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At least 343 records · Page 19Linked to original sources

PubMed2000

Sweat gland toxicity induced by bis (tributyltin) oxide: an ultrastructural and X-ray microanalysis study.

Acute toxicity of bis (tributyltin) oxide in the sweat glands in the rat footpad was investigated by electron microscopy and an energy-dispersive X-ray microanalyzer. Male Wistar rats received an intramuscular injection of 0.5 ml/kg bis (tributyltin) oxide. After 6-8 h, swelling of mitochondria appeared in the secretory cells of the sweat glands. After 12 h, the secretory cells began to show intracytoplasmic edema. After 16-20 h, secretory cells in some sweat glands showed marked hydropic degeneration with swollen cytoplasm. Using X-ray microanalysis, tin peaks were preferentially obtained from the swollen mitochondria of the affected secretory cells. Mitochondria dysfunction due to the toxic effects of bis (tributyltin) oxide induced changes in the secretory cells of rat sweat glands. After 24-48 h, the secretory portion of the sweat glands contained three types of cells: degenerating dark cells, regenerating cells carrying injured mitochondria, and light cells which were morphologically very similar to the cells in the transitional portion of the sweat gland. These light cells appeared to differentiate into active secretory cells after settling down in the secretory portion. Based on these observations, we concluded that the cells in the transitional portion could play an important role at least as reserve cells against secretory cell toxicity. In association with the regenerating process of the damaged secretory portions, increased mitotic activities were seen in different areas of all the dermal sweat ducts. The above-mentioned morphological observations for cell damage and subsequent regeneration and renewal ofsecretory cells in sweat gland intoxication have not been reported so far.

Animals↗

PubMed2003

Sweat lactate response between males with high and low aerobic fitness.

Sweat lactate indirectly reflects eccrine gland metabolism. However the potential influence of aerobic fitness on sweat lactate is not well-understood. Six males with high aerobic fitness [peak oxygen consumption ( VO(2)peak): 61.6 (2.5) ml.kg(-1).min(-1)] and seven males with low aerobic fitness [ VO(2)peak: 41.8 (6.4) ml.kg(-1).min(-1)] completed a maximal exertion cycling trial followed on a different day by 60 min of cycling (60 rev.min(-1)) in a 30 degrees C wet bulb globe temperature environment. Intensity was individualized at 90% of the ventilatory threshold ( V(E)/ VO(2) increase with no concurrent V(E)/ VCO(2) increase). Sweat samples were collected from the lumbar region every 10 min and analyzed for lactate concentration. Sweat rate (SR) was significantly greater ( p<0.05) for subjects with a high [1445 (254) ml.h(-1)] versus a low [1056 (261) ml.h(-1)] fitness level. Also, estimated total lactate excretion (SRxmean sweat lactate concentration) was marginally greater ( p=0.2) in highly fit males. However, repeated measures ANOVA showed no significant differences ( p>0.05) between groups for sweat lactate concentration at any time point. Current results show highly fit (vs. low fitness level) males have a greater sweat rate which is consistent with previous literature. However aerobic fitness and subsequent variations in SR do not appear to influence sweat lactate concentrations in males.

Adult↗

PubMed2002

Understanding gustatory sweating. What have we learned from Lucja Frey and her predecessors?

Gustatory sweating results from a disruption of the auriculotemporal nerve pathways. Damage to the nerve may cause a misdirected re-growth that results in parasympathetic innervation of sympathetic receptors and, therefore, facial sweating and flushing with gustatory stimulation. Over the past 300 years, the history of gustatory sweating has included observations of typhus-induced parotiditis, war injuries, and occupational accidents. Despite religious and personal persecution, Lucja Frey (1889-1943) systematically investigated gustatory sweating. Following the discovery of a German World War II document regarding Lucja Frey, an international committee was organized to research the history of gustatory sweating and of Dr. Frey's contributions to the understanding of the syndrome. Twenty original scientific publications from 1700 to 1950 on gustatory sweating were reviewed. Frey was the first to describe gustatory sweating as a disorder of both sympathetic and parasympathetic innervation. She proposed novel pathologic and pharmacologic mechanisms to explain the syndrome. Subsequent discoveries, including the work of André-Thomas in 1927, have provided a more complete understanding of gustatory sweating and the pathologic mechanism of aberrant neuronal regeneration.

