Study on the organization of cellular elements in the granulomatous lesion caused by chromoblastomycosis

Minotto, Renan; Edelweiss, Maria Isabel Albano; Scroferneker, Maria Lúcia

doi:10.1111/cup.13014

Cited by 7 publications

(5 citation statements)

References 16 publications

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“…Macrophages play central roles in host immune response against fungal infections ( 28 ). Likewise, these phagocytes are not only ubiquitous in CBM lesions but are also actively involved in the recognition of fungal cells and in the modulation of inflammatory responses against F. pedrosoi ( 4 , 29 , 30 ). In this context, we performed subsequent assays focused on macrophage-hyphae interaction, since we show here that hyphae are the F. pedrosoi infective morphotype most likely to be responsible for initiating the inflammatory response observed in CBM.…”

Section: Resultsmentioning

confidence: 99%

“…Macrophages are essential innate immunity cells that are critical for direct antifungal response. Macrophages, along with neutrophils and lymphocytes, are regularly observed within the chronic granulomatous lesions of CBM patients, displaying different degrees of maturation and activation, and they also form multinucleated giant cells that harbor fungi ( 29 , 30 ). In addition, F. pedrosoi cells can be detected in intracytoplasmic vacuoles of skin macrophages ( 61 ).…”

Section: Discussionmentioning

confidence: 99%

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The Major Chromoblastomycosis Etiologic Agent Fonsecaea pedrosoi Activates the NLRP3 Inflammasome

et al. 2017

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Fonsecaea pedrosoi is the main etiologic agent of chromoblastomycosis (CBM), one of the most prevalent subcutaneous mycosis in tropical and subtropical countries. CBM is a poorly characterized chronic infection that commonly starts after transcutaneous inoculation of conidia and saprophytic hyphae of F. pedrosoi. Recently, we have shown that unlike conidia, hyphae and muriform cells (the parasitic morphotype) of F. pedrosoi promotes an intense inflammatory response pattern in vivo, which comprises the production of an inflammasome-derived cytokine, IL-1β. Nonetheless, the mechanisms underlying IL-1β production and maturation upon F. pedrosoi infection and its functional output in the course of CBM remains unknown. We show here that F. pedrosoi hyphae, differently from conidia, induce IL-1β secretion in both bone marrow-derived dendritic cells and macrophages. Using inhibitors and knockout cells, we demonstrated that the mechanisms underlying IL-1β production by hyphae-infected macrophages were dependent on dectin-1, -2, and -3 receptors and the Syk-NF-kB signaling pathway. Furthermore, F. pedrosoi promoted a NLRP3-dependent inflammasome activation, which required potassium efflux, reactive oxygen species production, phagolysosomal acidification, and cathepsin B release as triggers. IL-1β processing and release was mediated primarily by caspase-1 and, to a lesser extent, by caspase-8-dependent cleavage. Finally, we showed using a murine CBM model that F. pedrosoi elicits a NLRP3-regulated IL-1β and interleukin-18 release in vivo, but without NLRP3 inflammasome activation interfering in the course of the experimental infection.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Major Chromoblastomycosis Etiologic Agent Fonsecaea pedrosoi Activates the NLRP3 Inflammasome

et al. 2017

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“…The species are differentiated through the conidiophores which are the spore like projections at the end of the branched hyphae. 1,2,5 What is common among them, aside from the black and brown pigment are the unique morphological and cellular plasticity that they manifest. Upon infection, celldifferentiation occurs and this leads to isodiametric swelling and cross-septation.…”

Section: Discussionmentioning

confidence: 99%

“…These changes form the muriform cells or the multinucleated giant cells with sclerotic bodies typically described as "copper pennies" upon histopathologic examination. 5,6 These muriform cells are directly associated with a marked granulomatous response with parakeratosis, pseudoepitheliomatous or pseudocarcinomatous hyperplasia, spongiosis, and increased lymphocytes. 1,2,5,7,8 Given the characteristic histopathological findings of muriform cells embedded in a granulomatous background, this leads to the scrutiny of misdiagnosis as leprosy and cutaneous tuberculosis.…”

Section: Discussionmentioning

confidence: 99%

Chromoblastomycosis, Overlooked and Undiagnosed: The Disease as a Mimic of other Neglected Tropical Diseases

Chamberlin¹,

Batac²,

Cubillan³

2019

Acta Med Philipp

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“…Initially, lesions develop as a papule that can further evolve into plaque, nodule, verrucous, or cicatricial appearance [27,30]. CBM lesions present a characteristic granulomatous reaction containing inflammatory infiltrates rich in neutrophils and macrophages forming multinucleated giant cells [31,32]. NETs released by neutrophils challenged with F. pedrosoi hyphae can kill fungal cells [33].…”

Section: Introductionmentioning

confidence: 99%

Zinc Starvation Induces Cell Wall Remodeling and Activates the Antioxidant Defense System in Fonsecaea pedrosoi

Santos,

Soares,

Oliveira

et al. 2024

JoF

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The survival of pathogenic fungi in the host after invasion depends on their ability to obtain nutrients, which include the transition metal zinc. This essential micronutrient is required to maintain the structure and function of various proteins and, therefore, plays a critical role in various biological processes. The host’s nutritional immunity limits the availability of zinc to pathogenic fungi mainly by the action of calprotectin, a component of neutrophil extracellular traps. Here we investigated the adaptive responses of Fonsecaea pedrosoi to zinc-limiting conditions. This black fungus is the main etiological agent of chromoblastomycosis, a chronic neglected tropical disease that affects subcutaneous tissues. Following exposure to a zinc-limited environment, F. pedrosoi induces a high-affinity zinc uptake machinery, composed of zinc transporters and the zincophore Pra1. A proteomic approach was used to define proteins regulated by zinc deprivation. Cell wall remodeling, changes in neutral lipids homeostasis, and activation of the antioxidant system were the main strategies for survival in the hostile environment. Furthermore, the downregulation of enzymes required for sulfate assimilation was evident. Together, the adaptive responses allow fungal growth and development and reveals molecules that may be related to fungal persistence in the host.

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Study on the organization of cellular elements in the granulomatous lesion caused by chromoblastomycosis

Abstract: The results indicated that the granuloma present in the cutaneous lesion of chromoblastomycosis is a mixed organized mycotic granuloma with high expression of the cellular components.

Cited by 7 publications

References 16 publications

The Major Chromoblastomycosis Etiologic Agent Fonsecaea pedrosoi Activates the NLRP3 Inflammasome

The Major Chromoblastomycosis Etiologic Agent Fonsecaea pedrosoi Activates the NLRP3 Inflammasome

Chromoblastomycosis, Overlooked and Undiagnosed: The Disease as a Mimic of other Neglected Tropical Diseases

Zinc Starvation Induces Cell Wall Remodeling and Activates the Antioxidant Defense System in Fonsecaea pedrosoi

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