Transient Repetitive Exposure to Low Level Light Therapy Enhances Collateral Blood Vessel Growth in The Ischemic Hindlimb of The Tight Skin Mouse

The tight skin mouse (Tsk^?/+) is a model of scleroderma characterized by impaired vasoreactivity, increased oxidative stress, attenuated angiogenic response to VEGF and production of the angiogenesis inhibitor angiostatin. Low‐level light therapy (LLLT) stimulates angiogenesis in myocardial infarction and chemotherapy‐induced mucositis. We hypothesize that repetitive LLLT restores vessel growth in the ischemic hindlimb of Tsk^?/+ mice by attenuating angiostatin and enhancing angiomotin effects in vivo. C57Bl/6J and Tsk^?/+ mice underwent ligation of the femoral artery. Relative blood flow to the foot was measured using a laser Doppler imager. Tsk^?/+ mice received LLLT (670 nm, 50 mW cm^?2, 30 J cm^?2) for 10 min per day for 14 days. Vascular density was determined using lycopersicom lectin staining. Immunofluorescent labeling, Western blot analysis and immunoprecipitation were used to determine angiostatin and angiomotin expression. Recovery of blood flow to the ischemic limb was reduced in Tsk^?/+ compared with C57Bl/6 mice 2 weeks after surgery. LLLT treatment of Tsk^?/+ mice restored blood flow to levels observed in C57Bl/6 mice. Vascular density was decreased, angiostatin expression was enhanced and angiomotin depressed in the ischemic hindlimb of Tsk^?/+ mice. LLLT treatment reversed these abnormalities. LLLT stimulates angiogenesis by increasing angiomotin and decreasing angiostatin expression in the ischemic hindlimb of Tsk^?/+ mice.     

High Final Energy of Low‐Level Gallium Arsenide Laser Therapy Enhances Skeletal Muscle Recovery without a Positive Effect on Collagen Remodeling

The aim of this study was to evaluate the effects of a Gallium Arsenide (GaAs) laser, using a high final energy of 4.8 J, during muscle regeneration after cryoinjury. Thirty Wistar rats were divided into three groups: Control (C, n = 10); Injured (I, n = 10) and Injured and laser treated (Injured/LLLT, n = 10). The cryoinjury was induced in the central region of the tibialis anterior muscle (TA). The applications of the laser (904 nm, 50 mW average power) were initiated 24 h after injury, at energy density of 69 J cm^?1 for 48 s, for 5 days, to two points of the lesion. Twenty‐four hours after the final application, the TA muscle was removed and frozen in liquid nitrogen to assess the general muscle morphology and the gene expression of TNF‐α, TGF‐β, MyoD, and Myogenin. The Injured/LLLT group presented a higher number of regenerating fibers and fewer degenerating fibers (P < 0.05) without changes in the collagen remodeling. In addition, the Injured/LLLT group presented a significant decrease in the expression of TNF‐α and myogenin compared to the injured group (P < 0.05). The results suggest that the GaAs laser, using a high final energy after cryoinjury, promotes muscle recovery without changing the collagen remodeling in the muscle extracellular matrix.     

Effect of Low‐Level Laser Therapy (660 nm) on Acute Inflammation Induced by Tenotomy of Achilles Tendon in Rats

In this study, we aimed to analyze the effects of low‐level laser therapy (LLLT; 660 nm) on levels of protein expression of inflammatory mediators after cutting Achilles tendon of rats. Thirty Wistar male rats underwent partial incisions of the left Achilles tendon, and were divided into three groups of 10 animals according to the time of euthanasia after injury: 6, 24 and 72 h. Each group was then divided into control group and LLLT group (treated with 100 mW, 3.57 W cm^?2, 0.028 cm², 214 J cm^?2, 6 J, 60 s, single point). In LLLT group, animals were treated once time per day until the time of euthanasia established for each group. The group treated with LLLT showed a significant reduction of IL‐1β compared with control groups at three time points (6 h: P = 0.0401; 24 h: P = 0.0015; 72 h: P = 0.0463). The analysis of IL‐6 showed significant reduction only in the LLLT group at 72 h compared with control group (P = 0.0179), whereas IL‐10 showed a significant increase in the treated group compared with control group at three experimental times (6 h: P = 0.0007; 24 h: P = 0.0256; 72 h: P < 0.0001). We conclude that LLLT is an important modulator of inflammatory cytokines release after injury in Achilles tendon.     

