Proinflammatory cytokine production by feline polymorphonuclear neutrophils after exposure to Microsporum canis (2023)

to suggest

small trace dogis a zoonotic dermatophyte that causes most cases of ringworm in dogs and cats (Weitzman and Summerbell, 1995; Chermette et al., 2008; Mignon and Monod, 2011). Since dermatophytes invade the tough keratinized skin structure, much effort has been devoted to characterizing secreted proteases as putative fungal virulence factors (Monod, 2008; Vermout et al., 2008), but few of them have been proven to be a causative agent of skin diseasesdog symbol(Descamps et al., 2002; Baldo et al., 2010; Bagut et al., 2012). In contrast, little attention has been paid to studying the host immune response to symbolEspecially other dermatophytes (Almeida, 2008, Mignon et al., 2008). Although dermatophytes reside on the surface of the skin, they can elicit an adaptive immune response. Cellular responses associated with delayed hypersensitivity (DTH) are known to correlate with clinical recovery and protection against reinfection (Calderon, 1989; Almeida, 2008; Mignon et al., 2008). The initial post-infection immunological events remain to be elucidated, including the role of innate immunity in mediating host-specific immune responses. The first epidermal cells encountered by dermatophytes during infection are keratinocytes, and a broad spectrum of cytokines can be produced when exposed to these fungi (Nakamura et al., 2002; Shiraki et al., 2006; Tani et al., 2007), including polymorphonuclear neutrophil (PMN) chemoattractants for IL-8 and proinflammatory TNFα (Nakamura et al., 2002). The first leukocytes to be recruited to sites of dermatophytosis infection are PMNs (Hay et al., 1988). Together with macrophages, these cells are known to be responsible for the elimination of dermatophytes (Calderon and Hay, 1987; Heddergott et al., 2012). Their potential role in inducing a specific immune response in dermatophytosis remains unknown, but can be reasonably assumed. Indeed, in other fungal and microbial infections, PMNs can initiate and regulate adaptive immune responses by interacting with dendritic cells and producing specific cytokines (Schaller et al., 2004; Megiovanni et al., 2006; Charmoy et al. et al., 2010) . The aim of this study was to assess the possible role of feline PMN in the early stagesdog symbolInfect. To this end, PMN was combined with variousdog symbolPMN-produced components and levels of specific cytokines were assessed.

partial fragment

Isolation of feline polymorphonuclear neutrophils

Cat blood is provided in good faith by veterinarians through blood donations conducted with the consent of the cat owner. The cats sampled were tame shorthair intact male or female young adult cats with no medical history. Clinical examination revealed no abnormalities. The cat tested negative for feline leukemia virus and feline immunodeficiency virus infection using the WITNESS® FeLV-FIV test (Prodivet, Eynatten, Belgium). Perform a fungal culture

PMNs produce TNFα, IL-1β and IL-8 after exposure todog symbolArthrospores

The amount of TNFα, IL-1β, IL-8 and IFNγ secreted by PMNs co-cultured with Arthrospores was assessed by capture ELISA. Stimulated PMNs produced significantly more TNFα (2.5-fold), IL-1β (8-fold) and IL-8 (25-fold) in culture supernatants compared to unstimulated PMNs, while IFNγ secretion was not affected. Stimulation Effects (Fig. 1) Cytokine responses assessed by ELISA were actually induced by arthrospores and not by potential endotoxin (LPS) contamination. Basically cytokines


The results obtained by ELISA showed that the response todog symbolUpon stimulation with live arthrospores, feline neutrophils secrete TNFα, IL-1β and IL-8, three proinflammatory cytokines. It has been proposed that PMNs play a protective role in other fungal infections by producing pro-inflammatory cytokines. in ain vitroIn an oral candidiasis model, the addition of human PMNs to the epithelium induced the production of IL-1α, IL-1β, TNFα and IL-8 (Schaller et al., 2004). commentParacoccidioides

Conflict of Interest Statement

Not a single one.

Thank you

This research was funded by3.4558.10 299vanResearch Funding Medical Sciences (FRSM).Yes. Yes and L.C. are scholarship recipients from FRIA (Fonds pour la Formation à la Recherche dans l'Industrie et dans l'Agriculture, 1000 Brussels, Belgium). ETB is a recipient of research grantsUniversity of ReunichiThe authors thank dr. L. Massart for the statistical analysis.

