Evidence for eosinophil recruitment, leukotriene B4 production and mast cell hyperplasia following Toxocara canis infection in rats

Carlos, D.; Machado, E.R.; Paula, L. De; Sá-Nunes, A.; Sorgi, C.A.; Jamur, Maria Célia; Oliver, Constance; Lima, W.T.; Faccioli, L.H.

doi:10.1590/s0100-879x2011000400008

Cited by 8 publications

(7 citation statements)

References 15 publications

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“…Because nematodes cannot synthesize AA [26], they must utilize the host’s AA to synthesize and release AA metabolites which are important to their survival and virulence. A previous study showed that the level of leukotriene was upregulated in T. canis infection at 3, 6, 18 and 24 dpi in Wistar rats [27]. Nematode-derived signals can directly induce leukotriene production by eosinophils and that leukotriene signaling is a major contributor to nematode-induced eosinophil accumulation in the lungs [28].…”

Section: Discussionmentioning

confidence: 99%

Serum metabolomic alterations in Beagle dogs experimentally infected with Toxocara canis

et al. 2019

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Background Toxocara canis, a globally distributed roundworm, can cause debilitating disease in dogs and humans; however, little is known about the metabolomic response of the hosts to T. canis infection. There is an increasing need to understand the metabolic mechanisms underlying the pathogenesis of T. canis infection in dogs. Here, we examined the metabolomic changes in Beagle dogsʼ serum following T. canis infection using LC-MS/MS. Results The metabolic profiles of Beagle dogsʼ serum were determined at 12 h, 24 h, 10 d and 36 d after oral infection with 300 infectious T. canis eggs by LC-MS/MS. We tested whether the T. canis-associated differentially abundant metabolites could distinguish the serum of infected dogs from controls, as measured by the area under the receiver operating characteristic (ROC) curve (AUC). The differentially expressed metabolites were further evaluated by principal components analysis and pathway enrichment analysis. A total of 5756 and 5299 ions were detected in ESI+ and ESI− mode, respectively. ROC curve analysis revealed nine and five metabolite markers, at 12 hpi and 24 hpi to 36 dpi, respectively, with potential diagnostic value for toxocariasis. The levels of taurocholate, estradiol, prostaglandins and leukotriene were significantly changed. Primary bile acid biosynthesis pathway, steroid hormone biosynthesis pathway and biosynthesis of unsaturated fatty acids pathway were significantly altered by T. canis infection. Conclusions These findings show that T. canis infection can induce several changes in the dog serum metabolome and that the metabolic signature associated with T. canis infection in dogs has potential for toxocariasis diagnosis.

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Section: Discussionmentioning

confidence: 99%

Serum metabolomic alterations in Beagle dogs experimentally infected with Toxocara canis

et al. 2019

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“…Mucosal and connective tissue MCs play important roles in defense against intestinal parasitosis, as it has been reported in infections with Trichinella spiralis ( 227 , 228 ), Strongyloides ratti ( 229 , 230 ) and Toxocara canis ( 231 ), among others ( 232 , 233 ). In addition, the MCs seem to play a crucial role in the decrease in the fertility rate of Heligmosomoides polygyrus ( 234 ).…”

Section: Antimicrobial Roles Of Mast Cellsmentioning

confidence: 98%

Responses of Mast Cells to Pathogens: Beneficial and Detrimental Roles

et al. 2021

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Mast cells (MCs) are strategically located in tissues close to the external environment, being one of the first immune cells to interact with invading pathogens. They are long living effector cells equipped with different receptors that allow microbial recognition. Once activated, MCs release numerous biologically active mediators in the site of pathogen contact, which induce vascular endothelium modification, inflammation development and extracellular matrix remodeling. Efficient and direct antimicrobial mechanisms of MCs involve phagocytosis with oxidative and non-oxidative microbial destruction, extracellular trap formation, and the release of antimicrobial substances. MCs also contribute to host defense through the attraction and activation of phagocytic and inflammatory cells, shaping the innate and adaptive immune responses. However, as part of their response to pathogens and under an impaired, sustained, or systemic activation, MCs may contribute to tissue damage. This review will focus on the current knowledge about direct and indirect contribution of MCs to pathogen clearance. Antimicrobial mechanisms of MCs are addressed with special attention to signaling pathways involved and molecular weapons implicated. The role of MCs in a dysregulated host response that can increase morbidity and mortality is also reviewed and discussed, highlighting the complexity of MCs biology in the context of host-pathogen interactions.

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“…Similar to PGD2, cysLTs also bind and activate two GPCRs, CysLT1 and CysLT2g. LTB4 is secreted in small quantities by activated mast cells and has an important role in the recruitment of neutrophils, eosinophils, and effector T lymphocytes (Goodarzi et al 2003;Carlos et al 2011). Leukotrienes function locally on the vascular endothelium by promoting rolling and recruitment of neutrophils and eosinophils, which contribute to host defense against bacterial infections (Malaviya and Abraham 2000;Carlos et al 2011).…”

Section: Mast Cell Mediatorsmentioning

confidence: 99%

“…LTB4 is secreted in small quantities by activated mast cells and has an important role in the recruitment of neutrophils, eosinophils, and effector T lymphocytes (Goodarzi et al 2003;Carlos et al 2011). Leukotrienes function locally on the vascular endothelium by promoting rolling and recruitment of neutrophils and eosinophils, which contribute to host defense against bacterial infections (Malaviya and Abraham 2000;Carlos et al 2011). In general, mast cell-released eicosanoids participate in the regulation of vascular permeability, smooth muscle contraction, the recruitment of immune effector cells, and they alter the patterns of antigen presentation (Boyce 2005).…”

Section: Mast Cell Mediatorsmentioning

confidence: 99%

Mast Cell Function

Silva

Jamur

Oliver

2014

J Histochem Cytochem.

464

221

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Since first described by Paul Ehrlich in 1878, mast cells have been mostly viewed as effectors of allergy. It has been only in the past two decades that mast cells have gained recognition for their involvement in other physiological and pathological processes. Mast cells have a widespread distribution and are found predominantly at the interface between the host and the external environment. Mast cell maturation, phenotype and function are a direct consequence of the local microenvironment and have a marked influence on their ability to specifically recognize and respond to various stimuli through the release of an array of biologically active mediators. These features enable mast cells to act as both first responders in harmful situations as well as to respond to changes in their environment by communicating with a variety of other cells implicated in physiological and immunological responses. Therefore, the critical role of mast cells in both innate and adaptive immunity, including immune tolerance, has gained increased prominence. Conversely, mast cell dysfunction has pointed to these cells as the main offenders in several chronic allergic/inflammatory disorders, cancer and autoimmune diseases. This review summarizes the current knowledge of mast cell function in both normal and pathological conditions with regards to their regulation, phenotype and role.

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Evidence for eosinophil recruitment, leukotriene B4 production and mast cell hyperplasia following Toxocara canis infection in rats

Cited by 8 publications

References 15 publications

Serum metabolomic alterations in Beagle dogs experimentally infected with Toxocara canis

Serum metabolomic alterations in Beagle dogs experimentally infected with Toxocara canis

Responses of Mast Cells to Pathogens: Beneficial and Detrimental Roles

Mast Cell Function

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