This review presents an overview about pharmaceutical and cosmetic topical products containing polymeric nanoparticles (nanospheres and nanocapsules), reporting the main preparation and characterization methods and the studies of penetration and transport of substances through the skin. The penetration and transport extent of those systems through the skin depends on the ingredients chemical composition, on the encapsulation mechanism influencing the drug release, on the size of nanoparticles and on the viscosity of the formulations. The polymeric nanoparticles are able to modify the activity of drugs, delay and control the drug release, and increase the drug adhesivity or its time of permanence in the skin. Briefly, the nanoparticles can be useful as reservoirs of lipophilic drugs to deliver them in the stratum corneum becoming an important strategy to control their permeation into the skin.

https://journals.sagepub.com/doi/pdf/10.1177/117739280700200002

Polymeric Nanoparticles, Nanospheres and Nanocapsules, for Cutaneous Applications

We investigated the role of Bruton's tyrosine kinase (Btk) in FcepsilonRI-dependent activation of mouse mast cells, using xid and btk null mutant mice. Unlike B cell development, mast cell development is apparently normal in these btk mutant mice. However, mast cells derived from these mice exhibited significant abnormalities in FcepsilonRI-dependent function. xid mice primed with anti-dinitrophenyl monoclonal IgE antibody exhibited mildly diminished early-phase and severely blunted late-phase anaphylactic reactions in response to antigen challenge in vivo. Consistent with this finding, cultured mast cells derived from the bone marrow cells of xid or btk null mice exhibited mild impairments in degranulation, and more profound defects in the production of several cytokines, upon FcepsilonRI cross-linking. Moreover, the transcriptional activities of these cytokine genes were severely reduced in FcepsilonRI-stimulated btk mutant mast cells. The specificity of these effects of btk mutations was confirmed by the improvement in the ability of btk mutant mast cells to degranulate and to secrete cytokines after the retroviral transfer of wild-type btk cDNA, but not of vector or kinase-dead btk cDNA. Retroviral transfer of Emt (= Itk/Tsk), Btk's closest relative, also partially improved the ability of btk mutant mast cells to secrete mediators. Taken together, these results demonstrate an important role for Btk in the full expression of FcepsilonRI signal transduction in mast cells.

/pdf/involvement-of-bruton-s-tyrosine-kinase-in-fceri-dependent-2zhc4352lx.pdf

Involvement of Bruton's Tyrosine Kinase in FcεRI-dependent Mast Cell Degranulation and Cytokine Production

Mast cells are pivotal effector cells in IgE-mediated allergic inflammatory diseases. Central for mast cell activation are signals from the IgE receptor FceRI, which induce cell degranulation with the release of preformed mediators and de novo synthesis of proinflammatory leukotrienes and cytokines. How these individual mast cell responses are differentially controlled is still unresolved. We identify B cell lymphoma 10 (Bcl10) and mucosa-associated lymphoid tissue 1 (Malt1) as novel key regulators of mast cell signaling. Mice deficient for either protein display severely impaired IgE-dependent late phase anaphylactic reactions. Mast cells from these animals neither activate nuclear factor κB (NF-κB) nor produce tumor necrosis factor α or interleukin 6 upon FceRI ligation even though proximal signaling, degranulation, and leukotriene secretion are normal. Thus, Bcl10 and Malt1 are essential positive mediators of FceRI-dependent mast cell activation that selectively uncouple NF-κB–induced proinflammatory cytokine production from degranulation and leukotriene synthesis.

/pdf/the-bcl10-malt1-complex-segregates-fceri-mediated-nuclear-9v6rv3bwtw.pdf

The Bcl10–Malt1 complex segregates FcεRI-mediated nuclear factor κB activation and cytokine production from mast cell degranulation

Involvement of unique mechanisms in the induction of scratching behavior in BALB/c mice by compound 48/80.

Scratching behavior was induced in 12 strains of mice and the frequency was compared. An injection of histamine at a dose of 50 nmol induced frequent scratching behavior only in ICR mice, although the same dose of serotonin induced frequent scratching behavior in all strains of mice except for A/J. Histamine (10 nmol), serotonin (1 nmol), substance P (50 nmol) and passive cutaneous anaphylaxis induced significant vascular permeability increase in BALB/c, ICR, ddY and NC/Nga mice. These four stimuli also induced frequent scratching behavior in ICR mice. However, they failed to induce substantial increase in the incidence of scratching in the other three strains, except for ddY, which exhibited a slight but significant increase against substance P injection. These results suggest that the ICR mouse is a good responder for scratching behavior against various stimuli, especially against histamine. Thus ICR mice may be suitable for studying mediators and/or mechanisms for itching.

Scratching behavior in various strains of mice.