Low‐Level Laser Therapy and Sodium Diclofenac in Acute Inflammatory Response Induced by Skeletal Muscle Trauma: Effects in Muscle Morphology and mRNA Gene Expression of Inflammatory Markers

Pharmacological therapy is widely used in the treatment of muscle injuries. On the other hand, low‐level laser therapy (LLLT) arises as a promising nonpharmacological treatment. The aim of this study was to analyze the effects of sodium diclofenac (topical application) and LLLT on morphological aspects and gene expression of biochemical inflammatory markers. We performed a single trauma in tibialis anterior muscle of rats. After 1 h, animals were treated with sodium diclofenac (11.6 mg g^‐1 of solution) or LLLT (810 nm; continuous mode; 100 mW; 3.57 W cm^?2; 1, 3 or 9 J; 10, 30 or 90 s). Histological analysis and quantification of gene expression (real‐time polymerase chain reaction—RT‐PCR) of cyclooxygenase 1 and 2 (COX‐1 and COX‐2) and tumor necrosis factor‐alpha (TNF‐α) were performed at 6, 12 and 24 h after trauma. LLLT with all doses improved morphological aspects of muscle tissue, showing better results than injury and diclofenac groups. All LLLT doses also decreased (P < 0.05) COX‐2 compared to injury group at all time points, and to diclofenac group at 24 h after trauma. In addition, LLLT decreased (P < 0.05) TNF‐α compared both to injury and diclofenac groups at all time points. LLLT mainly with dose of 9 J is better than topical application of diclofenac in acute inflammation after muscle trauma.     

Phototherapeutic Effect of Low‐Level Laser on Thyroid Gland of Gamma‐Irradiated Rats

One inescapable feature of life on the earth is exposure to ionizing radiation. The thyroid gland is one of the most sensitive organs to gamma‐radiation and endocrine disrupters. Low‐level laser therapy (LLLT) has been used to stimulate tissue repair, and reduce inflammation. The aim of this study was to gauge the value of using Helium–Neon laser to repair the damaged tissues of thyroid gland after gamma‐irradiation. Albino rats were used in this study (144 rats), divided into control, gamma, laser, and gamma plus laser‐irradiated groups, each group was divided into six subgroups according to time of treatment (total six sessions). Rats were irradiated once with gamma radiation (6 Gy), and an external dose of laser (Wavelength 632.8 nm, 12 mW, CW, Illuminated area 5.73 cm², 2.1 mW cm^?2, 120 s, 1.4 J, 0.252 J cm^?2) twice weekly localized on thyroid region of the neck, for a total of six sessions. Animals were sacrificed after each session. Analysis included thyroid function, oxidative stress markers, liver function and blood picture. Results revealed improvement in thyroid function, liver function and antioxidant levels, and the blood cells count after LLLT.     

Red Light Interferes in UVA‐Induced Photoaging of Human Skin Fibroblast Cells

The possible regulation mechanism of red light was determined to discover how to retard UVA‐induced skin photoaging. Human skin fibroblasts were cultured and irradiated with different doses of UVA, thus creating a photoaging model. Fibroblasts were also exposed to a subtoxic dose of UVA combined with a red light‐emitting diode (LED) for five continuous days. Three groups were examined: control, UVA and UVA plus red light. Cumulative exposure doses of UVA were 25 J cm^?2, and the total doses of red light were 0.18 J cm^?2. Various indicators were measured before and after irradiation, including cell morphology, viability, β‐galactosidase staining, apoptosis, cycle phase, the length of telomeres and the protein levels of photoaging‐related genes. Red light irradiation retarded the cumulative low‐dose UVA irradiation‐induced skin photoaging, decreased the expression of senescence‐associated β‐galactosidase, upregulated SIRT1 expression, decreased matrix metalloproteinase MMP‐1 and the acetylation of p53 expression, reduced the horizon of cell apoptosis and enhanced cell viability. Furthermore, the telomeres in UVA‐treated cells were shortened compared to those of cells in the red light groups. These results suggest that red light plays a key role in the antiphotoaging of human skin fibroblasts by acting on different signaling transduction pathways.     

