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Tartrate-Resistant Acid Phosphatase 5 (TRAP5) Promotes Eosinophil Migration During Allergic Asthma

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Názov: Tartrate-Resistant Acid Phosphatase 5 (TRAP5) Promotes Eosinophil Migration During Allergic Asthma
Autori: Padra, Medea, Bergwik, Jesper, Adler, Anna, Marcoux, Genevieve, Bhongir, Ravi K.V., Papareddy, Praveen, Egesten, Arne
Prispievatelia: Lund University, Faculty of Medicine, Department of Clinical Sciences, Lund, Section II, Respiratory Medicine, Allergology, and Palliative Medicine, Lunds universitet, Medicinska fakulteten, Institutionen för kliniska vetenskaper, Lund, Sektion II, Lungmedicin, allergologi och palliativ medicin, Originator, Lund University, Faculty of Medicine, Department of Clinical Sciences, Lund, Section III, Infection Medicine (BMC), Airways, pathogens, innate immunity, Lunds universitet, Medicinska fakulteten, Institutionen för kliniska vetenskaper, Lund, Sektion III, Infektionsmedicin, Luftvägar, patogener, immunförsvar, Originator, Lund University, Faculty of Medicine, Department of Clinical Sciences, Lund, Infect@LU, Lunds universitet, Medicinska fakulteten, Institutionen för kliniska vetenskaper, Lund, Infect@LU, Originator, Lund University, Faculty of Medicine, Department of Clinical Sciences, Lund, Section II, Respiratory Medicine, Allergology, and Palliative Medicine, Translational Respiratory Medicine, Lunds universitet, Medicinska fakulteten, Institutionen för kliniska vetenskaper, Lund, Sektion II, Lungmedicin, allergologi och palliativ medicin, Translationell lungmedicin, Originator, Lund University, Faculty of Medicine, Department of Clinical Sciences, Lund, Section III, Infection Medicine (BMC), Experimental Infection Medicine, Lunds universitet, Medicinska fakulteten, Institutionen för kliniska vetenskaper, Lund, Sektion III, Infektionsmedicin, Experimental Infection Medicine, Originator, Lund University, Faculty of Medicine, Department of Clinical Sciences, Lund, Section II, Respiratory Medicine, Allergology, and Palliative Medicine, Novel strategies targeting detrimental airway inflammation, Lunds universitet, Medicinska fakulteten, Institutionen för kliniska vetenskaper, Lund, Sektion II, Lungmedicin, allergologi och palliativ medicin, Nya strategier för att förhindra skadlig luftvägsinflammation, Originator, Lund University, Faculty of Medicine, Department of Clinical Sciences, Lund, Section II, Respiratory Medicine, Allergology, and Palliative Medicine, Hereditary angioedema (HAE) – epidemiology, genetics and pathophysiology, Lunds universitet, Medicinska fakulteten, Institutionen för kliniska vetenskaper, Lund, Sektion II, Lungmedicin, allergologi och palliativ medicin, Hereditärt angioödem (HAE) – epidemiologi, genetik och patofysiologi, Originator
Zdroj: American Journal of Respiratory Cell and Molecular Biology. 73(4):612-622
Predmety: Medical and Health Sciences, Clinical Medicine, Respiratory Medicine and Allergy, Medicin och hälsovetenskap, Klinisk medicin, Lungmedicin och allergi
Popis: Allergic asthma is characterized by Type 2 inflammation and eosinophilia. Tartrate-resistant acid phosphatase 5 (TRAP5; also referred to as acid phosphatase 5 [ACP5]) is a metallophosphatase expressed by alveolar macrophages that dephosphorylates osteopontin, a phosphoglycoprotein with increased expression in asthma. To investigate the role of TRAP5 during asthma, we used a murine model of ovalbumin (OVA)-induced allergic airway inflammation as well as IL-33–induced airway inflammation, including Trap52/2 and wild-type (WT) mice. Histological analyses of murine lung revealed that OVA-induced inflammation induced the formation of inflammatory lesions and increased mucus production in both WT and Trap52/2 mice. However, lower cytokine levels (including IL-5 and IL-13) were detected by multiplex immunoassay in Trap52/2 mice after OVA-induced inflammation. Furthermore, quantitative PCR analysis detected different gene expression profiles of Trap52/2 /OVA mice, including upregulation of Il-17a and downregulation of Il-33. Lower eosinophil numbers were measured in BAL fluid of Trap52/2 /OVA mice using flow cytometry analysis, whereas immunofluorescence staining revealed a high eosinophil number in lung tissue of both groups with OVA challenge. In the IL-33 model of Type 2 inflammation, both WT and Trap52/2 mice showed similar inflammatory responses with regard to cytokine levels and cell recruitment patterns. In vitro, eosinophil chemotaxis was facilitated by nonphosphorylated, but not phosphorylated, osteopontin, an effect inhibited by an a4b1 integrin inhibitor. The results suggest that TRAP5 is important in the recruitment of immune cells, including eosinophils, as well as in shaping the profile and amplification of the inflammatory response during allergic airway inflammation. Thus, TRAP5 may serve as a therapeutic target in allergic asthma.
Prístupová URL adresa: https://doi.org/10.1165/rcmb.2024-0304OC
Databáza: SwePub
Popis
Abstrakt:Allergic asthma is characterized by Type 2 inflammation and eosinophilia. Tartrate-resistant acid phosphatase 5 (TRAP5; also referred to as acid phosphatase 5 [ACP5]) is a metallophosphatase expressed by alveolar macrophages that dephosphorylates osteopontin, a phosphoglycoprotein with increased expression in asthma. To investigate the role of TRAP5 during asthma, we used a murine model of ovalbumin (OVA)-induced allergic airway inflammation as well as IL-33–induced airway inflammation, including Trap52/2 and wild-type (WT) mice. Histological analyses of murine lung revealed that OVA-induced inflammation induced the formation of inflammatory lesions and increased mucus production in both WT and Trap52/2 mice. However, lower cytokine levels (including IL-5 and IL-13) were detected by multiplex immunoassay in Trap52/2 mice after OVA-induced inflammation. Furthermore, quantitative PCR analysis detected different gene expression profiles of Trap52/2 /OVA mice, including upregulation of Il-17a and downregulation of Il-33. Lower eosinophil numbers were measured in BAL fluid of Trap52/2 /OVA mice using flow cytometry analysis, whereas immunofluorescence staining revealed a high eosinophil number in lung tissue of both groups with OVA challenge. In the IL-33 model of Type 2 inflammation, both WT and Trap52/2 mice showed similar inflammatory responses with regard to cytokine levels and cell recruitment patterns. In vitro, eosinophil chemotaxis was facilitated by nonphosphorylated, but not phosphorylated, osteopontin, an effect inhibited by an a4b1 integrin inhibitor. The results suggest that TRAP5 is important in the recruitment of immune cells, including eosinophils, as well as in shaping the profile and amplification of the inflammatory response during allergic airway inflammation. Thus, TRAP5 may serve as a therapeutic target in allergic asthma.
ISSN:10441549
15354989
DOI:10.1165/rcmb.2024-0304OC