炎症浸润细胞在曝光和非曝光部位皮肤中的组织学表现

目的 观察、比较曝光及非曝光部位皮肤中炎症浸润细胞的类型、数目,探讨其在光老化过程中的作用.方法 应用免疫组化法分别对23例女性健康志愿者前臂伸侧(曝光)和上臂内侧(非曝光部位)皮肤石蜡标本中的细胞表面抗原CD3、CD45RO、CD68进行检测,计数阳性细胞数目.不同部位阳性细胞数比较采用配对t检验,阳性细胞数与年龄的相关性采用Pearson相关分析.结果 曝光部位皮肤组织CD3、CD45RO、CD68阳性细胞数分别为(48.91±13.17)/mm2、(46.83±12.92)/mm2、(85.43±22.35)/mm2,非曝光部位分别为(40.61±11.57)/mm2、(38.00±10.11)/mm2、(73.48±16.21)/mm2,曝光部位均显著高于非曝光部位(P<0.01或<0.05).曝光部位皮肤组织CD3、CD45RO阳性细胞数与年龄呈正相关(r=0.56、0.56,P<0.01),曝光部位CD68及非曝光部位皮肤组织CD3、CD45RO、CD68阳性细胞数与年龄无相关性.结论 T淋巴细胞、巨噬细胞可能在光老化过程中发挥作用.

Abstract：

Objective To investigate the role of infiltrating inflammatory cells in photoaging process by comparing the type and number of these cells in sun-exposed and-unexposed skin.Methods The expression of CD3,CD45RO and CD68 were detected by immunohistochemieal staining in 46 paraffin-embeded skin samples from the extensor forearms(sun-exposed)and upper-inner arms(sun-unexposed) of 23 healthy female volunteers.The number of positive cells in sun-exposed and -unexposed sites was counted and statistically tested by paired samples t test,and Pearson correlation analysis was performed to assess the relationship between the number of positive cells and age of these volunteers.Results The number of cells positive for CD3,CD45RO and CD68 per square millimetre in sun-exposed skin was significantly higher than that in sun-unexposed skin(48.91±13.173 vs.40.61±11.571,46.83±12.915 vs.38.00±10.109,85.43±22.346 vs.73.48±16.208,respectively,P<0.01 or 0.05).The number of cells positive for CD3 and CD45RO increased significantly with age (r=0.557,0.555,respectively,both P<0.01) in the sun-exposed skin but not in sun-unexposed skin,and the number of CD68-positive cells was uncorrelated with age in either sunexposed or -unexposed skin.Conclusion T lymphocytes and macrophages may play a role in the process of photoaging.     

Visual Clues for the Histopathologic Diagnosis of Psoriasis: A Retrospective Case-Control Study

Objective: The histopathologic diagnosis of psoriasis remains challenging. This study aimed to uncover clues for the histopathologic diagnosis of psoriasis in patients whose lesions required differentiation from other inflammatory skin disorders.Methods: A retrospective analysis was conducted between psoriasis biopsy sections and other inflammatory skin diseases sections. The psoriasis and control groups were compared regarding the pathological characteristics, including the ? sign, hypogranulos...     

Oligo基因芯片和小鼠模型研究外阴阴道念珠菌病的发病机制

Objective To investigate the pathogenesis of vulvovaginal candidiasis.Methods Thirty mice were randomly and equally divided into 3 groups,i.e.,infected group treated with estrogen and innoculated with a clinical isolate of C. albicans,negative centrel group treated with estrogen and inoculated with physiological saline.blank control group without any treatment.All mice were kilied on day 7 after inoculation,vaginal tissue samples were obtained and subjected to pathological examination and staining.Total RNA was extracted from these samples as well as Candida isolates and reference strains,and hybridized with self-designed oligonucleotide chips.Then,signal value of vulvovaginal candidiasis-associated factors was compared between infected group and blank control group,and a 2-fold difference was considered as significant.Results Compared with the blank centrol group,the gene expression of 39 factors increased while that of 4 factors decreased in the infeeted group.In the case of host immunity,the expression of inflammatory chemokines generally inereased,and that of regulatory factors of adaptive immunity,including interleukin (IL)-1,IL-4,IL-6,IL-10,IL-12,tumor necrosis factor(TNF)-α,nuclear factor (NF)-κB and transforming growth factor (TGF)-β Was also enhanced to different degrees.TLR4,a humoral component of innate immune response,increased in all specimens from infected group,whereas Toll-like receptor(TLR)2 expression increased only in one third of these speciraens.The expression of virulent factors including EFG1 (a modulatory factor of hyphal formation),secreted aspartic proteinase (SAP)2,SAP4,SAP5,SAP6,SAP10,lipase(LIP)2,LIP4 and HWP(a major cell wall protein)1 increased in pathogenic strains.Among these differentially expressed genes,monocyte chemoattractant protein(MCP)-1,macrophage inflammatory protein(MIP)-1α,MIP-2,IL-1,TLR4,LIP4 and HWP1,which were involved in extracellular hydrolysis,hyphal formation,phenotypic switching and host native immunity,were increased significantly in all specimens from the infected group.Conclusions Both the deficiency of adaptive immunity and increased virulence of pathogen strains are involved in the pathogenesis of vulvovaginal candidiasis,and TLR4 possibly plays an important role in local immunity of hosts with vulvovaginal candidiasis.     