Low‐level Laser Therapy Ameliorates CCl4‐induced Liver Cirrhosis in Rats

This study investigated the effects of low‐level laser therapy (LLLT) in the liver function, structure and inflammation in a experimental model of carbon tetrachloride (CCl₄)‐induced liver cirrhosis. Wistar rats were divided into Control, LLLT, CCl₄ and CCl₄+LLLT groups. CCl₄ groups received CCl₄ (0.4 g kg^?1; i.p.), three times a week, for 12 weeks. A 830 nm LLLT was performed with a continuous wave, 35 mW, 2.5 J cm^?2 per point, applied to four points of the liver (right and left upper and lower extremities, in the four lobes of the liver) for 2 weeks. Liver structure and inflammation (cirrhotic areas, collagen deposition, inflammation, density of Kupffer and hepatic stellate cells) and function (aspartate aminotransferase, alkaline phosphatase, gamma glutamyltransferase, lactate dehydrogenase, total proteins and globulins) were evaluated. LLLT significantly reduced CCl₄‐increased aspartate aminotransferase (P < 0.001), alkaline phosphatase (P < 0.001), gamma‐glutamyl transferase (P < 0.001) and lactate dehydrogenase (P < 0.01) activity, as well as total proteins (P < 0.05) and globulins (P < 0.01). LLLT also reduced the number of cirrhotic areas, the collagen accumulation and the hepatic inflammatory infiltrate. Of note, LLLT reduced CCl₄‐increased number of Kupffer cells (P < 0.05) and hepatic stellate cells (P < 0.05). We conclude that LLLT presents beneficial effects on liver function and structure in an experimental model of CCl₄‐induced cirrhosis.     

Artocarpin‐enriched (Artocarpus altilis) Heartwood Extract Provides Protection Against UVB‐induced Mechanical Damage in Dermal Fibroblasts

This study aimed to evaluate the protective effect of artocarpin‐enriched (Artocarpus altilis) heartwood extract on the mechanical properties of UVB‐irradiated fibroblasts. Human skin fibroblasts were pretreated with 50 μg/mL^?1 extract and later irradiated with UVB (200 mJ/cm^?2). They were then cultured within three‐dimensional of free‐floating and tense collagen lattices. The pretreatment of fibroblasts with the extract prior to UVB radiation showed cells protection against UVB‐induced suppression of α‐SMA expression, fibroblast migration and contraction. These results reveal that the extract prevents mechanical damages induced by UVB irradiation in fibroblast‐embedded collagen lattices, and therefore, has a potential as a natural photo‐protectant.     

Effects of Laser Irradiation on Pulp Cells Exposed to Bleaching Agents

The aim of this study was to evaluate the effect of low‐level laser therapy (LLLT) on odontoblast‐like cells exposed to a bleaching agent. Mouse dental papilla cell‐23 cells were seeded in wells of 24‐well plates. Eight groups were established according to the exposure to the bleaching agent and LLLT (0, 4, 10 and 15 J cm^?2). Enamel–dentin disks were adapted to artificial pulp chambers, which were individually placed in wells containing Dulbecco's modified Eagle's medium (DMEM). A bleaching agent (35% hydrogen peroxide [BA35%HP]) was applied on enamel (15 min) to obtain the extracts (DMEM + BA35%HP components diffused through enamel/dentin disks). The extracts were applied (1 h) to the cells, and then subjected to LLLT. Cell viability (Methyl tetrazolium assay), alkaline phosphatase (ALP) activity, as well as gene expression of ALP, fibronectin (FN) and type I collagen, were evaluated. The bleaching procedures reduced the cell viability, ALP activity and gene expression of dentin proteins. Laser irradiation did not modulate the cell response; except for FN, as LLLT decreased the gene expression of this protein by the cells exposed to the BA35%HP. It can be concluded that BA35%HP decreased the activities of odontoblasts that were not recovered by the irradiation of the damaged cells with low‐level laser parameters tested.     

