Beta-defensin 36
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Beta-defensin 36

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Beta-defensin 36 is an antibacterial peptide isolated from Mus musculus.

Category
Functional Peptides
Catalog number
BAT-013694
Sequence
QKCWNLHGKCRHRCSRKESVYVYCTNGKMCCVKPKYQPKPKPWMF
1. Characterization of the β-defensin genes in giant panda
Zhi-Yi Zhang, He-Min Zhang, De-Sheng Li, Tie-Yi Xiong, Sheng-Guo Fang Sci Rep. 2018 Aug 17;8(1):12308. doi: 10.1038/s41598-018-29898-2.
β-Defensins are small antimicrobial proteins expressed in various organisms and have great potential for improving animal health and selective breeding programs. Giant pandas have a distinctive lineage in Carnivora, and it is unclear whether β-defensin genes have experienced different selective pressures during giant panda evolution. We therefore characterized the giant panda (Ailuropoda melanoleuca) β-defensin gene family through gap filling, TBLASTN, and HMM searches. Among 36 β-defensins identified, gastrointestinal disease may induce the expression of the DEFB1 and DEFB139 genes in the digestive system. Moreover, for DEFB139, a significant positive selection different from that of its homologs was revealed through branch model comparisons. A Pro-to-Arg mutation in the giant panda DEFB139 mature peptide may have enhanced the peptide's antimicrobial potency by increasing its stability, isoelectric point, surface charge and surface hydrophobicity, and by stabilizing its second β-sheet. Broth microdilution tests showed that the increase in net charge caused by the Pro-to-Arg mutation has enhanced the peptide's potency against Staphylococcus aureus, although the increase was minor. We expect that additional gene function and expression studies of the giant panda DEFB139 gene could improve the existing conservation strategies for the giant panda.
2. Clinicopathologic overlap of psoriasis, eczema, and psoriasiform dermatoses: A retrospective study of T helper type 2 and 17 subsets, interleukin 36, and β-defensin 2 in spongiotic psoriasiform dermatitis, sebopsoriasis, and tumor necrosis factor α inhibitor-associated dermatitis
Jarish N Cohen, Sarah Bowman, Zoltan G Laszik, Jeffrey P North J Am Acad Dermatol. 2020 Feb;82(2):430-439. doi: 10.1016/j.jaad.2019.08.023. Epub 2019 Dec 16.
Background: T helper (Th) type 17 and Th2 cells mediate psoriasis and eczema, respectively. Some dermatoses exhibit overlapping clinicopathologic features, and their immunopathology is relatively unexplored. Objective: To determine whether Th17 and Th2 subsets and interleukin (IL) 36 and β-defensin 2 (BD-2) markers of IL-17 signaling expression can discriminate between biopsy samples of psoriasis and eczematous/spongiotic dermatitis and to use those markers to immunophenotype cases with clinicopathologic overlap. Methods: A retrospective study was performed on biopsy samples of psoriasis, eczema/spongiotic dermatitis, sebopsoriasis, tumor necrosis factor α inhibitor-associated psoriasiform dermatitis, and ambiguous cases diagnosed as spongiotic psoriasiform dermatitis. Dual CD4/GATA3 and CD4/RORC, IL-36, and BD-2 immunohistochemistry was performed. Results: IL-36 and BD-2 were strongly expressed in biopsy samples of psoriasis compared with eczema/spongiotic dermatitis. No significant differences were observed in the percentages of Th2 and Th17 cells between disease types. Strong expression of IL-36 and BD-2 was observed in a subset of spongiotic psoriasiform dermatitis, sebopsoriasis, and tumor necrosis factor α inhibitor-associated psoriasiform dermatitis biopsy samples. Limitations: This was an exploratory study with a small sample size. No multiple testing adjustment was done. Clinical follow-up was limited. Conclusions: In cases with clinicopathologic overlap between psoriasis and spongiotic dermatitis, IL-36, and to a lesser extent BD-2, may be used to assess for a psoriasis-like/IL-17 phenotype, which could inform therapeutic clinical decisions.
3. HUMAN-BETA-DEFENSIN-1: PROGNOSTIC MARKER OF TUBERCULOSIS SEVERITY AND TREATMENT EFFECTIVENESS IN PULMONARY TUBERCULOSIS
Olha O Pohorielova, Olga S Shevchenko Wiad Lek. 2021;74(8):1839-1843.
Objective: The aim: Was to investigate human-beta-defensin-1 level in blood serum depending on tuberculosis severity and treatment ef f ectiveness. Patients and methods: Materials and methods: 100 patients with pulmonary tuberculosis and 20 healthy persons were included to the study. HBD-1 level was measured by ELISA in all the healthy persons and in all the patients at the treatment onset and at the end of initial phase of treatment. Additionally, the patients were examined with chest X-ray, sputum microscopy and culture, blood test and blood biochemistry. Results: Results: HBD-1 level was higher in patients with tuberculosis (21.5 ± 2.9 μmol/L) compared with healthy individuals (8.9 ± 2.5 μmol/L). A positive correlation of middle strength was found between the size of lung lesion and the level of HBD-1 and between the level of HBD-1 and the massiveness of bacterial excretion. We found weakly negative correlations between the level of HBD-1 at the beginning of treatment and parameters of life quality rated on sf-36 scale. Patients with initially high level of HBD-1 had preservation of bacterial excretion, as well as signs of inf l ammatory activity. In patients with an ef f ective intensive phase of treatment, the initial level of HBD-1. Conclusion: Conclusions: The larger pulmonary tuberculosis lesion, as well as the more pronounced clinical manifestations lead to the higher level of HBD-1. The possibility of using human-beta-defensin-1 as a prognostic marker of treatment ef f ectiveness is conf i rmed by the fact that human-beta-defensin-1 level prevails at the beginning of treatment in patients with subsequently non-ef f ective intensive phase of treatment.
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