History, 20th Century↗

PubMed1980

Low sweat electrolytes in a patient with cystic fibrosis.

A patient with the clinical syndrome of cystic fibrosis characterized by chronic pulmonary disease, infection with mucoid Pseudomonas aeruginosa, sinusitis, nasal polyposis, abnormal pancreatic bicarbonate response to secretin stimulation, but normal levels of trypsin and chymotrypsin in the duodenal drainage, and a sibling with autopsy-documented cystic fibrosis, is described. Sweat chloride ranged from 20 to 44 meq/liter and sweat sodium from 36 to 55 meq/liter. Immunoglobulin deficiency, alpha 1-antitrypsin deficiency, tuberculosis and abnormalities of ciliary ultrastructure were excluded. Review of sweat electrolytes in 213 patients with cystic fibrosis revealed that patients with normal pancreatic enzyme release have significantly lower sweat sodium and chloride concentrations (p < 0.0005) than do patients with pancreatic insufficiency. Chronic pulmonary disease, pancreatic insufficiency and elevated levels of sweat electrolytes comprise the classic diagnostic triad for cystic fibrosis. The expression of these features may be variable, but the sweat test remains the cardinal laboratory confirmation of the diagnosis. Over 98 percent of patients with cystic fibrosis have sweat chloride values greater than 60 meq/liter, 1 to 2 percent between 50 and 60 meq/liter, and only about one in 1,000, like our patient, less than 50 meq/liter. Patients with cystic fibrosis with borderline sweat chloride values frequently have chronic pulmonary disease but intact pancreatic enzyme release. In such patients, family history, ancillary clinical features and systemic exclusion of other syndromes assume special diagnostic importance.

Adult↗

PubMed1996

Transplanted sweat glands from mature and aged donors determine cholinergic phenotype and altered density of host sympathetic nerves.

Contact with sweat gland acini causes sympathetic neurons to switch from a catecholaminergic to a cholinergic phenotype during development and following experimental manipulations. Substantial reductions of cholinergic innervation have been shown in the sweat glands of ageing rats and humans. Using in oculo transplantation, we have now studied whether sweat gland target tissues retain the capacity to regulate changes in the phenotype of sympathetic neurons observed in maturity and old age, including a switch from catecholaminergic to cholinergic characters. Markers have been used which indicate changes in nerve fibre morphology (the pan-neuronal marker, PGP9.5) as well as neurotransmitter expression (acetylcholinesterase (AChE), vasocative intestinal polypeptide (VIP) and tyrosine hydroxylase (TH)). Sweat glands from young and old donor rats became reinnervated by an organotypic pattern of cholinergic host nerves. Surgical sympathectomy demonstrated that these cholinergic nerve fibres originate from sympathetic neurons of the host superior cervical ganglion (SCG). Retrograde tracing combined with staining for VIP (a marker associated with cholinergic phenotype in neurons supplying sweat glands) showed that SCG neurons projecting to irises with sweat gland implants may be induced to express VIP. We hypothesise that these neurons have been switched from their normal catecholaminergic phenotype to a cholinergic one by contact with the sweat gland implants. Transplants from old donors attracted a density of reinnervation by young host nerves which was appropriate to the age of the donor, thus old sweat glands received a significantly reduced density of innervation compared to young glands. Despite the reduced density of innervation, there was no obvious difference in the ability of young and old implants to induce the switch to a cholinergic phenotype, suggesting that different mechanisms regulate nerve growth and neurotransmitter phenotype.

Adrenergic Fibers↗

PubMed1996

Functional reinnervation of sweat glands in the adult cat paw by inappropriate postganglionic axons.

