell lines and monocyte-derived DCs (MoDCs) were pulsed with whole, live, wild-type Pg381 or isogenic major (DPG-3)-, minor (MFI)-, or double fimbriae (MFB)-deficient mutant P. gingivalis strains. The influence of blocking Abs, carbohydrates, full-length glycosylated HIV-1 gp120 envelope protein, and cytochalasin D on the uptake of strains and on the immune responses was determined in vitro. We show that the binding of minor fimbriated P. gingivalis strains to Raji cells and MoDCs is dependent on DC-SIGN, whereas the double fimbriae mutant strain does not bind. Binding to DC-SIGN on MoDCs is followed by the internalization of P. gingivalis into DC-SIGN-rich intracellular compartments, and MoDCs secrete low levels of inflammatory cytokines and remain relatively immature. Blocking DC-SIGN with HIV-1 gp120 prevents the uptake of minor fimbriated strains and deregulates the expression of inflammatory cytokines. Moreover, MoDCs promote a Th2 or Th1 effector response, depending on whether they are pulsed with minor or major fimbriated P. gingivalis strains, respectively, suggesting distinct immunomodulatory roles for the two adhesins of P. gingivalis.

The Correlation Between Cu2+ Resistance and Cu2+ Uptake in Strains of Yeasts and Moulds

ABSTRACTThe sensitivity of eighteen yeast and mould strains to Cu2+ was examined in correlation with the Cu2+ uptake and the pH changes during their growth. The tested strains were classified into three groups: sensitive, sub-tolerant and tolerant microorganisms. The increase in resistance of acid—producing strains to Cu2+ was associated with the decrease in metal uptake by microbial cells.

High-affinity glucose transport in Saccharomyces cerevisiae is under general glucose repression control.

Saccharomyces cerevisiae mutants defective in growth on low glucose concentration (lgn mutants) were isolated and screened for abnormal glucose transport. Nine complementation groups were identified, falling into two broad groups: those unable to significantly derepress high-affinity (low-Km) glucose uptake (lgn1, lgn4, lgn5, lgn7, and lgn8), and those with elevated repressed levels of high-affinity uptake that either derepress to normal or near normal levels of high-affinity uptake with loss of low-affinity transport (lgn2 and lgn3) or derepress only slightly, appearing to have an intermediate yet constitutive level of high-affinity transport (lgn6 and lgn9). Further analysis of the lgn mutations revealed pleiotropic phenotypes most consistent with the true defect being in regulation or expression of glucose repression and derepression. The kinetics of glucose uptake in strains carrying known mutations preventing derepression of glucose-repressible functions (snf1, snf2, snf4, and snf6) demonstrated that three of these mutations (snf1, snf4, and snf6) were similarly defective in derepression of high-affinity glucose uptake. The snf2 and snf5 mutations had no apparent effect on glucose uptake. Two mutations resulting in constitutive expression of glucose-repressible functions, cid1 and reg1, resulted in constitutive expression of high-affinity glucose uptake. These data support the conclusion that high-affinity glucose uptake in Saccharomyces cerevisiae is under general glucose repression control. The implications of other properties of these mutants are discussed.

Phagocytosis and intracellular killing of coagulase-negative staphylococci

The phagocytosis and intracellular killing of different coagulase-negative staphylococcal species by polymorphonuclear (PMN) leukocytes from one healthy donor were compared. The uptake of strains belonging to a given species varied from 60 to 80% with an average of 70% after 20 min incubation at 37 degrees C. Up to 95% of intracellular bacteria were killed after 10 min. There was no correlation between uptake capacity and species or biotype. The average rates of phagocytosis and killing strains whether isolated from urinary tract infections or from the skin were virtually the same.

Chloride uptake in strains of Scenedesmus obliquus

Summary Wild-type (#3) Scenedesmus obliquus, and mutants reported deficient in photosystem I (#8), photosystem II (#11) and cytochrome f (#50) were used to investigate the dependence of cellular chloride uptake on photosynthesis and respiration. The extent of the light-stimulation of chloride uptake rates from anaerobic solutions was in the same order as that of light-stimulation of O2 evolution, namely #3 ≫ #8 > #11 > #50. DCMU only partly inhibited the light-stimulated uptake in #3 and #8 and increased it in #11. The uptake rate by #3, #8 and #50 from aerobic solutions in the dark was the same, about 0.4–0.5 μmol (kg DW)−1 s−1; that of #11 was 0.13 μmol (kg DW)−1 s−1. O2 consumption under the same conditions was nearly equal in the four strains: 50–60 μmol (kgDW)−1 s−1. Sodium azide at 0.03–0.1 mM inhibited chloride uptake from dark, aerobic solutions and increased O2 consumption, in #3, #8 and #11. The results are discussed in terms of the mediation of chloride active transport by respiratory or photosynthetic ATP. Operation of Photosystem II does not seem essential and it is inferred that cyclic processes may support chloride uptake, in anaerobic solutions, in the light with DCMU present. An inhibition of chloride uptake from dark, anaerobic solutions, by sodium azide, may be a direct effect on a membrane-located transport mechanism or on substrate-level phosphorylation (an «energy limitation»).

Histidine Uptake in Strains of Neurospora crassa with Normal and Mutant Transport Systems

Kinetic parameters for three systems of active histidine uptake by germinated conidia of Neurospora crassa have been measured. Each system appears to follow typical Michaelis-Menten kinetics when studied separately from the other systems. Under the conditions studied, the general amino acid transport system was found to account for the major portion of histidine uptake from low concentrations. Three types of transport mutants with altered growth inhibition patterns were selected in a histidine auxotroph. Growth of one mutant, type bas(a), could be inhibited by the addition of methionine to a histidine-supplemented medium, and another type, neu(a), could be inhibited by the addition of arginine. These mutants were shown to be lacking active histidine uptake by the basic amino acid and neutral amino acid transport systems, respectively. Another type of double mutant (his-3, neu(r)) could be inhibited only by the addition of very high concentrations of methionine in the presence of arginine and histidine, and the mutation appeared to have altered the specificity of the neutral amino acid permease.