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In this research, the occurrence of hygienic quality and histamine in commercial brined and dried milkfish products, and the effects of brine concentrations on the quality of brined and dried milkfish, were studied. Brined and dried milkfish products (n = 20) collected from four retail stores in Taiwan were tested to investigate their histamine-related quality. Among them, five tested samples (25%, 5/20) had histamine contents of more than 5 mg/100 g, the United States Food and Drug Administration guidelines for scombroid fish, while two (10%, 2/20) contained 69 and 301 mg/100 g of histamine, exceeding the 50 mg/100 g potential hazard level. In addition, the effects of brine concentrations (0%, 3%, 6%, 9%, and 15%) on the chemical and bacteriological quality of brined and dried milkfish during sun-drying were evaluated. The results showed that the aerobic plate count (APC), coliform, water activity, total volatile basic nitrogen (TVBN), and histamine content values of the brined and dried milkfish samples decreased with increased brine concentrations, whereas those of salt content and thiobarbituric acid (TBA) increased with increasing brine concentrations. The milkfish samples prepared with 6% NaCl brine had better quality with respect to lower APC, TVBN, TBA, and histamine levels.

M2-polarization and the tumoricidal to tumor-promoting transition are commonly observed with tumor-infiltrating macrophages after interplay with cancer cells or/and other stroma cells. Our previous study indicated that macrophage M2-polarization can be induced by extracellular HSP90α (eHSP90α) secreted from endothelial-to-mesenchymal transition-derived cancer-associated fibroblasts. To extend the finding, we herein validated that eHSP90α-induced M2-polarized macrophages exhibited a tumor-promoting activity and the promoted tumor tissues had significant increases in microvascular density but decreases in CD4 + T-cell level. We further investigated the signaling pathways occurring in eHSP90α-stimulated macrophages. When macrophages were exposed to eHSP90α, CD91 and toll-like receptor 4 (TLR4) functioned as the receptor/co-receptor for eHSP90α binding to recruit interleukin (IL)-1 receptor-associated kinases (IRAKs) and myeloid differentiation factor 88 (MyD88), and next elicited a canonical CD91/MyD88-IRAK1/4-IκB kinase α/β (IKKα/β)-nuclear factor-κB (NF-κB)/interferon regulatory factor 3 (IRF3) signaling pathway. Despite TLR4-MyD88 complex-associated activations of IKKα/β, NF-κB and IRF3 being well-known as involved in macrophage M1-activation, our results demonstrated that the CD91-TLR4-MyD88 complex-associated IRAK1/4-IKKα/β-NF-κB/IRF3 pathway was not only directly involved in M2-associated CD163, CD204, and IL-10 gene expressions but also required for downregulation of M1 inflammatory cytokines. Additionally, Janus kinase 2 (JAK2) and tyrosine kinase 2 (TYK2) were recruited onto MyD88 to induce the phosphorylation and activation of the transcription factor signal transducer and activator of transcription-3 (STAT-3). The JAK2/TYK2-STAT-3 signaling is known to associate with tumor promotion. In this study, the MyD88-JAK2/TYK2-STAT-3 pathway was demonstrated to contribute to eHSP90α-induced macrophage M2-polarization by regulating the expressions of M1- and M2-related genes, proangiogenic protein vascular endothelial growth factor, and phagocytosis-interfering factor Sec22b.