Horses are unusual in producing protein-rich sweat for thermoregulation, a major component of which is latherin, a highly surface-active, non-glycosylated protein. The amino acid sequence of latherin, determined from cDNA analysis, is highly conserved across four geographically dispersed equid species (horse, zebra, onager, ass), and is similar to a family of proteins only found previously in the oral cavity and associated tissues of mammals. Latherin produces a significant reduction in water surface tension at low concentrations (≤1 mg ml−1), and therefore probably acts as a wetting agent to facilitate evaporative cooling through a waterproofed pelt. Neutron reflection experiments indicate that this detergent-like activity is associated with the formation of a dense protein layer, about 10 Å thick, at the air-water interface. However, biophysical characterization (circular dichroism, differential scanning calorimetry) in solution shows that latherin behaves like a typical globular protein, although with unusual intrinsic fluorescence characteristics, suggesting that significant conformational change or unfolding of the protein is required for assembly of the air-water interfacial layer. RT-PCR screening revealed latherin transcripts in horse skin and salivary gland but in no other tissues. Recombinant latherin produced in bacteria was also found to be the target of IgE antibody from horse-allergic subjects. Equids therefore may have adapted an oral/salivary mucosal protein for two purposes peculiar to their lifestyle, namely their need for rapid and efficient heat dissipation and their specialisation for masticating and processing large quantities of dry food material.
Sweating has a variety of functions in mammals including pheromone action, excretion of waste products and maintenance of the skin surface ecosystem. In a small number of mammalian species, which includes humans and the Equidae, it also has an important role in thermoregulation. This review is focused specifically on the thermoregulatory role of sweat in Equidae and the causes of sweating failure (anhidrosis). The first part describes the glandular appearance, sweat composition, and output rates; and considers the latest theories on the glandular control and secretory mechanisms. It is concluded that the glands are not directly innervated but are controlled by the interplay of neural, humoral and paracrine factors. The secretory mechanism is not as simple as previously thought and is mediated by the dynamic interaction of activating pathways, including autocrine control not only of the secretory process but probably also of secretory cell reproduction, growth, and death.
No nerve fibres were found near the apocrine gland, suggesting that any catecholamine influence is through humoral effects and that glands could be influenced by beta-adrenoceptor subtypes and purinoceptors. Blockage of both these types of receptors offers a route to controlling apocrine secretion from axillary glands and reducing the opportunity for the development of bromhidrosis.
The present finding of the absence of structural defects in the glands indicates that future studies should concentrate on the investigation of neurohumoral or secretory cell metabolic abnormalities.
The condition of anhidrosis is described in this review, and the latest theories on the causal factors are explored. The evidence supports the hypothesis that anhidrosis is an inappropriate response to prolonged climatic stress (generally combined heat and high humidity), which can be evoked in a small (approximately 10 +/- 5%) proportion of the equine population. It is caused by gradual failure of the glandular secretory cell processes, initiated by desensitization and subsequent down-regulation of the cell receptors as a result of continued adrenaline-driven hyperactivity. It progresses through secretory failure and culminates in gradual, probably irreversible, glandular dedifferentiation and ultimate degeneration. There is a need for considerably more research on the secretory and transcriptional processes to document the changes arising within the glandular secretory mechanism as a prelude to development of a corrective treatment.
SUMMARYWe have explored the factors that may regulate membrane permeability in a cell line (NCL-SG3) derived from the human sweat gland epithelium. lonomycin increased the rate of 1251-efflux from preloaded cells and this action appeared to be due to an increase in intracellular free calcium ([Ca2+]). The ionomycin-evoked increase in 1251-efflux was reduced in cells that were exposed either to barium or to valinomycin in the presence of a high concentration of external potassium. It thus appears that a fraction of the ionomycin-evoked increase in 1251-efflux is due to the activation of potassium channels and experiments using 8"Rb+ also suggested that ionomycin increased the rate of potassium efflux, an effect which was totally abolished by barium. Blockade of Na+-K+-2Cl1-cotransport and of Cl--HCO exchange reduced the basal rate of 1251-efflux and the ionomycin-evoked increase in 1251-efflux from control cells and from cells depolarized by valinomycin. These transport systems thus contribute to anion efflux, although [Ca2+]-dependent chloride channels also appear to be present. Acetylcholine increases [Ca2+] [Ca2+]i, but this hormone did evoke cyclic-3',5'-adenosine monophosphate (cyclic AMP) production. However, membrane permeability was riot under adrenergic control, as the cells did not appear to express functional, cyclic AMP-dependent anion channels. This may be because they were not fully differentiated under the culture conditions. ATP consistently evoked a dose-dependent increase in anion efflux that appeared to be mediated by [Ca2+]i. The increase in [Ca2+]i was initiated by the release of calcium from a limited internal store and was subsequently sustained by calcium influx. UTP and ADP also increased [Ca2+]i, whereas adenosine, AMP and x,/i-methylene ATP were without effect. These data thus suggest that a subclass of type 2 purine receptor, which is functionally coupled to phosphoinositidase C, is present in these cells.
For several decades now, researchers, professional bodies, governments, and journals such as the journal of Experimental Dermatology have worked to reduce the number of animals used in experimentation. This review centres on investigations into how human sweat glands produce sweat and how that research has evolved over the years. It is hoped that this review will show that as methodologies advanced, sweat gland research has come to rely less and less on a variety of animal models as investigative tools and information is being primarily obtained through human and mouse material, with a view to further reductions in using animal models.
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