淋球菌opa基因分型方法的建立与评估

Objective To establish a molecular typing method (opa-typing) for Neisseria gonorrhoeae, and to evaluate its performance based on epidemiological data. Methods Twenty-six gonorrhea patients were recruited from March to April 2006 at two sites, including 17 cases from the STD Clinic of Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College and 9 cases from the STD Clinic of Shandong Provincial Institute of Dermatology. Of the 26 patients, 6 were from three known sexual links, while the remaining 20 patients did not have any sexual contact with each other. The opa gene was amplified by using PCR from Neisseria gonorrhoeae isolates from these patients followed by overnight digestion with restriction enzymes Taq Ⅰ and Hpa Ⅱ. The enzyme digestion band patterns were analyzed using the Cel-Compar program. Results The opa gene was successfully amplified from all the 26 Neisseria gonorrhoeae strains, and restrictedly digested by endonucleases Taq Ⅰ and Hpa Ⅱ . Identical band patterns were observed between patients with sexual links, but not among the remaining 20 patients. Conclusions The results of opatyping of Neisseria gonorrhoeae coincide with the information on sexual behaviour provided by patients. Opatyping may serve as a reliable tool in sexual network analysis.     

淋球菌opa基因分型方法的建立与评估

Objective To establish a molecular typing method (opa-typing) for Neisseria gonorrhoeae, and to evaluate its performance based on epidemiological data. Methods Twenty-six gonorrhea patients were recruited from March to April 2006 at two sites, including 17 cases from the STD Clinic of Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College and 9 cases from the STD Clinic of Shandong Provincial Institute of Dermatology. Of the 26 patients, 6 were from three known sexual links, while the remaining 20 patients did not have any sexual contact with each other. The opa gene was amplified by using PCR from Neisseria gonorrhoeae isolates from these patients followed by overnight digestion with restriction enzymes Taq Ⅰ and Hpa Ⅱ. The enzyme digestion band patterns were analyzed using the Cel-Compar program. Results The opa gene was successfully amplified from all the 26 Neisseria gonorrhoeae strains, and restrictedly digested by endonucleases Taq Ⅰ and Hpa Ⅱ . Identical band patterns were observed between patients with sexual links, but not among the remaining 20 patients. Conclusions The results of opatyping of Neisseria gonorrhoeae coincide with the information on sexual behaviour provided by patients. Opatyping may serve as a reliable tool in sexual network analysis.     

淋球菌opa基因分型方法的建立与评估

Objective To establish a molecular typing method (opa-typing) for Neisseria gonorrhoeae, and to evaluate its performance based on epidemiological data. Methods Twenty-six gonorrhea patients were recruited from March to April 2006 at two sites, including 17 cases from the STD Clinic of Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College and 9 cases from the STD Clinic of Shandong Provincial Institute of Dermatology. Of the 26 patients, 6 were from three known sexual links, while the remaining 20 patients did not have any sexual contact with each other. The opa gene was amplified by using PCR from Neisseria gonorrhoeae isolates from these patients followed by overnight digestion with restriction enzymes Taq Ⅰ and Hpa Ⅱ. The enzyme digestion band patterns were analyzed using the Cel-Compar program. Results The opa gene was successfully amplified from all the 26 Neisseria gonorrhoeae strains, and restrictedly digested by endonucleases Taq Ⅰ and Hpa Ⅱ . Identical band patterns were observed between patients with sexual links, but not among the remaining 20 patients. Conclusions The results of opatyping of Neisseria gonorrhoeae coincide with the information on sexual behaviour provided by patients. Opatyping may serve as a reliable tool in sexual network analysis.     

