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        <datestamp>2026-10-01T17:34:05Z</datestamp>
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          <dc:title>&lt;p&gt;Raw data 2.&lt;/p&gt;</dc:title>
          <dc:creator>Pasinee Sangsiwarit (23748827)</dc:creator>
          <dc:creator>Wisitsak Phoksawat (25157794)</dc:creator>
          <dc:creator>Nattiya Teawtrakul (6490541)</dc:creator>
          <dc:creator>Sonwit Phanabamrung (22918172)</dc:creator>
          <dc:creator>Parama Budmala (25157797)</dc:creator>
          <dc:creator>Ariya Chindamporn (430921)</dc:creator>
          <dc:creator>Pratsanee Hiengrach (6208559)</dc:creator>
          <dc:subject>Microbiology</dc:subject>
          <dc:subject>Cell Biology</dc:subject>
          <dc:subject>Molecular Biology</dc:subject>
          <dc:subject>Physiology</dc:subject>
          <dc:subject>Environmental Sciences not elsewhere classified</dc:subject>
          <dc:subject>Ecology</dc:subject>
          <dc:subject>Sociology</dc:subject>
          <dc:subject>Immunology</dc:subject>
          <dc:subject>Biological Sciences not elsewhere classified</dc:subject>
          <dc:subject>Developmental Biology</dc:subject>
          <dc:subject>Hematology</dc:subject>
          <dc:subject>remain incompletely understood</dc:subject>
          <dc:subject>impaired host defense</dc:subject>
          <dc:subject>ex vivo &lt;/</dc:subject>
          <dc:subject>neutrophil extracellular trap</dc:subject>
          <dc:subject>higher fungal burdens</dc:subject>
          <dc:subject>pythium insidiosum &lt;/</dc:subject>
          <dc:subject>including killing activity</dc:subject>
          <dc:subject>div &gt;&lt; p</dc:subject>
          <dc:subject>using neutrophils isolated</dc:subject>
          <dc:subject>thalassemia patients exposed</dc:subject>
          <dc:subject>insidiosum &lt;/</dc:subject>
          <dc:subject>killing activity</dc:subject>
          <dc:subject>significantly higher</dc:subject>
          <dc:subject>neutrophil functions</dc:subject>
          <dc:subject>phagocytic activity</dc:subject>
          <dc:subject>neutrophils isolated</dc:subject>
          <dc:subject>isolated neutrophils</dc:subject>
          <dc:subject>underlying mechanisms</dc:subject>
          <dc:subject>tropical regions</dc:subject>
          <dc:subject>threatening disease</dc:subject>
          <dc:subject>therapeutic strategies</dc:subject>
          <dc:subject>significantly diminished</dc:subject>
          <dc:subject>phagocytic capacity</dc:subject>
          <dc:subject>patient group</dc:subject>
          <dc:subject>often life</dc:subject>
          <dc:subject>iron overload</dc:subject>
          <dc:subject>increased susceptibility</dc:subject>
          <dc:subject>immune dysregulation</dc:subject>
          <dc:subject>human pythiosis</dc:subject>
          <dc:subject>highly susceptible</dc:subject>
          <dc:subject>healthy group</dc:subject>
          <dc:subject>healthy controls</dc:subject>
          <dc:subject>functional alterations</dc:subject>
          <dc:subject>findings demonstrate</dc:subject>
          <dc:subject>contributed mechanistically</dc:subject>
          <dc:subject>causative agent</dc:subject>
          <dc:description>&lt;div&gt;&lt;p&gt;Patients with β-thalassemia are highly susceptible to &lt;i&gt;Pythium insidiosum&lt;/i&gt;, the causative agent of human pythiosis, a severe and often life-threatening disease in tropical regions. This vulnerability has been associated with iron overload and immune dysregulation. However, the underlying mechanisms of impaired host defense, especially in neutrophils, remain incompletely understood. This study investigated neutrophil function in response to &lt;i&gt;P. insidiosum&lt;/i&gt; zoospores, using neutrophils isolated from β-thalassemia patients and comparing their responses with those from healthy controls. &lt;i&gt;Ex vivo&lt;/i&gt; study, isolated neutrophils were co-incubated with &lt;i&gt;P. insidiosum&lt;/i&gt; zoospores, then evaluated for pathogen-killing activity, neutrophil extracellular trap (NET) formation, and phagocytic capacity. Neutrophils isolated from β-thalassemia patients exhibited significantly reduced fungicidal activity, as indicated by higher fungal burdens in comparison with healthy controls. In addition, NET formation was significantly diminished in the neutrophils isolated from the patient group, reflecting impaired extracellular pathogen containment. Similarly, phagocytic activity in the neutrophils isolated from the healthy group was significantly higher than in the patient group. These findings demonstrate that impairments of neutrophil functions, including killing activity, NET formation, and phagocytic capacity, contributed mechanistically to the increased susceptibility to &lt;i&gt;P. insidiosum&lt;/i&gt; in patients with β-thalassemia. This study highlights the importance of targeting innate immune dysfunction in the development of therapeutic strategies for human pythiosis.&lt;/p&gt;&lt;/div&gt;</dc:description>
          <dc:date>2026-10-01T17:34:01Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.1371/journal.pone.0359846.s002</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/_p_Raw_data_2_p_/34048513</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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