Quoted by (15)

  • Oxidative stress response in rats experimentally infected with Sporothrix schenckii

    2017, Microbial pathogenesis

    Quote excerpt:

    The current work suggests that rats affected by sporotrichosis may develop oxidative stress, as indicated by increased lipid peroxidation and antioxidant enzyme activity. Lipid peroxidation directly influences the pathogenesis of parasitic and fungal diseases [15,16], as well as the stimulation of pro-inflammatory cytokines during fungal infections [17,18]. The occurrence of lipid peroxidation in S. schenckii infection may increase proinflammatory cytokines, leading to membrane damage through the Fenton reaction, as observed in dogs with dermatophytosis [6].

    The aim of this study was to assess whether oxidative stress occurs in experimentally infected ratsSporotrichum schenckii,and its possible impact on the pathogenesis of diseases. Thirty rats were divided into two groups: group A (uninfected, n=18) and group B (infectedStreptococcus schenk,n = 21). Blood samples were collected on days 15, 30 and 40 post-infection (PI). Six rats in group A and seven rats in group B were bled at each sampling time. Measure TBARS (thiobarbituric acid reactive substances) levels in serum samples to assess lipid peroxidation. In addition, catalase (CAT) and superoxide dismutase (SOD) activities, known as biomarkers of antioxidant levels, were validated in whole blood. Serum levels of pro-inflammatory cytokines (IFN-γ, TNF-α and IL-6) were measured, indicating that these inflammatory mediators had higher levels in infected rats (P<0.001). Rats with sporotrichosis showed significantly higher (p<0.01) TBARS levels at 40 days post-infection compared to uninfected animals, the number of days increased significantly (p<0.01) and SOD activity increased by day 40 after infection (p<0.01). Infected rats had enlarged testes, granulomas in the testicular sac, granulomas in the liver, and follicular hyperplasia in the spleen. All tissues (testis, spleen and liver) showed inflammation associated with many fungal structures. These results suggest that the intense inflammatory response (serum and tissue) in sporotrichosis is a possible mechanism of redox imbalance and thus oxidative stress in experimentally infected rats.

  • Evaluation of Immunogenicity and Protective Efficacy of Microsporum Canis Secreted Components with Monophosphoryl Lipid A Adjuvant in a Guinea Pig Vaccine Study

    2015, Veterinary Microbiology

    Quote excerpt:

    A P-value <0.05 was considered statistically significant. Mycoplasma canis SC induced proinflammatory cytokine production in feline PMNs (Cambier et al., 2013) represented an attractive antigen to test in vaccine studies. These components were tested for their ability to elicit a DTH response in immunized guinea pigs, i.e. spontaneous recovery from experimental infection with M. canis.

    small trace dogis the most common dermatophyte in pets and is of zoonotic concern, but there is currently no effective vaccine to prevent dermatophytosis. The aim of this work was to assess the immunogenicity and protective efficacy of the secretory component (SC).dog symbolIn guinea pig vaccine studies as an experimental model, it was supplemented with monophosphoryl lipid A (MPLA). Animals were inoculated with SC in MPLA adjuvant, MPLA adjuvant alone or PBS 3 times every other week up to 42 days prior to inoculationdog symbolInfect. Weekly monitoring of the development of dermatophytosis symptoms and blinded assessment of dermatophytosis persistence. Antibody responses to SCs and levels of interferon (IFN) γ and interleukin 4 expressed in peripheral blood mononuclear cells were assessed during the study or at the end of the study, respectively. Animals receiving MPLA had significantly lower clinical scores than animals receiving PBS. However, no significant difference was observed between guinea pigs vaccinated SC vaccinated with MPLA adjuvant and those receiving MPLA alone. The results also showed that vaccination induced a strong antibody response against SC and an increase in IFNγ mRNA levels. Our results indicate that the MPLA adjuvant used in this vaccine study is self-inducingdog symbolInfect. Although they elicit delayed-type hypersensitivity in guinea pigs, SCs did not confer protection under the current experimental conditions.

  • Experimental model of dermatophytosis

    2021, dermatophytes and dermatophytosis

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    The newspaper then considers the morning and evening rush hours together as a single-mode bottleneck (all cars), with the same travelers sharing the same expected time. A timetable penalty function for positively determined morning departures and evening arrivals with specific properties shows that there is a user equilibrium in which commuters travel in the same order during the two peak periods. The results are used to illustrate user equilibriums in two cases: (i) commuters have uncorrelated morning and evening schedule preferences, and (ii) commuters must work fixed shifts but have flexibility in when to start. Finally, consider the special case of the car and public transport: commuters have the same desire during the morning and evening rush hours. Commuters should use the same pattern in both directions, and a full user balance solution reveals the number of commuters using cars and public transport and the time period between each peak in public transport use.

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Copyright © 2012 Elsevier B.V. All rights reserved.