点阵激光、射频和激光溶脂技术在紧肤除皱中的应用

点阵激光、射频和激光溶脂技术可以延缓皮肤的老化,特别是皮肤的光老化,在改善皮肤松弛和皱纹上各有优势.点阵激光、射频和激光溶脂技术已被用于改善皮肤皱纹,紧致皮肤.与其他紧肤、除皱方法相比,具有安全性高、不良反应少、患者耐受性好的优点,为希望皮肤年轻化的人群提供了一种微创、痛苦小而效果较明显的新选择.

Abstract：

Fractional lasers ,radiofrequency and laser lipolysis can delay skin aging ,especially photoaging,and each of them has its own advantages in improving skin slackness and wrinkles.These techniques have been applied to skin tightening and rhytidectomy.Compared with other methods,they show a higher safety with less side effects and better compliance,and provide a new option for skin rejuvenation.     

Telomere length of the skin in association with chronological aging and photoaging

BACKGROUND: Telomere shortening has been implicated in cellular senescence, which may cause certain aging phenotypes. OBJECTIVE: To reveal whether telomere shortening is associated with chronological aging and/or photoaging of the skin, we measured telomere length in the epidermis and in the dermis from sun-protected and from sun-exposed sites of the skin. METHODS: Seventy-six specimens of epidermis from sun-protected sites and 24 specimens of epidermis from sun-exposed sites were analyzed. Sixty specimens of the dermis were also analyzed. In six cases, epidermal specimens from sun-protected and from sun-exposed sites of the same individual were analyzed. RESULTS: Comparison of telomere lengths revealed that the epidermis has shorter telomeres than the dermis. Telomere length in the epidermis and in the dermis was reduced with age, and average telomere shortening rates in the epidermis and in the dermis were 9 and 11 bp/yr, respectively. Unexpectedly, telomere length was not significantly different between epidermis from sun-exposed sites and from sun-protected sites. CONCLUSION: We could not show the evidence that telomere shortening is associated with photoaging of the skin.     

Gene expression profiling analysis of solar lentigo in relation to immunohistochemical characteristics

BACKGROUND: Solar lentigo appears as dark brown spots that occur on sun-exposed areas and is considered to be a hallmark of aged skin. Although considerable knowledge about acute pigmentation has recently been accumulated, little is yet known about the mechanisms underlying chronic- and delayed-type hyperpigmentation, such as solar lentigo. OBJECTIVES: To clarify further the mechanisms underlying the development of solar lentigo, we carried out gene expression analysis in skin biopsy specimens obtained from human solar lentigines using DNA microarray analysis. METHODS: Two pairs of skin specimens were obtained from solar lentigo and adjacent sun-exposed normal skin, as well as normal skin on the buttocks of 16 volunteers aged 40-55 years. One set of specimens was frozen and RNA was extracted for microarray and the other set was prepared for histological sections and analysed by antibodies and probes. RESULTS: Sixty-five genes were upregulated more than 1.8-fold in solar lentigo compared with adjacent control skin and seven melanocyte-related genes were included. Compared with sun-protected skin, many inflammation-related genes were upregulated in solar lentigo, and compared with sun-exposed control skin, upregulation of genes related to fatty-acid metabolism was apparent in solar lentigo. Moreover, we found downregulation of cornified envelope-related genes, which suggests suppression of cornification in the epidermis in solar lentigo. Immunohistochemically, larger numbers of TRP1-positive cells were found in the basal layer of solar lentigo than in normal skin. Fatty acid-related genes were highly expressed in the epidermis as detected by in situ hybridization, and they were much more prominent in the lesional skin of solar lentigo. However, cycling epidermal cells detectable with Ki67 antibody were fewer in the lesional skin of solar lentigo. Expression of filaggrin and involucrin was decreased in the lesional skin, where the number of cell layers of the stratum corneum was significantly higher than in normal skin. CONCLUSIONS: The results of the present microarray analysis of solar lentigo, demonstrating upregulation of genes related to inflammation, fatty-acid metabolism and melanocytes and downregulation of cornified envelope-related genes, suggest that solar lentigo is induced by the mutagenic effect of repeated ultraviolet light exposures in the past, leading to the characteristic enhancement of melanin production, together with decreased proliferation and differentiation of lesional keratinocytes on the background of chronic inflammation.     

