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Effects of human immunoglobulins on Cryptococcus neoformans morphology and proteome

ABSTRACT: Cryptococcus neoformans (Cn) is the main cause of fungal meningitis (CM) in people living with HIV. Perturbations in levels of normal immunoglobulin (Ig) levels are observed in these individuals, but their association with CM pathogenesis is unclear. Here, we investigated the physical and biological effects of normal human immunoglobulins (not elicited by known cryptococcal infection), IgM, IgG, and IgA on Cn (strain H99). Each isotype affected the growth, surface morphology, and proteome of Cn. However, IgA had the most prominent effect. It induced growth inhibition after 24 h of co-culture with Cn, altered the structural organization of capsular fibers, and significantly reduced protein synthesis and proteins associated with intracellular glucuronoxylomannan (GXM) synthesis, such as those mediating transport of sugar precursors to Golgi and the cyclic AMP (cAMP) pathway. Together with prior data showing an association between reduced plasma IgA and HIV-associated CM, our findings suggest that the influence on human IgA on Cn pathogenesis warrants further investigation.

INSTRUMENT(S):

ORGANISM(S): Cryptococcus Neoformans

SUBMITTER: Marlon D M Santos

LAB HEAD: Taiane N de Souza

PROVIDER: PXD072710 | Pride | 2026-01-26

REPOSITORIES: Pride

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			Action	DRS
	20230811_150123_Haroldo_28_1.raw	Raw
	20230811_150123_Haroldo_28_1.yada.ctxt	Other
	20230811_150123_Haroldo_28_2.raw	Raw
	20230811_150223_Haroldo_29_1.raw	Raw
	20230811_150223_Haroldo_29_3.raw	Raw

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Project description:Assessment of the extent to which the altered profiles of miRNA expression influence viral replication and latency, as well as the efficiency of host defenses, may be useful for understanding the basis of the HIV-1-related alterations in cellular physiology and immunologic control. To this end, three patient groups were enrolled. One group consisted of subjects who were classified as M-CM-)lite control long-term non-progressors (M-CM-)LTNP). A second study group was HIV-1-positive subjects, who were antiretroviral therapy naive. A third group was multiply exposed to HIV-1, but uninfected (MEU). This study allowed us to investigate the existence of a CD4+T- lymphocytes miRNAs signature able to discriminate among different stages of HIV-1 infection, and to evaluate whether the exposure to HIV-1 antigen is sufficient to change the miRNA profile. MicroRNAs inhibit HIV-1 expression by either modulating host innate immunity or by directly interfering with viral mRNAs. We evaluated the expression of 377 miRNAs in CD4+ T cells from HIV-1 M-CM-)lite LTNP (M-CM-)LTNP), naive and multiply exposed uninfected individuals (MEU) and we observed that the M-CM-)LTNP patients clustered with naive, whereas all MEU subjects grouped together. The discriminatory power of miRNAs showed that 21 miRNAs significantly differentiated M-CM-)LTNP from MEU and 23 miRNAs distinguished naive from MEU, while only 1 (miR-155) discriminated M-CM-)LTNP from naive. We proposed that miRNA expression may discriminate between HIV-1 infected and exposed but negative individuals. Analysis of miRNAs expression after exposure of healthy CD4+T cells to gp120 in vitro confirmed our hypothesis that a miRNA profile could be the result not only of a productive infection, but also of the exposure to HIV-1 products that leave a signature in immune cells. The comparison of normalized Dicer and Drosha expression in ex vivo and in vitro conditions revealed that these enzymes did not affect the change of miRNA profiles, supporting the existence of a Dicer-independent biogenesis pathway. We have compared miRNA profiles of CD4+ T-lymphocytes from 18 HIV-1-exposed subjects with healthy CD4+ T-lymphocytes following exposure to gp120 using a RT-qPCR assay.

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Effects of human immunoglobulins on Cryptococcus neoformans morphology and proteome

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