Sympathetic postganglionic neurons were allowed to reinnervate the hairless skin of the cat paw pad, normally supplied by the tibial nerve, after suturing the central stump of the superficial peroneal nerve (supplying both hairy and hairless skin, eight animals) or of the sural nerve (supplying only hairy skin, seven animals) to the distal stump of the tibial nerve. Neural activation of sweat glands was studied by the starch iodine method and by recording the skin potential from the skin surface. Postganglionic neurons were activated by electrical stimulation of peripheral nerves or reflexly. There was good functional reinnervation of sweat glands by sudomotor neurons in all animals. The superficial peroneal nerve contains a few fibers that normally supply < 20% of the sweat glands on the foot pads. When this nerve regenerated into the innervation territory of the tibial nerve, sudomotor fibers consistently made functional contacts with sweat glands on the pads in all animals. These functional contacts were always weaker than those in the controls. Electrical stimulation of the sural nerve does not activate sweat glands in the paw pads of normal animals, indicating that this nerve does not contain postganglionic sudomotor axons. When the sural nerve regenerated into the foot pads, electrical stimulation activated some sweat glands in five of seven animals. We conclude that sudomotor neurons have a high capacity to functionally reinnervate sweat glands in the adult cat. There was also evidence that some noradrenergic vasoconstrictor neurons might take on "cholinergic features' in the adult animal when they reinnervate sweat glands suggesting that the peripheral target can specify the phenotypic properties of postganglionic neurons in the adult animal.

Animals↗

PubMed1996

Transplanted sweat glands from mature and aged donors determine cholinergic phenotype and altered density of host sympathetic nerves.

Contact with sweat gland acini causes sympathetic neurons to switch from a catecholaminergic to a cholinergic phenotype during development and following experimental manipulations. Substantial reductions of cholinergic innervation have been shown in the sweat glands of ageing rats and humans. Using in oculo transplantation, we have now studied whether sweat gland target tissues retain the capacity to regulate changes in the phenotype of sympathetic neurons observed in maturity and old age, including a switch from catecholaminergic to cholinergic characters. Markers have been used which indicate changes in nerve fibre morphology (the pan-neuronal marker, PGP9.5) as well as neurotransmitter expression (acetylcholinesterase (AChE), vasocative intestinal polypeptide (VIP) and tyrosine hydroxylase (TH). Sweat glands from young and old donor rats became reinnervated by an organotypic pattern of cholinergic host nerves. Surgical sympathectomy demonstrated that these cholinergic nerve fibres originate from sympathetic neurons of the host superior cervical ganglion (SCG). Retrograde tracing combined with staining for VIP (a marker associated with cholinergic phenotype in neurons supplying sweat glands) showed that SCG neurons projecting to irises with sweat gland implants may be induced to express VIP. We hypothesise that these neurons have been switched from their normal catecholaminergic phenotype to a cholinergic one by contact with the sweat gland implants. Transplants from old donors attracted a density of reinnervation by young host nerves which was appropriate to the age of the donor, thus old sweat glands received a significantly reduced density of innervation compared to young glands. Despite the reduced density of innervation, there was no obvious difference in the ability of young and old implants to induce the switch to a cholinergic phenotype, suggesting that different mechanisms regulate nerve growth and neurotransmitter phenotype.

Adrenergic Fibers↗

PubMed1982

Sweating in the intact horse and isolated perfused horse skin.

1. In intact horses, heat-induced sweating occurred initially as pulses, then as a continuous, synchronously fluctuating discharge. 2. I.V. adrenaline (Adr) induced sweating immediately; isoprenaline (Isop) elicited sweating after a delay; and phenylephrine (PhE) had no sudorific effect. 3. In isolated perfused skin, PhE induced an immediate small sweat discharge, Isop a slower sustained output and Adr a biphasic discharge. alpha- and beta-adrenergic antagonists blocked the first and second phases, respectively, of Adr-induced sweating. 4. The observed sweating patterns are consistent with independent activation of alpha-adrenergic myoepithelium and beta-adrenergic secretory cells in the sweat glands. 5. Microcirculatory changes apparently also influenced sweat discharge.

Animals↗

PubMed2004

Severity of compensatory sweating after thoracoscopic sympathectomy.

BACKGROUND: Compensatory sweating is a well-known side effect after sympathectomy for hyperhidrosis. It is often claimed to correlate with the extent of sympathectomy, but results from the literature are conflicting, and few have actually considered differences in the intensity of compensatory sweating. METHODS: A total of 158 patients underwent thoracoscopic sympathectomy for primary hyperhidrosis or blushing, or both. Sympathectomy was performed bilaterally at Th2 for facial hyperhidrosis/blushing (n = 49), Th2-3 for palmar hyperhidrosis (n = 62), and Th2-4 for axillary hyperhidrosis (n = 47). RESULTS: Follow-up by questionnaire was possible in 94% of patients after a median of 26 months. Compensatory sweating occurred in 89% of patients and was so severe in 35% that they often had to change their clothes during the day. The frequency of compensatory sweating was not significantly different among the three groups, but severity was significantly higher after Th2-4 sympathectomy for axillary hyperhidrosis (p = 0.04). Gustatory sweating occurred in 38% of patients, and 16% of patients regretted the operation. CONCLUSIONS: Compensatory and gustatory sweating were remarkably frequent side effects after thoracoscopic sympathectomy for primary hyperhidrosis. We found no significant difference between the level of sympathectomy and the occurrence of compensatory sweating. However, it appears that this is the first study to demonstrate that severe sweating is significantly more frequent after Th2-4 sympathectomy for axillary hyperhidrosis. We encourage informing patients thoroughly about these side effects before surgery.