Passive cutaneous anaphylaxis (PCA) was elicited both in the ear and in the dorsal skin of 13 strains of mice at the same time and assessed quantitatively by measuring the amount of extravasated dye. Body pigments of colored mice such as DBA/2 (chocolate), C3H/He (brown) and C57BL/6 (black) did not interfere with the measurement of dye. In the ear response, ICR was a higher responder, C57BL/6 and BALB/c-nu/nu were lower responder strains. In the dorsal skin response, however, ICR was a lower responder, BALB/c-nu/nu, Hairless and WBB6F1-+/+ were higher responders. WBB6 F1-W/Wv was a nonresponder in both responses. The ear response was highly reproducible and the dorsal skin response of each strain was 1/2-1/10 of its ear response except for BALB/c-nu/nu. The PCA bluing regions on the dorsal skin of BALB/c-nu/nu were clearly delineated and the response was almost comparable to its ear response.

Homologous Passive Cutaneous Anaphylaxis in Various Strains of Mice.

Several attempts were made to elucidate the possible role of histamine, serotonin, leukotrienes C4 (LTC4) and D4 (LTD4), and prostaglandin E1 (PGE1) as vascular permeability increasing factors involved in 48-hour homologous passive cutaneous anaphylaxis (PCA) in the mouse ear. Increased vascular permeability in the mouse ear caused by the mediator injection or PCA was assessed quantitatively by measuring the amount of extravasated dye. In skin reactions, all of the mediators used in the present study significantly increased vascular permeability. The most potent mediator was serotonin, which increased the vascular permeability from a concentration of 10(-8) g/ml, and the activity was about 100 times higher than that of histamine on a weight basis. Vascular permeability increasing activity of LTC4 was about 10 times higher than that of histamine, and LTD4 and PGE1 were also more potent than histamine. Increases of vascular permeability caused by histamine, serotonin, LTC4 and LTD4 were significantly potentiated by injecting 10(-6) g/ml of PGE1 simultaneously. Histamine-, serotonin- and LTC4-induced skin reactions in the mouse ear were suppressed significantly by the administrations of chlorpheniramine, methysergide and FPL 55712, respectively. In contrast, though chlorpheniramine and methysergide suppressed also mouse ear PCA (about 50 and 40%, respectively), neither FPL 55712, indomethacin nor BW 755C suppressed it. These results strongly suggest that the most important mediator involved in mouse ear PCA is histamine and that serotonin also plays an important role in the increase of vascular permeability caused by PCA. Despite their potent vascular permeability increasing activity LTC4, LTD4 and PGE1 do not seem to play an important role in mouse ear PCA.

Studies on Vascular Permeability Increasing Factors Involved in 48-Hour Homologous PCA in the Mouse Ear.

Reduction of antigen-induced contraction of sensitized guinea-pig tracheal smooth muscle in vitro by calmodulin inhibitors.

To compare the receptors for cysteinyl-leukotriene (cys-LT) in rat skin with those in other tissues, we investigated the effects of specific cys-LT receptor antagonists (FPL 55712, LY171883, MCI-826 and L-648051) on cys-LT-induced cutaneous reactions in rats and mice, and on cys-LT-induced contractile responses in rat stomach smooth muscle. We also studied the effects of these drugs on homologous passive cutaneous anaphylaxis. The four cys-LT receptor antagonists dose dependently inhibited cys-LT-induced cutaneous reactions in mouse ear, but failed to inhibit passive cutaneous anaphylaxis and the histamine-induced cutaneous reaction. In rats, only MCI-826 inhibited cys-LT-induced cutaneous reactions although the other three drugs failed to inhibit these reactions. In contrast, the cys-LT-induced contractile responses of rat stomach smooth muscle were inhibited by all these drugs in a concentration-dependent manner. These results suggest that cys-LT receptors in rat skin have an affinity different from that of receptors in mouse skin and rat stomach. They also suggest that cys-LTs are not involved in passive cutaneous anaphylaxis in mice and rats.

Leukotriene Receptors in the Skin of Rats differ from those of Mouse Skin or Rat Stomach Strip.

Immunoglobulin E (IgE) antibody production against Dermatophagoides farinae extract (mite antigen) was studied in female BALB/c mice. When mice were immunized with mite antigen and aluminium hydroxide gel (alum) intraperitoneally at intervals of 30 d, good primary, secondary and tertiary IgE antibody responses were observed. In the absence of adjuvant, a subcutaneous injection of mite antigen failed to induce the primary IgE antibody response. However, good IgE antibody responses were observed after the secondary immunization given 30 d after the primary immunization. Furthermore, 5 weekly injections of mite antigen alone also induced the IgE antibody production. Intranasal administrations of mite antigen alone also induced the IgE antibody production in mice. Two exposures to mite antigen, intranasally, were sufficient for eliciting low IgE antibody production. The response was significantly potentiated by the administration of islet-activating protein obtained from culture fluids of Bordetella pertussis. These results indicate that the intranasal administration of mite antigen is very effective for eliciting the IgE antibody production.

Immunoglobulin E antibody production against house dust mite, Dermatophagoides farinae, in mice.

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