Publications by authors named "A Lauren R Goundry"

Article Synopsis
  • * In studies, neutrophils from susceptible BALB/c mice produced more NETs when infected compared to the more resistant C57BL/6 mice, who were better at phagocytosis and had genes associated with that process upregulated.
  • * The research suggests that the balance between NET formation and phagocytic activity plays a crucial role in how susceptible different mouse strains are to Leishmania infection, with specific neutrophil subsets contributing to
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Trypanosoma cruzi is the causative agent of Chagas disease, a chronic pathology that affects the heart and/or digestive system. This parasite invades and multiplies in virtually all nucleated cells, using a variety of host cell receptors for infection. T.

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The protozoan causes Human African Trypanosomiasis, also known as sleeping sickness, and penetrates the central nervous system, leading to meningoencephalitis. The Cathepsin L-like cysteine peptidase of has been implicated in parasite penetration of the blood-brain barrier and its activity is modulated by the chagasin-family endogenous inhibitor of cysteine peptidases (ICP). To investigate the role of ICP in bloodstream form, -null (Δ) mutants were generated, and lines re-expressing (Δ).

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Subtilisin proteases, found in all organisms, are enzymes important in the post-translational steps of protein processing. In Leishmania major and L. donovani, this enzyme has been described as essential to their survival; however, few compounds that target subtilisin have been investigated for their potential as an antileishmanial drug.

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Macrophages play critical roles in inflammation and defense against pathogens, as well as in the return to tissue homeostasis. Macrophage subpopulations displaying antagonistic phenotypes are generally classified as proinflammatory M1, implicated in antipathogen and antitumoral activities, or as anti-inflammatory M2, associated with tissue repair. Granulocytic and monocytic myeloid-derived suppressor cells recruited from the bone marrow to tissues and phagocytosis of apoptotic neutrophils can attenuate macrophage microbicidal activity.

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