Adolescent↗

PubMed2006

Measurement of cytokines in sweat patches and plasma in healthy women: validation in a controlled study.

Cytokines have been detected by ELISA in a variety of body fluids. Recycling immunoaffinity chromatography (RIC) coupled with laser-induced fluorescence detection is a highly sensitive and specific method, which allows simultaneous measurements of many analytes in small volumes of biological fluids. This method has been applied to plasma, cervical secretions and other body fluids, but has not previously been applied to sweat. The aim of this study was to validate the RIC methodology in sweat for measurements of IL-1alpha, IL-1beta, IL-6, TNF-alpha, IL-8 and TGF-beta. Two sweat patches were applied for 24 h on the torso, and blood was collected at one time point during this period in nine healthy women. Cytokines were measured in paired samples of plasma and sweat. Cytokines were detected in sweat in similar concentrations to plasma. Linear regression analysis confirmed that sweat levels of these cytokines accounted for a large percentages of variance in plasma levels: IL-1alpha (R2 = 0.70, p = 0.005), IL-1beta (R2 = 0.79, p = 0.003), IL-6 (R2 = 0.52, p = 0.03), TNF-alpha (R2 = 0.95, p < 0.0001), IL-8 (R2 = 0.81, p = 0.001) and TGF-beta (R2 = 0.94, p = 0.0003). These findings indicate that cytokine levels measured in sweat are informative of circulating levels and that sweat patches combined with RIC represents a viable non-invasive method to measure cytokines in ambulatory settings over time. This method is unobtrusive and requires minimal active compliance on the part of the subjects being studied, without pain or stress. This approach can open a new generation of studies to address the effects of environmental factors on immune responses in a wide range of different settings.

Case-Control Studies↗

PubMed1994

Clinical evaluation of the macroduct sweat collection system and conductivity analyzer in the diagnosis of cystic fibrosis.

The purposes of this study were to compare sweat tests used in diagnosing cystic fibrosis (CF), as performed with the Macroduct collection system, with those utilizing the more laborious quantitative pilocarpine iontophoresis test (QPIT), and to ascertain the efficacy of the Sweat-Chek conductivity analyzer in eliminating some possibly unnecessary chloride analyses. A Macroduct sweat test was performed on one arm and a QPIT on the other on 1090 patients, 93 of whom had CF. Of these, 514 patients (43 with CF) also had a conductivity determination on the Macroduct sweat sample. All subjects were referred to the laboratory of one of us (K.B.H.) for sweat testing. Of the QPIT samples, 0.7% were inadequate, as were 6.1% of those from the Macroduct system. When sodium and chloride concentrations from the two tests were compared, the standard errors of the estimate were 3.90 and 3.85, respectively. Agreement within 8 mEq/L could then be expected with 95% confidence limits. With use of the Sweat-Chek analyzer, no patient with CF was found to have a conductivity of less than 90 mmol/L, whereas 430 (91%) of the non-CF subjects had a conductivity of less than 50 mmol/L. None of those 430 subjects had a sweat chloride value > 32 mmol/L. We conclude that the Macroduct collection system provides results equally as satisfactory as those provided by the QPIT and that the Sweat-Chek analyzer frequently eliminates the necessity of measuring chloride concentrations.

Adolescent↗

PubMed2005

Gene delivery to human sweat glands: a model for cystic fibrosis gene therapy.