Photodynamic Inactivation of Bacterial and Yeast Biofilms With a Cationic Porphyrin

The efficiency of 5,10,15,20‐tetrakis(1‐methylpyridinium‐4‐yl)porphyrin tetra‐iodide (Tetra‐Py⁺‐Me) in the photodynamic inactivation of single‐species biofilms of Staphylococcus aureus, Pseudomonas aeruginosa and Candida albicans and mixed biofilms of S. aureus and C. albicans was evaluated. The effect on the extracellular matrix of P. aeruginosa was also assessed. Irradiation with white light up to an energy dose of 64.8 J cm^?2 in the presence of 20 μm of Tetra‐Py⁺‐Me caused significant inactivation in all single‐species biofilms (3–6 log reductions), although the susceptibility was attenuated in relation to planktonic cells. In mixed biofilms, the inactivation of S. aureus was as efficient as in single‐species biofilms but the susceptibility of C. albicans decreased. In P. aeruginosa biofilms, a reduction of 81% in the polysaccharide content of the matrix was observed after treatment with a 20 μm PS concentration and a total light dose of 64.8 J cm^?2. The results show that the Tetra‐Py⁺‐Me causes significant inactivation of the microorganisms, either in biofilms or in the planktonic form, and demonstrate that polysaccharides of the biofilm matrix may be a primary target of photodynamic damage.     

Low Level Light Therapy Modulates Inflammatory Mediators Secreted by Human Annulus Fibrosus Cells during Intervertebral Disc Degeneration In Vitro

Intervertebral disc degeneration (IVD) is one of the important causes of low back pain and is associated with inflammation induced by interaction between macrophages and the human annulus fibrosus (AF) cells. Low‐level light therapy (LLLT) has been widely known to regulate inflammatory reaction. However, the effect of LLLT on macrophage‐mediated inflammation in the AF cells has not been studied till date. The aim of this study is to mimic the inflammatory microenvironment and to investigate the anti‐inflammatory effect of LLLT at a range of wavelengths (405, 532 and 650 nm) on the AF treated with macrophage‐like THP‐1 cells conditioned medium (MCM) containing proinflammatory cytokines and chemokines (interleukin‐1beta, tumor necrosis factor‐alpha, interleukin‐6 and 8). We observed that AF cells exposed to MCM secrete significantly higher concentrations of IL‐6, IL‐8, IL‐1β and TNF‐α. LLLT markedly inhibited secretion of IL‐6 at 405 nm in a time‐dependent manner. Level of IL‐8 was significantly decreased at all wavelengths in a time‐dependent manner. We showed that MCM can induce the inflammatory microenvironment in AF cells and LLLT selectively suppressed IL‐6 and 8 levels. The results indicate that LLLT is a potential method of IVD treatment and provide insights into further investigation of its anti‐inflammation effect on IVD.     

The Injury and Cumulative Effects on Human Skin by UV Exposure from Artificial Fluorescence Emission

The injury and cumulative effects of UV emission from fluorescence lamp were studied. UV intensity from fluorescence lamp was measured, and human skin samples (hips, 10 volunteers) were exposed to low‐dose UV irradiation (three times per week for 13 consecutive weeks). Three groups were examined: control group without UV radiation; low‐dose group with a cumulative dose of 50 J cm^?2 which was equivalent to irradiation of the face during indoor work for 1.5 years; and high‐dose group with 1000 J cm^?2 cumulative dose equivalent to irradiation of the face during outdoor activities for 1 year. Specific indicators were measured before and after UVA irradiation. The findings showed that extending the low‐dose UVA exposure decreased the skin moisture content and increased the transepidermal water loss as well as induced skin color changes (decreased L* value, increased M index). Furthermore, irradiated skin showed an increased thickness of cuticle and epidermis, skin edema, light color and unclear staining collagen fibers in the dermis, and elastic fiber fragmentation. In addition, MMP‐1, p53 and SIRT1 expression was also increased. Long‐term exposure of low‐dose UVA radiation enhanced skin photoaging. The safety of the fluorescent lamp needs our attention.     