Photoageing shows histological features of chronic skin inflammation without clinical and molecular abnormalities

BACKGROUND: Photodamage is characterized by degradation of collagen and accumulation of abnormal elastin in the superficial dermis. Mast cells and macrophages, which are found in higher numbers in photoaged skin, have been implicated in this process. OBJECTIVES: To analyse the phenotype of haematopoietic-derived infiltrating cells in photodamaged skin. METHODS: Chronically sun-exposed (preauricular) and control sun-protected (postauricular) skin was recovered from eight healthy subjects undergoing cosmetic surgery (facial lifting). RESULTS: Histological analysis showed that sun-exposed skin harboured more infiltrating mononuclear cells than sun-protected skin. Cellular infiltrates were found at the periphery of areas of elastolysis around hair follicles in sun-exposed sites, whereas they were found in the interfollicular dermis around blood vessels and around hair follicles in sun-protected samples. Immunohistochemical analysis revealed an increased number of mast cells, macrophages and CD4+ CD45RO+ T cells in sun-exposed dermis as well as a higher number of CD1a+ dendritic cells in sun-exposed epidermis, compared with the sun-protected samples. Thus photoageing displays histological features of chronic skin inflammation. However, no molecular sign of inflammation was observed and we even found a decreased expression of interleukin-1beta mRNA in sun-exposed compared with sun-protected sites. Furthermore, the patients' skin looked normal and did not display any clinical inflammation. CONCLUSIONS: Collectively, these data show that chronic ultraviolet irradiation induces alterations of innate immune cells which are recruited in sun-exposed skin without being activated.     

Changes in S100A8 expression in UV-irradiated and aged human skin in vivo

S100A8, a calcium-binding protein, is associated with keratinocyte differentiation, inflammation and wound healing. S100A8 is induced by various skin stresses and diseases, which suggests that S100A8 plays a role in those processes. However, it has not been reported how the expression of S100A8 is affected during skin aging or whether S100A8 plays a role in the skin aging process. In this study, we investigated the changes in S100A8 mRNA and protein following acute UV irradiation to human buttock skin and by intrinsic aging and photoaging in human sun-protected (upper-inner arm) and sun-exposed (forearm) skin of elderly subjects. Real-time PCR, western blot and immunohistochemical staining analyses of UV-irradiated young buttock skin revealed that S100A8 protein expression was increased at 24 h (3.0-fold) and 48 h (4.4-fold) after UV irradiation. S100A8 mRNA and protein were more highly expressed by 2.3- and 4.0-fold, respectively, in the sun-protected skin of elderly people than in that of young people. In addition, the sun-exposed skin of elderly expressed more S100A8 mRNA and protein than the sun-protected skin of the same individuals. In immunohistochemical staining, facial (photoaged) skin ≥72 years showed higher epidermal expression of S100A8 than that of the other age groups. Based on the above results, our data suggest that the expression of S100A8 is affected by acute UV irradiation, intrinsic aging and photoaging processes.     

Density and proportions of the epidermal T cell population in human sun-exposed skin differ from those in sun-protected skin: preliminary immunohistochemical study

Epidermal T cells, which are found in clinically normal human skin, show topographic differences in density and proportions; however, the mechanisms and the biological consequences of such differences are still unknown. In a previous work, we showed that epidermal T cells are altered in number and composition after a single exposure to solar-simulated radiation (SSR). The purposes of the present investigation were, first, to compare the density of epidermal T cells and the proportion of T cell subpopulations in habitually sun-exposed versus sun-protected sites; second, to determine the effects of repetitive exposures to SSR on the latter cell populations. Biopsies from habitually sun-exposed, sun-protected and solar-simulated-exposed skin of 28 healthy volunteers were taken and immunohistochemistry was performed on cryostat sections. Compared with sun-protected sites, epidermal CD3⁺ T cell numbers of habitually sun-exposed sites were significantly lower. Double staining showed that the number of CD3⁺CD8⁺ T cells was significantly lower in sun-exposed than in sun-protected skin, whereas the numbers of CD3⁺CD4⁺ T cells were similar in both sites. Therefore, the CD4/CD8 ratio was markedly higher in sun-exposed compared to sun-protected sites. Moreover, repeated exposures of sun-protected skin to SSR induced a significant reduction in number of epidermal CD3⁺ T cells. The mean number of epidermal CD3⁺CD8⁺ double stained cells significantly decreased after such exposures, while the epidermal CD3⁺CD4⁺ T cell subpopulation was not significantly changed. In conclusion, both chronically sun-exposed skin and repeatedly SSR-exposed skin show a decrease in density of epidermal CD3⁺ and CD3⁺CD8⁺ T cells. We hypothesize that such sun-induced changes may weaken the immunosurveillance capacity of the skin and therefore increase the occurrence of skin cancer.     