Gene therapy vectors are mostly studied in cultured cells, rodents, and sometimes in non-human primates, but it is useful to test them in human tissue prior to clinical trials. In this study, we investigated the possibility of using human sweat glands as a model for testing cystic fibrosis (CF) gene therapy vectors. Human sweat glands are relatively easy to obtain from skin biopsy, and can be tested for CFTR function. Using patients' sweat glands could provide a safe model to study the efficacy of CF gene therapy. As the first step to explore using sweat glands as a model for CF gene therapy, we examined various ex vivo gene delivery methods for a helper-dependent adenovirus (HD-Ad) vector. Gene delivery to sweat glands in skin organ culture was studied by topical application, intradermal injection or submerged culture. We found that transduction efficiency can be enhanced by pretreating isolated sweat glands with dispase, which suggests that the basement membrane is a critical barrier to gene delivery by adenoviral vectors. Using this approach, we showed that Cftr could be efficiently delivered to and expressed by the epithelial cells of sweat glands with our helper-dependent adenoviral vector containing cytokeratin 18 regulatory elements. Based on this study we propose that sweat glands might be used as an alternative model to study CF gene therapy in humans.

Adenoviridae↗

PubMed2006

Generation of multiple stable dermcidin-derived antimicrobial peptides in sweat of different body sites.

Antimicrobial peptides (AMPs) are effector molecules of innate immunity. Dermcidin (DCD), a recently discovered AMP with broad-spectrum activity, is produced constitutively by the eccrine sweat glands and secreted into sweat. In this study, we investigated the proteolytic processing, site-specific expression, and stability of DCD peptides in eccrine sweat. Using surface-enhanced laser desorption ionization time-of-flight mass spectrometry (SELDI-TOF-MS) and reversed-phase high-pressure liquid chromatography analysis, we identified in eccrine sweat 14 proteolytically processed DCD peptides. Semiquantitative SELDI-TOF-MS analysis indicated that processing of DCD-1L is individually different, but generates a few dominant peptides. At body sites with a high probability for contact with pathogenic microorganisms, a high amount of antimicrobial active DCD peptides was detected in sweat. Furthermore, we show that the secretion rate of DCD is constant during a period of prolonged sweating and that DCD peptides are stable in sweat over several hours. Other known AMPs like the human cathelicidin LL-37 and alpha- or beta-defensins were not detected in significant quantity in eccrine sweat. Owing to the durable and abundant presence, DCD-derived peptides contribute to the first line of defense by building a constant barrier that overlies the epithelial skin.

Adult↗

PubMed2000

Operative field contamination by the sweating surgeon.

BACKGROUND: There are a number of factors relating to the host, bacteria and wound that are important in the development of wound infection. The effect of the surgeon sweating has not been previously reported. METHODS: Ten surgeons performed a mock total hip joint operation under sterile conditions while not sweating and then repeated the operation while sweating. Settle plates were used to quantify the bacterial counts in the operative field in both phases. RESULTS: For each subject a mean of 3.3 colony forming units (c.f.u.) were present in the non-sweating phase and 6.9 c.f.u. were present in the sweating phase (P < 0.05). Organisms grown were normal skin flora. CONCLUSION: The sweating surgeon may be more likely to contaminate the surgical field than the non-sweating surgeon. It is important for orthopaedic surgeons, especially those performing joint replacement surgery, to be aware of this and to take measures to minimize sweating in the operating theatre.

Adult↗

PubMed2000

Effects of high and low blood lactate concentrations on sweat lactate response.

Sweat lactate results from eccrine gland metabolism, however, the possible clearance of blood lactate through sweat has not been resolved. On separate days in an environmental chamber (32 +/- 1 C) 12 subjects completed a constant load (CON) (30 min at 40% VO2 max) and an interval cycling trial (INT) (15 one-min intervals at 80% VO2 max, each separated by one min rest) each designed to elicit different blood lactate responses. Each 30 min cycling trial was preceded by 15 min warm-up (30 watts) and followed by 15 min passive rest. Sweat and blood were analyzed for lactate concentration at 15, 25, 35, 45, and 60 min during CON and INT. Total body water loss was used to calculate sweat rate (ml/hr). Blood lactate was significantly greater (p < or = 0.05) at 25, 35, 45, and 60 min during INT compared to CON (approximately 5 mmol/L vs 1.5 mmol/L). Sweat lactate was not significantly different (p>0.05) between trials at any time (approximately 10 mmol/L). Sweat rates (approximately 600ml/hr) and estimated total lactate secretion were not significantly different (CON vs. INT) (p > 0.05). Elevated blood lactate was not associated with changes in sweat lactate concentration. Sweat lactate seems to originate in eccrine glands independent of blood lactate.

