Publications by authors named "Goundry A"

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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Visceral leishmaniasis is associated with hepato-splenomegaly and altered immune and hematological parameters in both preclinical animal models and humans. We studied mouse experimental visceral leishmaniasis caused by Leishmania infantum and Leishmania donovani in BALB/c mice using dual RNA-seq to investigate the transcriptional response of host and parasite in liver and spleen. We identified only 4 species-specific parasite expressed genes (SSPEGs; log2FC >1, FDR <0.

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is a protozoan parasite that causes visceral leishmaniasis, provoking liver and spleen tissue destruction that is lethal unless treated. The parasite replicates in macrophages and modulates host microbicidal responses. We have previously reported that neutrophil elastase (NE) is required to sustain intracellular growth in macrophages through the induction of interferon beta (IFN-β).

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Trypanosoma brucei rhodesiense is one of the causative agents of Human African Trypanosomiasis (HAT), known as sleeping sickness. The parasite invades the central nervous system and causes severe encephalitis that is fatal if left untreated. We have previously identified ecotin-like inhibitors of serine peptidases, named ISPs, in trypanosomatid parasitic protozoa.

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Leishmania major is the causative agent of the neglected tropical disease, cutaneous leishmaniasis. In the mouse, protective immunity to Leishmania is associated with inflammatory responses. Here, we assess the dynamics of the inflammatory responses at the lesion site during experimental long-term, low-dose intradermal infection of the ear, employing noninvasive imaging and genetically modified L.

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Article Synopsis
  • Helminth parasites pose significant health issues worldwide, with limited treatment options primarily designed for animals and restricted due to ineffective screening systems.
  • This study investigates the use of bioluminescence imaging with luminol to visualize immune responses to filarial parasites in mice, aiming to differentiate between live and dead worms for future drug screening.
  • While the technique detects immune responses to early infections, it struggles to reveal adult worm presence, indicating a need for more targeted reagents to enhance live imaging capabilities.
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Background: Sexually transmitted infections (STIs) such as chlamydia and gonorrhoea are largely symptomless diseases which, left untreated, can result in serious complications including infertility. Fertility problems currently affect approximately one in seven couples in the UK and there is increasing demand for couples seeking reproductive technologies. Young people are at greatest risk of contracting STIs, therefore this study aimed to identify young people's knowledge and beliefs about the link between untreated STIs and infertility.

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Leishmania ISPs are ecotin-like natural peptide inhibitors of trypsin-family serine peptidases, enzymes that are absent from the Leishmania genome. This led to the proposal that ISPs inhibit host serine peptidases and we have recently shown that ISP2 inhibits neutrophil elastase, thereby enhancing parasite survival in murine macrophages. In this study we show that ISP1 has less serine peptidase inhibitory activity than ISP2, and in promastigotes both are generally located in the cytosol and along the flagellum.

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Stress exerts profound inhibitory effects on reproductive function by suppressing the pulsatile release of gonadotrophin-releasing hormone (GnRH) and therefore luteinising hormone (LH). This effect is mediated in part via the corticotrophin-releasing factor (CRF) system, although another potential mechanism is via GABAergic signalling within the medial preoptic area (mPOA) because this has known inhibitory influences on the GnRH pulse generator and shows increased activity during stress. In the present study, we investigated the role of the preoptic endogenous GABAergic system in stress-induced suppression of the GnRH pulse generator.

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