The Reversibility of UV‐B Induced Alterations in Optical Properties of the Rabbit Cornea Depends on Dose of UV Irradiation

Solar UVB radiation evokes photokeratitis, accompanied by increased corneal hydration and changes in corneal transparency, resulting in increased light absorption. Corneal optical properties are disturbed and visual acuity decreased. The aim of this study was to investigate the reversibility of these UVB‐induced changes. Rabbit corneas were irradiated with UVB doses of 0.5 J cm^?2 or 1.01 J cm^?2 during 4 days. Some rabbits were sacrificed after the last irradiation and some 2 months later. Corneas were investigated spectrophotometrically for light absorption, and corneal hydration was evaluated by central corneal thickness with an ultrasonic pachymeter. Corneal impression cytologies were examined immunohistochemically for proinflammatory cytokines and malondialdehyde. The increased corneal light absorption, hydration and the staining of immunohistochemical markers found in corneas after irradiation returned to normal values during 2 months in corneas irradiated with the lower UVB dose. In contrast, in corneas irradiated with the higher UVB dose, a moderate but statistically significant increase in corneal light absorption, hydration and positive immunohistochemical stainings remained as residual changes. This was in contrast to normal corneas, where the staining of proinflammatory cytokines as well as malondialdehyde was negative. In conclusion, the reversibility of UVB‐induced disturbances was dependent on UVB dose.     

Efficacy of Low‐Dose Ultraviolet A‐1 Phototherapy for Parapsoriasis/Early‐Stage Mycosis Fungoides

Mycosis fungoides (MF) and parapsoriasis (PP) are major dermatologic conditions for which phototherapy continues to be a successful and valuable treatment option. UVA‐1 phototherapy is effective in the management of cutaneous T‐cell mediated diseases. The aim of the study was to evaluate the efficacy and safety of low‐dose UVA‐1 phototherapy for the management of PP/early‐stage MF. A total of 30 patients, diagnosed with MF (n:19) or PP (n:11) were enrolled to the study. All patients were managed with low‐dose UVA‐1 (20 or 30 J cm^?2). Response was assessed clinically and immunohistochemically. UVA‐1 treatment led to clinical and histological complete remission (CR) in 11 of 19 MF patients (57.9%), partial remission (PR) in three of 19 (15.8%), after a mean cumulative dose of 1665 (range, 860–3120) J cm^?2 and mean number of 73 exposure (range, 43–107) sessions. Five patients with PP (45.5%) showed CR, and PR was observed in six patients with PP (54.5%) after a mean cumulative dose of 1723 (range, 1060–3030) J cm^?2 and mean number of 74 exposure (range, 53–101) sessions. We conclude that low‐dose UVA‐1 therapy seems to be an effective, safe, and well‐tolerated treatment option for patients with PP/early‐stage MF.     

Photodynamic and Nail Penetration Enhancing Effects of Novel Multifunctional Photosensitizers Designed for The Treatment of Onychomycosis

Novel multifunctional photosensitizers (MFPSs), 5,10,15‐tris(4‐N‐methylpyridinium)‐20‐(4‐phenylthio)‐[21H,23H]‐porphine trichloride (PORTH) and 5,10,15‐tris(4‐N‐methylpyridinium)‐20‐(4‐(butyramido‐methylcysteinyl)‐hydroxyphenyl)‐[21H,23H]‐porphine trichloride (PORTHE), derived from 5,10,15‐Tris(4‐methylpyridinium)‐20‐phenyl‐[21H,23H]‐porphine trichloride (Sylsens B) and designed for treatment of onychomycosis were characterized and their functionality evaluated. MFPSs should function as nail penetration enhancer and as photosensitizer for photodynamic treatment (PDT) of onychomycosis. Spectrophotometry was used to characterize MFPSs with and without 532 nm continuous‐wave 5 mW cm^?2 laser light (± argon/mannitol/NaN₃). Nail penetration enhancement was screened (pH 5, pH 8) using water uptake in nails and fluorescence microscopy. PDT efficacy was tested (pH 5, ± argon/mannitol/NaN₃) in vitro with Trichophyton mentagrophytus microconida (532 nm, 5 mW cm^?2). A light‐dependent absorbance decrease and fluorescence increase were found, PORTH being less photostable. Argon and mannitol increased PORTH and PORTHE photostability; NaN₃ had no effect. PDT (0.6 J cm^?2, 2 μm ) showed 4.6 log kill for PORTH, 4.4 for Sylsens B and 3.2 for PORTHE (4.1 for 10 μm ). Argon increased PORTHE, but decreased PORTH PDT efficacy; NaN₃ increased PDT effect of both MFPSs whereas mannitol increased PDT effect of PORTHE only. Similar penetration enhancement effects were observed for PORTH (pH 5 and 8) and PORTHE (pH 8). PORTHE is more photostable, effective under low oxygen conditions and thus realistic candidate for onychomycosis PDT.     

