{
  "abstract": "Neutrophils are essential for host defense against most invasive fungal pathogens, yet their role in cryptococcosis remains paradoxical. Neutropenia is not a recognized risk factor for cryptococcal disease, and an early study reported that neutrophil depletion improves survival in mice, supporting the prevailing view that these cells are dispensable. Here we re-examined this question using Ly6G-specific depletion strategies. Contrary to prior reports, neutrophil-depleted mice infected with Cryptococcus neoformans succumbed significantly more rapidly than isotype-treated controls. Accelerated mortality occurred without any increase in pulmonary fungal burden at 24h, 48h, or day 7, or in brain and spleen at day 7, indicating host-mediated rather than pathogen-driven death. This phenotype was independent of mouse genetic background, depletion antibody, inoculum, and fungal strain. Within 24h, neutrophil depletion provoked an early chemokine and IL-17A response, followed by pronounced pulmonary accumulation of inflammatory monocytes and macrophages by day 7. Strikingly, the increased mortality associated with neutrophil depletion was completely absent in Ccr2-/- mice, implicating CCR2-dependent inflammatory responses in disease severity. Together, these findings reveal a previously underappreciated protective function of neutrophils during cryptococcosis, whereby they constrain inflammatory monocyte-associated immunopathology and promote host survival independently of measurable changes in fungal burden.",
  "abstract_shown": true,
  "affiliations": [
    "The University of Tennessee Health Science Center"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "name": "M. C. Harden-Pruitt"
    },
    {
      "name": "R. G. Rebekah"
    },
    {
      "affs": [
        0
      ],
      "name": "C. R. Hole"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/9empycy3zqk38.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.10.26.762039",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.10.26.762039v1.full",
  "id": "9empycy3zqk38",
  "issns": [
    "2692-8205"
  ],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.10.26.762039v1",
  "language": "en",
  "licence": "CC-BY-ND",
  "licence_label": "CC BY-ND",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "microbiology"
    ],
    [
      "heading",
      "Article"
    ],
    [
      "openalex",
      "2713|Fungal Infections and Studies"
    ]
  ],
  "openalex": "W7223830387",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.10.26.762039v1.full.pdf",
  "pmcid": "PMC13733911",
  "pmid": "42990408",
  "published": "2026-10-26",
  "publisher": "Cold Spring Harbor Laboratory Preprints",
  "ris": "https://research.draconitic.com/paper/9empycy3zqk38.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:29:54Z",
      "native_id": "10.64898/2026.10.26.762039",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.10.26.762039v1"
    },
    {
      "first_seen": "2026-11-08T12:23:35Z",
      "native_id": "PMC13733911",
      "source": "pmc",
      "url": "https://doi.org/10.64898/2026.10.26.762039"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:microbiology",
      "subfield": "microbiology"
    }
  ],
  "title": "Neutrophils Restrain CCR2-Dependent Monocyte Immunopathology During Pulmonary Cryptococcosis.",
  "title_text": "Neutrophils Restrain CCR2-Dependent Monocyte Immunopathology During Pulmonary Cryptococcosis.",
  "type": "preprint",
  "updated_at": "2026-11-08T12:23:35Z",
  "url": "https://research.draconitic.com/paper/9empycy3zqk38",
  "venue": "bioRxiv",
  "versions": []
}