表皮p63和CD44与年龄及曝光部位的相关性

目的 探讨p63与CD44在皮肤衰老过程中与年龄、紫外线的关系。方法 采用免疫组化方法检测121例正常全厚皮肤标本中p63与CD44的表达,光镜下观察并计算表皮基底层p63阳性细胞百分比,用图像分析软件image proplus 6.0测量表皮层p63与CD44表达的吸光度值。结果 ①表皮基底层p63阳性细胞百分比与年龄呈负相关（r = -0.218,P < 0.05）,51 ~ 79岁组最低;但在曝光部位、半曝光部位与非曝光部位间的差异无统计学意义。②表皮p63的表达强度与年龄在曝光部位呈负相关（r = -0.389,P = 0.010）,在半曝光部位无相关性,在非曝光部位呈正相关（r = 0.341,P < 0.05）;三个部位表达强度的差异在10 ~ 30岁组无统计学意义,在31 ~ 50岁组与51 ~ 79岁组由强至弱依次为非曝光部位、半曝光部位、曝光部位。③表皮CD44的表达强度与年龄之间呈微弱负相关（r = -0.083,P < 0.05）,10 ~ 30岁组最高;但在曝光部位、半曝光部位与非曝光部位间的差异无统计学意义。结论 表皮基底层p63阳性细胞百分比、表皮CD44的表达强度和年龄呈负相关,和紫外线照射量无关。表皮p63表达强度在31 ~ 50岁组与51 ~ 79岁组的表达强度依曝光多少而递减。     

DNA repair capacities of cutaneous fibroblasts: effect of sun exposure, age and smoking on response to an acute oxidative stress

BACKGROUND: Sun irradiation causes skin ageing and cancer through the accumulation of damage to cell components. Intrinsic ageing is also associated with accumulation of oxidized macromolecules. OBJECTIVES: In this study we investigated the effects of sun exposure on response to an acute in vitro oxidative stress (H(2)O(2)) using normal human fibroblasts prepared from biopsies from 10 volunteers taken from sun-protected and sun-exposed sites. METHODS: Time-course experiments measuring repair of DNA strand-breaks and formamidopyrimidine DNA N-glycosylase-sensitive sites were conducted using the single-cell gel electrophoresis (comet) assay. RESULTS: Our results demonstrated that repair of strand-breaks was slower in sun-exposed compared with sun-protected cells. Interestingly, ageing was also associated with decreased DNA repair capacities for single-strand breaks in both sun-exposed and sun-protected cells whereas for formamidopyrimidine glycosylase (Fpg)-sensitive sites, this feature was in evidence only in sun-protected cells. Smoking, associated with age, was shown to have a markedly negative impact on DNA repair. CONCLUSIONS: Taken together our data suggest that stresses like ageing, sun exposure and smoking might have an additive effect contributing to the overall heterogeneity and decrease of DNA repair capacities in human cells and so increase the danger of sun exposure for health. They also emphasize the importance of the quality of the biological samples when repair studies on skin cells are to be conducted.     