Fisetin Inhibits UVB‐induced Cutaneous Inflammation and Activation of PI3K/AKT/NFκB Signaling Pathways in SKH‐1 Hairless Mice

Solar ultraviolet B (UVB) radiation has been shown to induce inflammation, DNA damage, p53 mutations and alterations in signaling pathways eventually leading to skin cancer. In this study, we investigated whether fisetin reduces inflammatory responses and modulates PI3K/AKT/NFκB cell survival signaling pathways in UVB‐exposed SKH‐1 hairless mouse skin. Mice were exposed to 180 mJ cm^?2 of UVB radiation on alternate days for a total of seven exposures, and fisetin (250 and 500 nmol) was applied topically after 15 min of each UVB exposure. Fisetin treatment to UVB‐exposed mice resulted in decreased hyperplasia and reduced infiltration of inflammatory cells. Fisetin treatment also reduced inflammatory mediators such as COX‐2, PGE₂ as well as its receptors (EP1–EP4) and MPO activity. Furthermore, fisetin reduced the level of inflammatory cytokines TNFα, IL‐1β and IL‐6 in UVB‐exposed skin. Fisetin treatment also reduced cell proliferation markers as well as DNA damage as evidenced by increased expression of p53 and p21 proteins. Further studies revealed that fisetin inhibited UVB‐induced expression of PI3K, phosphorylation of AKT and activation of the NFκB signaling pathway in mouse skin. Overall, these data suggest that fisetin may be useful against UVB‐induced cutaneous inflammation and DNA damage.     

Hybrid phospholipid bilayer coatings for separations of cationic proteins in capillary zone electrophoresis

Protein separations in CZE suffer from nonspecific adsorption of analytes to the capillary surface. Semipermanent phospholipid bilayers have been used to minimize adsorption, but must be regenerated regularly to ensure reproducibility. We investigated the formation, characterization, and use of hybrid phospholipid bilayers (HPBs) as more stable biosurfactant capillary coatings for CZE protein separations. HPBs are formed by covalently modifying a support with a hydrophobic monolayer onto which a self‐assembled lipid monolayer is deposited. Monolayers prepared in capillaries using 3‐cyanopropyldimethylchlorosilane (CPDCS) or n‐octyldimethylchlorosilane (ODCS) yielded hydrophobic surfaces with lowered surface free energies of 6.0 ± 0.3 or 0.2 ± 0.1 mJ m^?2, respectively, compared to 17 ± 1 mJ m^?2 for bare silica capillaries. HPBs were formed by subsequently fusing vesicles comprised of 1,2‐dilauroyl‐sn‐glycero‐3‐phosphocholine or 1,2‐dioleoyl‐sn‐glycero‐3‐phosphocholine to CPDCS‐ or ODCS‐modified capillaries. The resultant HPB coatings shielded the capillary surface and yielded reduced electroosmotic mobility (1.3–1.9 × 10^?4 cm² V^?1s^?1) compared to CPDCS‐ and ODCS‐modified or bare capillaries (3.6 ± 0.2 × 10^?4 cm² V^?1s^?1, 4.8 ± 0.4 × 10^?4 cm² V^?1s^?1, and 6.0 ± 0.2 × 10^?4 cm² V^?1s^?1, respectively), with increased stability compared to phospholipid bilayer coatings. HPB‐coated capillaries yielded reproducible protein migration times (RSD ≤ 3.6%, n ≥ 6) with separation efficiencies as high as 200 000 plates/m.     