Adult↗

PubMed2005

Sweat lactate, ammonia, and urea in rugby players.

The purpose of this study was to investigate sweat lactate, ammonia, and urea excretion in rugby players. Fifteen elite amateur rugby players volunteered to participate. The study was conducted during competitive matches in the official season. Plasma and sweat concentrations of lactate, ammonia, and urea were measured before and after the matches. Peak values for creatine kinase activity were observed 24 h after the match. There was no significant change between time points for blood lactate concentration but secretion rate per unit surface and time was significantly reduced after the match. Sweat ammonia concentration increased significantly during the match; values were significantly reduced after 24 h and still remained low at 72 h. Secretion rate was also reduced from 24 h. Urea concentration was significantly reduced at 48 h, while secretion rates decreased at 24 h and 48 h. Lactate in blood was significantly elevated during the match but not thereafter. Blood ammonia was significantly elevated during the match and did not differ from the resting values at 24 or 48 h. Urea in blood tended to decrease during the match, with a significant reduction at 24 h. Significant positive correlations were observed between blood and sweat concentrations for urea and ammonia but not for lactate. Sweat rate correlated positively with sweat lactate secretion. The fact that part of the ammonia formed during exercise is lost with sweat indicates the importance of the purine nucleotide cycle during rugby matches. Our data also confirm that sweat lactate concentration is not influenced by circulatory blood lactate in rugby players.

Adult↗

PubMed1997

Lactate and ammonia concentration in blood and sweat during incremental cycle ergometer exercise.

It is known that the concentrations of ammonia and lactate in blood increase during incremental exercise. Sweat also contains lactate and ammonia. The aim of the present study was to investigate the physiological response of lactate and ammonia in plasma and sweat during a stepwise incremental cycle ergometer exercise test in ten subjects. During this test lactate and ammonia were measured in blood obtained from the earlobe and in sweat collected in a bag attached to the back of the subject. At the end of each interval this bag was emptied for measuring lactate and ammonia. A disproportional increase in the concentration of lactate and ammonia in blood was found, in sweat a disproportional decrease. The lactate concentrations in sweat were higher than those in blood. We hypothesise that lactate in sweat is produced from glycogen granules of the clear cell of the eccrine gland. This lactate production results in acidification of sweat, which facilitates the diffusion of ammonia from eccrine duct cell to duct lumen. It is uncertain how far duct cell ammonia originates from plasma, the duct cell itself might produce ammonia. Part of the ammonia in sweat could come from the breakdown of urea by skin bacteria.

Adult↗

PubMed2005

Cathepsin D is present in human eccrine sweat and involved in the postsecretory processing of the antimicrobial peptide DCD-1L.

The protein pattern of healthy human eccrine sweat was investigated and 10 major proteins were detected from which apolipoprotein D, lipophilin B, and cathepsin D (CatD) were identified for the first time in human eccrine sweat. We focused our studies on the function of the aspartate protease CatD in sweat. In vitro digestion experiments using a specific fluorescent CatD substrate showed that CatD is enzymatically active in human sweat. To identify potential substrates of CatD in human eccrine sweat LL-37 and DCD-1L, two antimicrobial peptides present in sweat, were digested in vitro with purified CatD. LL-37 was not significantly digested by CatD, whereas DCD-1L was cleaved between Leu(44) and Asp(45) and between Leu(29) and Glu(30) almost completely. The DCD-1L-derived peptides generated in vitro by CatD were also found in vivo in human sweat as determined by surface-enhanced laser desorption/ionization (SELDI) mass spectrometry. Furthermore, besides the CatD-processed peptides we identified additionally DCD-1L-derived peptides that are generated upon cleavage with a 1,10-phenanthroline-sensitive carboxypeptidase and an endoprotease. Taken together, proteolytic processing generates 12 DCD-1L-derived peptides. To elucidate the functional significance of postsecretory processing the antimicrobial activity of three CatD-processed DCD-1L peptides was tested. Whereas two of these peptides showed no activity against Gram-positive and Gram-negative bacteria, one DCD-1L-derived peptide showed an even higher activity against Escherichia coli than DCD-1L. Functional analysis indicated that proteolytic processing of DCD-1L by CatD in human sweat modulates the innate immune defense of human skin.

Amino Acid Sequence↗