What major cytokine is responsible for the stimulation of neutrophil production? ›

Outside the bone marrow, neutrophil production is also regulated by a cytokine network that involves interleukin (IL)-23 produced by phagocytes and IL-17 produced by T lymphocytes.

Do neutrophils make cytokines? ›

It is evident that neutrophils express/produce cytokines belonging to various families, mostly including pro-inflammatory/anti-inflammatory cytokines, chemokines, immunoregulatory cytokines, tumor necrosis factor (TNF) superfamily members, and angiogenic/fibrogenic factors.

What causes proinflammatory cytokines? ›

Proinflammatory cytokines are produced predominantly by activated macrophages and are involved in the up-regulation of inflammatory reactions. There is abundant evidence that certain pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α are involved in the process of pathological pain.

Do neutrophils release pro-inflammatory cytokines? ›

It is evident that neutrophils express/produce cytokines belonging to various families, mostly including pro-inflammatory/anti-inflammatory cytokines, chemokines, immunoregulatory cytokines, tumor necrosis factor (TNF) superfamily members, and angiogenic/fibrogenic factors.

What inflammatory cytokines are on neutrophils? ›

An important issue is that both cytokines and chemokines may also act as priming agents of neutrophils.
Neutrophil cytokines review.
Cytokines TypeExpressed by Neutrophils in Vitro
Proinflammatory cytokinesIL-1-α, IL-1-β
Anti-inflammatory cytokinesIL-1 receptor antagonist (IL-1Ra)
17 more rows

Why do neutrophils increase in inflammation? ›

Neutrophils dominate the early stages of inflammation and set the stage for repair of tissue damage by macrophages. These actions are orchestrated by numerous cytokines and the expression of their receptors, which represent a potential means for inhibiting selective aspects of inflammation.

What effect do cytokines have on neutrophils? ›

Under normal circumstances, cytokines, such as TNF-α, IL-1, IL-2, IL-6, and IL-8 trigger the neutrophil-endothelial cell adhesion, facilitating cells' migration to the inflamed site [14].

How do you reduce proinflammatory cytokine production? ›

One of the most effective of these mechanisms is the role of physical activity in reducing the production of pro-inflammatory cytokines due to strengthening the immune system. Other mechanisms that can affect adipose tissue include reducing inflammation in the tissue and finally improving hypoxia.

How do you treat proinflammatory cytokines? ›

Management and Treatment

First, your healthcare provider will give you medication to reduce inflammation. This may include corticosteroids or drugs that target specific cytokines (like siltuximab, tocilizumab and anakinra). Depending on your symptoms, other treatments may be necessary.

What happens when proinflammatory cytokines are released? ›

Interleukin (IL)-1 and tumor necrosis factor (TNF) are proinflammatory cytokines, and when they are administered to humans, they produce fever, inflammation, tissue destruction, and, in some cases, shock and death.

What stimulates the release of inflammatory cytokines? ›

During infection, bacterial and viral products, such as bacterial lipopolysaccharide (LPS), cause the release of cytokines from immune cells. These cytokines can reach the brain by several routes. Furthermore, cytokines, such as interleukin-1 (IL-1), are induced in neurons within the brain by systemic injection of LPS.

What cytokine attracts neutrophils to the site of infection? ›

Neutrophils are attracted to the site of infection by chemokines such as IL-8, CXCL1, and CXCL2 [50], and can cause epithelial damage. IL-8 is the most potent neutrophil chemoattractant, which is released by the epithelial cells lining the airways [46].

What cytokines affect neutrophils? ›

The pro-inflammatory cytokines IL-1α, IL-1β, IL-6, IL-16, IL-18, and macrophage migration inhibitory factor (MIF), along with enzymes released from neutrophil granules (including neutrophil elastase, myeloperoxidase, azurocidin, enolase-1, and lysozyme) [26], are believed to contribute to the immunopathogenesis of CSS ...

What cytokines attract neutrophils? ›

Neutrophils also release immunoregulatory cytokines such as IFN-γ, which recruits macrophages, and G-CSF, which ultimately stimulates neutrophil production and aids in extended neutrophil presence, and many other factors (reference Table 1 for more factors) [6].

What cytokine receptors are on neutrophils? ›

Important type II cytokine receptors on neutrophils are receptors for IFNα, IFNβ, IFNγ and the inhibitory IL-10 cytokine. Sharing of receptor chains between type II cytokine receptors is less common. Type I and type II cytokine receptors are involved in a number of neutrophil functions.

Which cytokine is responsible for the chemotaxis of neutrophils? ›

Interleukin 8

IL8, also known as neutrophil chemotactic factor or CXCL8, is primarily produced by macrophages, but can also be released by hepatocytes and other cells.


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