Effectiveness of the Photoactive Dye Methylene Blue versus Caspofungin on the Candida parapsilosis Biofilm in vitro and ex vivo

This research studied the effectiveness of the photoactive compound methylene blue (MB) activated with red LED light (576–672 nm) compared to that of caspofungin (CAS) on 1 Candida albicans and 3 Candida parapsilosis strains. Results were evaluated in terms of SMIC₅₀ for CAS or in PDI (photodynamic inactivation)‐SMIC₅₀ for MB (minimal inhibitory concentration inhibiting sessile biofilm to 50% in comparison to the control without CAS or after irradiation in comparison to the control without MB). While all strains were susceptible to CAS in planktonic form, the SMIC₅₀ was determined to be >16 μg mL^?1 when CAS was added to a 24 h biofilm. However, PDI‐MIC_50s (1.67 mW cm^?2, fluence 15 J cm^?2) were 0.0075–0.03 mmol L^?1. For biofilm, PDI‐SMIC_50s were in the range from 0.7 to 1.35 mmol L^?1. MB concentration of 1 mmol L^?1 prevented a biofilm being formed ex vivo on mouse tongues after irradiation regardless of the application time, in contrast to CAS, which was only effective at a concentration of 16 μg mL^?1 when it was added at the beginning of biofilm formation. PDI seems to be a promising method for the prevention of microbial biofilms that do not respond significantly to conventional drugs.     

Guinea Pig Skin,a Model for Epidermal Cellular and Molecular Changes Induced by UVR in vivo and in vitro: Effects on Mycobacterium bovis Bacillus Calmette–Guérin Vaccination

Previously, we reported that ultraviolet B‐radiation (UVR) suppressed Bacillus Calmette–Guérin (BCG) vaccine‐induced resistance to Mycobacterium tuberculosis in guinea pigs (GP). Herein, we investigated the cellular and molecular changes within the irradiated GP epidermis and the in vivo effect of supernatants from UV‐irradiated (200 J m^?2) epidermal cells (UV‐sup) on M. bovis BCG vaccination. UVR increased the number of nucleated keratinocytes in the skin, but caused a decrease in the proportions of CD25⁺T cells. In the spleen, UVR resulted in a decrease in the proportions of T‐cell subsets including CD25⁺T cells, and major histocompatibility complex (MHC) class II⁺ and CD14⁺ cells. Similarly, significant up‐regulation of several cytokine mRNAs including IL‐10 was also observed. Furthermore, UV‐sup significantly reduced the MHC class II expression in peritoneal cells and reduced T‐cell proliferation to ConA. The proliferation to purified protein derivative (PPD) was restored to normal levels by anti‐IL‐10 antibody. The UV‐sup when injected into BCG‐vaccinated GP significantly diminished the skin test response and T‐cell proliferation to PPD and up‐regulated the expression of IL‐10, IL‐4, IL‐1β and Foxp3 mRNAs in the lymph node or spleen. Thus, whole body UVR induces profound cellular and molecular changes and injection of UV‐sup from epidermal cells mimics the effect of whole body UVR in BCG‐vaccinated GP.     

Histopathological Analysis of UVB and IR Interaction in Rat Skin

To determine the chronic skin effects caused by the interaction of infrared and ultraviolet B radiations, male Rattus norvegicus (Wistar) (2 months old) were exposed for 15 days to infrared radiation (600–1500 nm, with a peak at 1000 nm, n = 12) for 30 min (1080 J cm^?2) (IRo); to ultraviolet B radiation (peak emission at 313 nm, n = 9) for 90 min (55.08 J cm^?2) (UVB); to infrared radiation followed after 90 min by ultraviolet B (n = 6) (IRUVB) and to ultraviolet B followed after 90 min by infrared radiation (n = 9) (UVBIR). Skin samples were collected and histopathological analysis showed the presence of acanthosis, parakeratotic and orthokeratotic hyperkeratosis, intraepidermal pustules, keratin pearls, detachment of epidermis, collagen necrosis, inflammatory infiltrate, vasodilation, basal cell vacuolization and superficial dermis degeneration both in UVB and UVBIR treatments. IRUVB animals showed the same characteristics as above except for parakeratotic hyperkeratosis, keratin pearls and superficial dermis degeneration. To conclude, infrared radiation exposure after ultraviolet B irradiation increases skin damage without protecting the tissue, while infrared radiation exposure before ultraviolet B irradiation showed a protective effect against ultraviolet skin damage.