Photoaging-associated changes in epidermal proliferative cell fractions in vivo

The epidermis is a dynamic epithelium with constant renewal throughout life. Epidermal homeostasis depends on two types of proliferative cells, keratinocyte stem cells (KSCs), and transit amplifying (TA) cells. In the case of chronologic aging, levels of KSCs tend to decrease and change functionally. However, little is known about the effect of photoaging on epidermal proliferative subtype populations. The aim of this study was to validate involucrin/β1-integrin ratio as a molecular marker of epidermal photoaging, and to investigate the effects of photoaging caused by chronic UV exposure on the proliferative subtype populations. A total of 15 male volunteers (age range 20–24 and 77–85 years, Fitzpatrick skin phototype III–IV) provided sun-exposed and sun-protected skin samples for real-time RT-PCR, Western blot analysis and immunostaining. Fractional changes in proliferative subtype populations in photoaged and chronologically aged skins were analyzed by flow cytometry. The expression of β1-integrin was found to be significantly reduced in photoaged skin and ratios of the expressions of involucrin to β1-integrin were increased 2.6-fold only in elderly subjects. Interestingly, immunostaining of the sun-exposed skins of elderly subjects showed aberrant β1-integrin expression over the basal layer and greater numbers of Ki-67-positive cells than in sun-protected buttock skin. Flow cytometric analysis revealed that the proportion of KSCs to TA cells was reversed in sun-exposed and sun-protected skins of elderly subjects. Our results suggest that KSC numbers may be lower in photoaged skin than in chronologically aged skin and could be applied to hyperplastic pattern of photoaging. These findings suggest that the epidermis of photoaged skin is impaired in terms of its proliferative potential by attempting to repair chronic UV exposure and that photoaging may be associated with alteration in the two proliferative cell fractions.     

The incidence of both tandem duplications and the common deletion in mtDNA from three distinct categories of sun-exposed human skin and in prolonged culture of fibroblasts

The use of mtDNA damage as a biomarker of cumulative sunlight exposure in human skin is a relatively new field of research. Previous investigations have simply compared the frequency of occurrence of the mtDNA common deletion (CD), and to a much lesser extent that of tandem duplications (TDs), to distinguish between sun-protected and sun-exposed skin. This approach is limited because non-melanoma skin cancer is predominantly formed on body sites that are "usually" sun-exposed as opposed to sites that are "occasionally" sun-exposed and as such they differ in their cumulative UV exposure. This study addresses this limitation by investigating the frequency of occurrence of the CD and TDs in 116 age-matched human skin samples taken from three different sun-exposed body sites. There was a greater frequency of the mtDNA damage in "usually" sun-exposed compared to "occasionally" sun-exposed body sites for both the CD and the TDs (P < 0.0001 and P = 0.058, respectively). In addition, we identified a 260 bp triplication of the mtDNA D-loop for the first time in skin. No evidence of the CD or TDs was observed in sun-protected (ie rarely exposed) skin (n = 20). Comparatively little is known about mtDNA damage in prolonged skin cell culture. We have furthered this work by studying the level of the CD and the frequency of the TDs during continued culture of human fibroblasts derived from skin samples taken from usually sun-exposed sites (n = 7 patients). The level of the CD decreases with culture, whereas the frequency of TDs can be maintained.     

Acute exposure of human skin to ultraviolet or infrared radiation or heat stimuli increases mast cell numbers and tryptase expression in human skin in vivo

Background  Mast cells are key effector cells in diverse immunological and pathological processes. It is still unclear why there are more mast cells at peripheral and sun-exposed skin sites than at sun-protected sites.
Objectives  To investigate changes in mast cell numbers associated with natural ageing and photoageing, and to observe the effects of ultraviolet (UV) and infrared (IR) radiation and heat on the prevalence of mast cells and tryptase expression in human skin in vivo .
Methods  Sun-exposed and sun-protected skin samples were taken from individuals in four different age groups. UV, IR or heat-treated buttock skin of young volunteers was also obtained. Mast cells were quantified by immunohistochemical staining of mast cell-specific tryptase and chymase. The expression of tryptase was determined by Western blotting.
Results  Both sun-exposed and sun-protected skin showed a gradual decrease in total mast cells (MC_Total) number with ageing. The number of mast cells in sun-exposed skin was significantly higher than that in sun-protected skin. After UV irradiation (2 minimal erythema doses), MC_Total and mast cells expressing tryptase and chymase were significantly increased at 24 and 48 h postirradiation. After IR irradiation (3 minimal heating doses) and heat treatment (43 °C for 90 min), MC_Total reached peak induction at 8 and 48 h after stimulation, respectively. Tryptase expression was also clearly upregulated by UV, IR and heat.
Conclusions  Our data demonstrate that mast cell numbers decreased with ageing in human skin. Also, mast cells may be activated and recruited by UV, IR and heat. These findings should further our understanding of the reason for the high prevalence of mast cells at peripheral sun-exposed skin sites.