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Acacia caven (Mol.) Molina pollen causes pollinosis in South America. The aim of this work was to isolate, purify, and characterize the proteolytic enzymes of A. caven pollen, and study their influence on allergy. A series of chromatographic steps were applied to purify the proteolytic extract of A. caven pollen. The purified fraction was partially characterized, and then it was assayed on airway bioactive peptides (substance P, vasoactive intestinal peptide, and bradykinin), and peptide degradation was visualized by direct protein sequencing. The cellular detachment of an airway‐derived epithelial cell line (A‐549) was measured by methylene blue binding assay. The degradation of proteins from intercellular junctions (occludin, claudin, and E‐cadherin) was visualized by Western blot. A 75‐kDa peptidase, named acaciain peptidase, was purified and classified as a serine peptidase. Acaciain peptidase degraded bioactive peptides involved in the maintenance and recovery of the bronchomotor tone; it caused cellular detachment of A‐549 cell line, and degradation of intercellular junction proteins. Acaciain peptidase can alter the integrity of the epithelium barrier, causing cell permeability, increasing the allergic sensitization and exacerbating the overall bronchoconstrictive effect detected in asthmatic lungs. This novel serine peptidase constitutes a relevant therapeutic target in the treatment of allergic disorders. [ABSTRACT FROM AUTHOR]

In cephalopod hatchlings there is a transitional period considered critical, in which the digestive system undergoes morphophysiological changes associated with the passage from the consumption of vitelline reserves to an independent feeding. During this period, the characterization of the digestive dynamics and growth is key information to define their nutritional requirements under culture. Octopus tehuelchus , which has become increasingly interesting for cultivation, is a species endemic to South America with holobenthic development and large juveniles. In this work, the enzymatic and cytological changes of the digestive gland (DG) along with the variation in body weight and size of O. tehuelchus hatchlings were evaluated when reared at 16 °C under two feeding treatments: fed with the isopod Exosphaeroma sp. and starved. In fed juveniles, the predatory activity began a few hours after hatching; and up to 6 days post hatching (DPH) there was neither somatic growth nor cellular differentiation of the DG, but there was an activation of acid enzymes. From 6 to 10 DPH, there was an increase in the size and weight of juveniles, and the maturation of the DG began with the appearance of heterolysosomes and heterophagosomes. Furthermore, lipases activity reached its maximum level and there was a considerable increase in both alkaline phosphatases and peptidases. From 15 to 25 DPH, the DG became fully mature and the lipase activity reached minimum levels, while the alkaline peptidases continued increasing. At the end of the experiment, at 25 DPH, fed juveniles doubled their weight. In the starved juveniles, neither somatic growth nor cytological differentiations of the DG were registered. Besides, in this treatment, acid phosphatases and lipase activities (i.e. enzymes related to yolk consumption) remained at basal levels or decreased over time, even with yolk platelets still present, suggesting that the consumption of yolk reserves would be delayed, regulating the survival time. In fed juveniles, the ingestion of isopods seems to act as a modulating factor of the digestive activity, triggering an increment in the activity of lipases, acid phosphatases, as well as alkaline peptidases which are related to the digestion of exogenous food. It is concluded that morphological and physiological changes during the digestive maturation are related to the ingestion of Exosphaeroma sp. In this sense, this isopod species would be a suitable food which promotes the rapid growth of O. tehuelchus during their early post-hatching stage under culture. • The consumption of yolk reserves is regulated according to the availability of food. • A feeding based on Exosphaeroma sp. has a positive effect on growth of Octopus tehuelchus juveniles. • Growth and digestive gland differentiation are seen from the second week of life in fed hatchlings. • The energy available from yolk is used for maintenance and not for development in non-fed juveniles. [ABSTRACT FROM AUTHOR]

Abstract: Tripeptidyl-peptidase 1 (TPP1) null or residual activity occurs in neuronal ceroid lipofuscinosis (NCL) with underlying TPP1/CLN2 mutations. A survey of 25 South American CLN2 affected individuals enabled the differentiation of two phenotypes: classical late-infantile and variant juvenile, each in approximately 50% of patients, with residual TPP1 activity occurring in approximately 32%. Each individual was assigned to one of three subgroups: (I) n=11, null TPP1 activity in leukocytes; (II) n=8, residual TPP1 activity of 0.60–15.85nmol/h/mg (nr 110–476); (III) n=6, activity not measured in leukocytes. Curvilinear bodies (CB) appeared in almost all studied CLN2 subjects; the only exceptions occurred in cases of subgroup II: two individuals had combined CBs/fingerprints (FPs), and one case had pure FPs. There were 15 mutations (4 first published in this paper, 3 previously observed in South America by our group, and 8 previously observed by others). In subgroup I, mutations were either missense or nonsense; in subgroups II and III, mutations prevailed at the non-conserved intronic site, c.887−10A>G (intron 7), and to a lesser extent at c.89+5G>C (intron 2), in heterozygous combinations. Grouping phenotypically and genetically known individuals on the basis of TPP1 activity supported the concept that residual enzyme activity underlies a protracted disease course. The prevalence of intronic mutations at non-conserved sites in subgroup II individuals indicates that some alternative splicing might allow some residual TPP1 activity. [Copyright &y& Elsevier]

Zika virus (ZIKV) is a mosquito-borne flavivirus, and its infection may cause severe neurodegenerative diseases. The outbreak of ZIKV in 2015 in South America has caused severe human congenital and neurologic disorders. Thus, it is vitally important to determine the inner mechanism of ZIKV infection. Here, our data suggested that the ubiquitin-specific peptidase 38 (USP38) played an important role in host resistance to ZIKV infection, during which ZIKV infection did not affect USP38 expression. Mechanistically, USP38 bound to the ZIKV envelope (E) protein through its C-terminal domain and attenuated its K48-linked and K63-linked polyubiquitination, thereby repressed the infection of ZIKV. In addition, we found that the deubiquitinase activity of USP38 was essential to inhibit ZIKV infection, and the mutant that lacked the deubiquitinase activity of USP38 lost the ability to inhibit infection. In conclusion, we found a novel host protein USP38 against ZIKV infection, and this may represent a potential therapeutic target for the treatment and prevention of ZIKV infection. [ABSTRACT FROM AUTHOR]